[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 100 of about 1511
1. Acién P, Abad M, Mayol MJ, Garcia S, Garde J: Primary squamous cell carcinoma of the ovary associated with endometriosis. Int J Gynaecol Obstet; 2010 Jan;108(1):16-20
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary squamous cell carcinoma of the ovary associated with endometriosis.
  • OBJECTIVE: To analyze the clinical, therapeutic, and pathologic features of published cases presenting primary squamous cell carcinoma (SCC) of the ovary associated with endometriosis.
  • METHODS: A case report, 15 cases of infiltrating SCC of the ovary associated with or arising from endometriosis, and 1 case of synchronous carcinoma in situ in the cervix and ovary from a review of the literature were studied.
  • RESULTS: Young age, advanced stage of the disease, and hypogastric pain were frequent at the time of diagnosis.
  • The tumor was associated with 80% patient mortality in the first few months.
  • Adjuvant chemotherapy with paclitaxel and carboplatin or cisplatin appeared to improve the results.
  • The best therapeutic results are obtained with paclitaxel and carboplatin or cisplatin after radical surgery.
  • [MeSH-major] Carcinoma, Squamous Cell / pathology. Endometriosis / complications. Ovarian Neoplasms / pathology
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Age Factors. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Chemotherapy, Adjuvant / methods. Cisplatin / administration & dosage. Female. Humans. Middle Aged. Neoplasm Staging. Neoplasms, Multiple Primary. Paclitaxel / administration & dosage. Prognosis. Uterine Cervical Neoplasms / pathology


2. Yarlett N, Waters WR, Harp JA, Wannemuehler MJ, Morada M, Bellcastro J, Upton SJ, Marton LJ, Frydman BJ: Activities of DL-alpha-difluoromethylarginine and polyamine analogues against Cryptosporidium parvum infection in a T-cell receptor alpha-deficient mouse model. Antimicrob Agents Chemother; 2007 Apr;51(4):1234-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Activities of DL-alpha-difluoromethylarginine and polyamine analogues against Cryptosporidium parvum infection in a T-cell receptor alpha-deficient mouse model.
  • The in vivo effectiveness of a series of conformationally restricted polyamine analogues alone and selected members in combination with DL-alpha-difluoromethylarginine against Cryptosporidium parvum infection in a T-cell receptor alpha-deficient mouse model was tested.
  • Polyamine analogues were selected from the extended bis(ethyl)-sym-homospermidine or bis(ethyl)-spermine backbone having cis or trans double bonds at the center of the molecule.
  • The cis isomers were found to have significantly greater efficacy in both preventing and curing infection in a mouse model than the trans polyamine analogues when tested in a T-cell receptor alpha-deficient mouse model.
  • When tested in combination with DL-alpha-difluoromethylarginine, the cis-restricted analogues were found to be more effective in preventing oocyst shedding.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. (L)-ARGININE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Med Chem. 1998 Nov 19;41(24):4723-32 [9822543.001]
  • [Cites] Mol Biochem Parasitol. 1997 Sep;88(1-2):35-42 [9274865.001]
  • [Cites] Diagn Microbiol Infect Dis. 1999 Jul;34(3):245-62 [10403104.001]
  • [Cites] Pflugers Arch. 1999 Sep;438(4):445-51 [10519136.001]
  • [Cites] Wiad Parazytol. 1999;45(2):125-8 [16886452.001]
  • [Cites] Mol Biochem Parasitol. 2007 Apr;152(2):170-80 [17289169.001]
  • [Cites] Biochem J. 2000 Jan 1;345 Pt 1:69-75 [10600640.001]
  • [Cites] J Neurochem. 2000 May;74(5):2201-8 [10800966.001]
  • [Cites] Antimicrob Agents Chemother. 2000 Oct;44(10):2891-4 [10991882.001]
  • [Cites] J Med Chem. 2001 Feb 1;44(3):390-403 [11462979.001]
  • [Cites] J Med Chem. 2001 Feb 1;44(3):404-17 [11462980.001]
  • [Cites] Microbes Infect. 2002 Aug;4(10):1047-58 [12191655.001]
  • [Cites] Mini Rev Med Chem. 2002 Dec;2(6):553-63 [12370040.001]
  • [Cites] Biochem J. 2003 Feb 15;370(Pt 1):19-28 [12477380.001]
  • [Cites] Biochem Biophys Res Commun. 2003 May 16;304(4):605-11 [12727196.001]
  • [Cites] Biochem J. 2003 Nov 15;376(Pt 1):1-14 [13678416.001]
  • [Cites] Pediatr Res. 1978 Aug;12(8):830-3 [683740.001]
  • [Cites] Methods Enzymol. 1983;94:158-61 [6621384.001]
  • [Cites] Biochem J. 1988 Jan 1;249(1):33-6 [3124824.001]
  • [Cites] Biochem J. 1988 Oct 1;255(1):197-202 [3143356.001]
  • [Cites] Crit Rev Microbiol. 1988;16(2):113-59 [3067976.001]
  • [Cites] Biochem J. 1989 May 15;260(1):1-10 [2673211.001]
  • [Cites] Cancer Res. 1989 Nov 15;49(22):6226-31 [2804970.001]
  • [Cites] Am J Physiol. 1990 Apr;258(4 Pt 1):G576-84 [2333971.001]
  • [Cites] FASEB J. 1993 May;7(8):653-61 [8500690.001]
  • [Cites] Science. 1994 Feb 18;263(5149):966-9 [7906055.001]
  • [Cites] Bioessays. 1993 Aug;15(8):561-6 [8135771.001]
  • [Cites] FEMS Microbiol Lett. 1994 May 1;118(1-2):45-9 [8013881.001]
  • [Cites] J Am Vet Med Assoc. 1994 Jul 1;205(1):86-91 [7928557.001]
  • [Cites] Life Sci. 1995;56(26):2319-30 [7791519.001]
  • [Cites] Infect Immun. 1996 May;64(5):1854-7 [8613403.001]
  • [Cites] Am J Vet Res. 1996 Nov;57(11):1586-8 [8915434.001]
  • [Cites] J Parasitol. 1997 Aug;83(4):746-50 [9267420.001]
  • [Cites] Eur J Biochem. 1999 Feb;259(3):933-8 [10092884.001]
  • (PMID = 17242149.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI40320; United States / NIAID NIH HHS / AI / AI43931; United States / NIAID NIH HHS / AI / AI45739
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiprotozoal Agents; 0 / Polyamines; 69955-43-7 / alpha-(difluoromethyl)arginine; 94ZLA3W45F / Arginine
  • [Other-IDs] NLM/ PMC1855503
  •  go-up   go-down


3. Ramoni S, Cusini M, Gaiani F, Arancio L, Alessi E: Penile intraepithelial carcinoma treated with imiquimod 1% in an HIV-positive patient. J Dermatolog Treat; 2009;20(3):177-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Penile intraepithelial carcinoma treated with imiquimod 1% in an HIV-positive patient.
  • [MeSH-major] Aminoquinolines / therapeutic use. Carcinoma in Situ / drug therapy. Cell Transformation, Neoplastic / pathology. HIV Infections / diagnosis. Penile Neoplasms / drug therapy
  • [MeSH-minor] Administration, Topical. Anti-HIV Agents / therapeutic use. Condylomata Acuminata / complications. Condylomata Acuminata / drug therapy. Condylomata Acuminata / pathology. Dose-Response Relationship, Drug. Drug Administration Schedule. Follow-Up Studies. Humans. Immunohistochemistry. Male. Neoplasm Staging. Penile Diseases / complications. Penile Diseases / drug therapy. Penile Diseases / pathology. Risk Assessment. Time Factors. Treatment Outcome

  • Genetic Alliance. consumer health - HIV.
  • MedlinePlus Health Information. consumer health - HIV/AIDS.
  • Hazardous Substances Data Bank. Imiquimod .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19016064.001).
  • [ISSN] 1471-1753
  • [Journal-full-title] The Journal of dermatological treatment
  • [ISO-abbreviation] J Dermatolog Treat
  • [Language] eng
  • [Publication-type] Case Reports; Letter
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Aminoquinolines; 0 / Anti-HIV Agents; 99011-02-6 / imiquimod
  •  go-up   go-down


Advertisement
4. Hancock AA, Buckner SA, Brune ME, Esbenshade TA, Ireland LM, Katwala S, Milicic I, Meyer MD, Kerwin JF Jr, Williams M: Preclinical pharmacology of fiduxosin, a novel alpha(1)-adrenoceptor antagonist with uroselective properties. J Pharmacol Exp Ther; 2002 Feb;300(2):478-86
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Fiduxosin (3-[4-((3aR,9bR)-cis-9-methoxy-1,2,3,3a,4,9b-hexahydro-[1]-benzopyrano[3,4-c]pyrrol-2-yl)butyl]-8-phenyl-pyrazino[2',3':4,5] thieno-[3,2-d]pyrimidine-2,4(1H,3H)-dione; ABT-980) was tested in radioligand binding assays, isolated tissue bioassays, intraurethral pressure (IUP) tests in isoflurane-anesthetized dogs, and blood pressure analyses in spontaneously hypertensive rats (SHR).
  • Fiduxosin had higher affinity for cloned human alpha(1a)- (0.16 nM) and alpha(1d)-adrenoceptors (0.92 nM) in radioligand binding studies compared with alpha(1b)-adrenoceptors (25 nM) or in isolated tissue bioassays [pA(2) values of 8.5-9.6 for alpha(1A)-receptors in rat vas deferens or canine prostate strips, 8.9 at alpha(1D)-adrenoceptors (rat aorta), compared with 7.1 at alpha(1B)-adrenoceptors (rat spleen)].
  • The area under the curve (AUC(0-->60) min) for the hypotensive response was dose related with a log index value for fiduxosin of 5.23, indicating a selectivity of 770-fold comparing IUP to MAP effects.
  • Preferential antagonism of alpha(1A)- and alpha(1D)- versus alpha(1B)-adrenoceptors in vitro, blockade of putative alpha(1L)-sites in vitro, and selective effects on lower urinary tract function versus blood pressure in vivo by fiduxosin suggest the potential utility of this compound for the treatment of BPH.
  • [MeSH-major] Adrenergic alpha-1 Receptor Antagonists. Adrenergic alpha-Antagonists / pharmacology. Heterocyclic Compounds, 3-Ring / pharmacology. Pyrimidinones / pharmacology. Urinary Tract / drug effects
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Dogs. Humans. In Vitro Techniques. Male. Mice. Muscle Contraction / drug effects. Muscle, Smooth / drug effects. Muscle, Smooth, Vascular / drug effects. Prostatic Hyperplasia / drug therapy. Rabbits. Radioligand Assay. Rats. Rats, Inbred SHR. Urethra / drug effects. Urethra / physiology. Urodynamics / drug effects. Vas Deferens / drug effects

  • BindingDB. BindingDB .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11805207.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-1 Receptor Antagonists; 0 / Adrenergic alpha-Antagonists; 0 / Heterocyclic Compounds, 3-Ring; 0 / Pyrimidinones; W9O92HYT6I / fiduxosin
  •  go-up   go-down


5. Huang Z, Timerbaev AR, Keppler BK, Hirokawa T: Determination of cisplatin and its hydrolytic metabolite in human serum by capillary electrophoresis techniques. J Chromatogr A; 2006 Feb 17;1106(1-2):75-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Cisplatin is for a long time in clinical use as efficient antitumor drug.
  • The success in cisplatin-based chemotherapy, however, strongly depends on how careful the drug's dosages are monitored in order to reduce severe side-effects and overcome cellular resistance.
  • The use of micellar electrokinetic chromatography with direct UV detection is described for the determination of intact cisplatin in human serum.
  • The main product of drug's hydrolytic metabolism, cis-diammineaquachloroplatinum(II), was quantified using capillary zone electrophoresis in combination with indirect UV detection and on-line transient isotachophoresis preconcentration.
  • The detection limits of platinum species studied were about 2-3 micromol l(-1) that allows the proposed methods to be applied for quantification of the administered levels of cisplatin as well as drug's active metabolite.

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16203005.001).
  • [ISSN] 0021-9673
  • [Journal-full-title] Journal of chromatography. A
  • [ISO-abbreviation] J Chromatogr A
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


6. Shariat SF, Chade DC, Karakiewicz PI, Scherr DS, Dalbagni G: Update on intravesical agents for non-muscle-invasive bladder cancer. Immunotherapy; 2010 May;2(3):381-92
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Update on intravesical agents for non-muscle-invasive bladder cancer.
  • Major controversies still exist with regard to the indication, type and regimen of intravesical therapy for non-muscle-invasive bladder cancer.
  • Other areas of controversy are the criteria for response/failure of treatment and for decisions regarding secondary intravesical therapy versus radical cystectomy.
  • In this article, we analyze the different intravesical therapeutic strategies and compare their safety and efficacy.
  • Well-designed clinical trials have found that the addition of bacillus Calmette-Guerin (BCG) to transurethral resection (TUR) decreases the risk for both disease recurrence and progression.
  • These encouraging results are sustained even in patients with recurrent or aggressive disease, including patients whose prior intravesical chemotherapy has failed.
  • Most investigators believe that the efficacy of BCG therapy can be maximized with maintenance therapy.
  • Mitomycin C (MMC), the most commonly used intravesical chemotherapy to date, decreases the risk of disease recurrence but not disease progression when used after TUR compared with TUR alone.
  • For patients at high risk of disease progression, BCG with maintenance therapy should be the preferred primary intravesical therapeutic strategy.
  • However, MMC can be considered as a viable alternative for patients with papillary tumors (no carcinoma in situ) that are at low or intermediate risk of disease progression.
  • Combination intravesical therapy may be more successful than single-agent strategies.
  • Intravesical therapy failures indicate the need to include radical cystectomy as an option in the management decision.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. BCG Vaccine / therapeutic use. Cystectomy / methods. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Administration, Intravesical. Combined Modality Therapy. Humans. Mitomycin / administration & dosage. Mitomycin / therapeutic use. Taxoids / administration & dosage. Taxoids / therapeutic use. Treatment Outcome

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. MITOMYCIN C .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Epidemiol. 2000 Jul;53(7):676-80 [10941943.001]
  • [Cites] Cochrane Database Syst Rev. 2000;(4):CD001986 [11034738.001]
  • [Cites] Anticancer Res. 2001 Jan-Feb;21(1B):765-9 [11299841.001]
  • [Cites] J Natl Cancer Inst. 2001 Apr 18;93(8):597-604 [11309436.001]
  • [Cites] J Autoimmun. 2001 May;16(3):235-40 [11334488.001]
  • [Cites] J Urol. 2001 May;165(5):1488-91 [11342902.001]
  • [Cites] Acta Oncol. 2001;40(2-3):371-90 [11441942.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3193-8 [12149290.001]
  • [Cites] J Urol. 2002 Nov;168(5):1964-70 [12394686.001]
  • [Cites] J Urol. 2003 Jan;169(1):90-5 [12478111.001]
  • [Cites] J Clin Oncol. 2003 Feb 15;21(4):697-703 [12586808.001]
  • [Cites] Cytokine. 2003 Jan 7;21(1):17-26 [12668155.001]
  • [Cites] J Urol. 2003 May;169(5):1702-5 [12686812.001]
  • [Cites] J Urol. 2003 May;169(5):1706-8 [12686813.001]
  • [Cites] Eur Urol. 2003 Oct;44(4):429-34 [14499676.001]
  • [Cites] J Urol. 2004 Jan;171(1):153-7 [14665865.001]
  • [Cites] Eur Urol. 2004 Mar;45(3):304-13; author reply 313 [15036675.001]
  • [Cites] J Urol. 1999 Apr;161(4):1124-7 [10081852.001]
  • [Cites] Surgery. 1970 Jul;68(1):158-63; discussion 163-4 [10483463.001]
  • [Cites] Am J Clin Oncol. 2004 Oct;27(5):522-8 [15596924.001]
  • [Cites] J Urol. 2005 May;173(5):1518-25 [15821471.001]
  • [Cites] J Urol. 2005 Jul;174(1):86-91; discussion 91-2 [15947584.001]
  • [Cites] Eur Urol. 2005 Aug;48(2):333-8 [15963631.001]
  • [Cites] J Urol. 2005 Oct;174(4 Pt 1):1242-7 [16145378.001]
  • [Cites] Urology. 2005 Dec;66(6 Suppl 1):4-34 [16399414.001]
  • [Cites] BJU Int. 2006 May;97(5):997-1001 [16542342.001]
  • [Cites] J Urol. 2006 Jun;175(6):2004-10 [16697786.001]
  • [Cites] J Urol. 2000 Apr;163(4):1124-9 [10737480.001]
  • [Cites] Eur Urol. 2009 Aug;56(2):247-56 [19409692.001]
  • [Cites] Urology. 2010 Jan;75(1):134-7 [19913890.001]
  • [Cites] J Urol. 2004 Jun;171(6 Pt 1):2186-90, quiz 2435 [15126782.001]
  • [Cites] BJU Int. 2004 Mar;93(4):485-90 [15008714.001]
  • [Cites] BJU Int. 2004 Mar;93(4):491-4 [15008715.001]
  • [Cites] Aging Cell. 2004 Aug;3(4):195-208 [15268753.001]
  • [Cites] Immunology. 1966 Feb;10(2):127-36 [5932899.001]
  • [Cites] Lancet. 1969 Apr 5;1(7597):697-9 [4182654.001]
  • [Cites] J Natl Cancer Inst. 1972 Jul;49(1):119-30 [4338767.001]
  • [Cites] J Urol. 1976 Aug;116(2):180-3 [820877.001]
  • [Cites] Cancer. 1983 Apr 1;51(7):1323-6 [6337700.001]
  • [Cites] Urology. 2004 Apr;63(4):682-6; discussion 686-7 [15072879.001]
  • [Cites] J Urol. 2000 Jan;163(1):73-8 [10604317.001]
  • [Cites] Eur Urol. 2000;37 Suppl 1:33-6 [10575271.001]
  • [Cites] Cancer. 1987 Aug 1;60(3):326-33 [3594369.001]
  • [Cites] J Urol. 1987 Aug;138(2):295-8 [3298694.001]
  • [Cites] Prog Clin Biol Res. 1989;310:35-50 [2672021.001]
  • [Cites] J Urol. 1990 Jul;144(1):68-71; discussion 71-2 [2113590.001]
  • [Cites] N Engl J Med. 1991 Oct 24;325(17):1205-9 [1922207.001]
  • [Cites] Urol Clin North Am. 1992 Aug;19(3):529-39 [1636237.001]
  • [Cites] Urol Clin North Am. 1992 Aug;19(3):573-80 [1636241.001]
  • [Cites] J Urol. 1993 Apr;149(4):744-8 [8455235.001]
  • [Cites] Urol Int. 1993;51(2):67-72 [8351757.001]
  • [Cites] J Urol. 1995 Mar;153(3 Pt 2):934-41 [7853578.001]
  • [Cites] J Urol. 1995 May;153(5):1444-50 [7714962.001]
  • [Cites] Int J Urol. 1996 Mar;3(2):98-100; discussion 101 [8689518.001]
  • [Cites] J Urol. 1996 Sep;156(3):962-6 [8709374.001]
  • [Cites] J Urol. 1996 Dec;156(6):1934-40, discussion 1940-1 [8911360.001]
  • [Cites] J Urol. 1997 Jul;158(1):62-7 [9186324.001]
  • [Cites] Clin Cancer Res. 1998 Jan;4(1):139-43 [9516962.001]
  • [Cites] Eur Urol. 1998;33(3):285-8; discussion 289 [9555553.001]
  • [Cites] Urology. 1985 Feb;25(2):119-23 [3881870.001]
  • [Cites] J Urol. 1985 Jul;134(1):40-7 [3892050.001]
  • [Cites] Urol Int. 1986;41(4):254-9 [3538593.001]
  • [Cites] J Clin Oncol. 1987 Mar;5(3):441-9 [3546618.001]
  • [Cites] Urology. 2006 Jun;67(6):1216-23 [16765182.001]
  • [Cites] J Clin Oncol. 2006 Jun 20;24(18):2729-34 [16782913.001]
  • [Cites] J Clin Oncol. 2006 Jul 1;24(19):3075-80 [16809732.001]
  • [Cites] Urol Oncol. 2006 Jul-Aug;24(4):344-8 [16818189.001]
  • [Cites] J Urol. 2007 Jan;177(1):75-9; discussion 79 [17162005.001]
  • [Cites] ScientificWorldJournal. 2006;6:2617-25 [17619739.001]
  • [Cites] Eur Urol. 2007 Oct;52(4):1123-29 [17383080.001]
  • [Cites] Eur Urol. 2007 Nov;52(5):1398-406 [17485161.001]
  • [Cites] J Urol. 2007 Dec;178(6):2314-30 [17993339.001]
  • [Cites] Urol Oncol. 2008 Mar-Apr;26(2):137-40 [18312931.001]
  • [Cites] J Urol. 2008 Jun;179(6):2164-9 [18423745.001]
  • [Cites] Urology. 2008 Jun;71(6):1161-5 [18279920.001]
  • [Cites] Eur Urol. 2008 Nov;54(5):971-3 [18585842.001]
  • [Cites] Scand J Urol Nephrol Suppl. 2008 Sep;(218):12-20 [19054893.001]
  • [Cites] J Urol. 2009 Mar;181(3):1040-5 [19150551.001]
  • [Cites] BJU Int. 2009 May;103(10):1368-74 [19338566.001]
  • [Cites] Eur Urol. 2000 Apr;37(4):470-7 [10765079.001]
  • [ErratumIn] Immunotherapy. 2014;6(11):1238
  • (PMID = 20635902.001).
  • [ISSN] 1750-7448
  • [Journal-full-title] Immunotherapy
  • [ISO-abbreviation] Immunotherapy
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA082088; United States / NCI NIH HHS / CA / T32 CA082088
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BCG Vaccine; 0 / Taxoids; 15H5577CQD / docetaxel; 50SG953SK6 / Mitomycin
  • [Other-IDs] NLM/ NIHMS643681; NLM/ PMC4247174
  •  go-up   go-down


7. Tse GM, Yeung DK, King AD, Cheung HS, Yang WT: In vivo proton magnetic resonance spectroscopy of breast lesions: an update. Breast Cancer Res Treat; 2007 Sep;104(3):249-55
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In vivo proton magnetic resonance spectroscopy ((1)H-MRS) has been demonstrated to be successful in the differentiation of benign and malignant breast lesions in a non-invasive manner by detecting increased levels of composite choline (Cho) compounds.
  • Currently there is molecular evidence of increased Cho metabolism in breast cancer cells.
  • Most test cases were infiltrating duct carcinoma, but infiltrating lobular, medullary, mucinous and adenoid cystic carcinomas were also positive by (1)H-MRS.
  • Large lesional size is a pre-requisite for (1)H-MRS testing, and technical problems account for some of the false negative results.
  • Another potential of (1)H-MRS is to assess patients' response to neoadjuvant chemotherapy.
  • In ductal carcinoma in situ, the results of (1)H-MRS on the limited number of cases were negative.
  • Normal breast tissue was almost always negative by (1)H-MRS, whereas, lactating breast tissue showed positivity with a slightly different spectrum on further analysis.
  • With the clinical use of stronger field MR scanners and better coils, the sensitivity of (1)H-MRS may be further improved.
  • With these improvements, (1)H-MRS may potentially be useful in detection of smaller malignant lesions, characterization of malignant lesions into non-invasive or invasive, and as an invaluable tool in disease progression monitoring.
  • [MeSH-major] Breast Neoplasms / diagnosis. Breast Neoplasms / pathology. Magnetic Resonance Spectroscopy / methods
  • [MeSH-minor] Breast / pathology. Carcinoma / metabolism. Carcinoma, Ductal, Breast / diagnosis. Carcinoma, Ductal, Breast / pathology. Choline / metabolism. Disease Progression. False Positive Reactions. Female. Humans. Protons. Reproducibility of Results. Sensitivity and Specificity

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CHOLINE CHLORIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17051424.001).
  • [ISSN] 0167-6806
  • [Journal-full-title] Breast cancer research and treatment
  • [ISO-abbreviation] Breast Cancer Res. Treat.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Protons; N91BDP6H0X / Choline
  • [Number-of-references] 36
  •  go-up   go-down


8. Okuno M, Kojima S, Matsushima-Nishiwaki R, Tsurumi H, Muto Y, Friedman SL, Moriwaki H: Retinoids in cancer chemoprevention. Curr Cancer Drug Targets; 2004 May;4(3):285-98
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Retinoids in cancer chemoprevention.
  • We review the therapeutic and preventive applications of a retinoid analog (vitamin A and its derivatives) for human cancers.
  • Chemoprevention of cancer is an intervention in the carcinogenic process by chemical agents that block or reverse the malignant transformation of cells.
  • Retinoids are prime candidates for cancer chemoprevention since cancer is characterized by abnormal growth with a lack of differentiation, which could be modified by retinoids.
  • A number of experimental and clinical studies have been performed in the past two decades with retinoids showing that they inhibit or reverse the carcinogenic process in some organs, including hematological malignancy as well as premalignant and malignant lesions in the oral cavity, head and neck, breast, skin and liver.
  • We particularly focus upon the therapeutic application of all-trans RA (atRA) to acute promyelocytic leukemia (APL) and on the preventive approach to hepatocellular carcinoma (HCC) by a synthetic retinoid analog, acyclic retinoid.
  • PML-RAR alpha works as a dominant negative receptor in the leukemic cells, interfering with the normal function of RAR alpha and/or PML, which in turn results in the arrest of cell maturation at the stage of promyelocytes.
  • AtRA therapy has become standard in the treatment of APL.
  • Acyclic retinoid suppresses the phosphorylation of RXR alpha, restores its function in the presence of its endogenous ligand, 9-cis RA, and thereby induces apoptosis of the cancer cells.
  • Eradication of (pre)malignant clones ('clonal deletion') from the liver is suggested as a mechanism of the chemopreventive effect.
  • Further development of more effective retinoids as well as their use in combination with other classes of anticancer agents including immunopreventive drugs like interferons may provide strategies for cancer prevention.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Neoplasms / prevention & control. Retinoids / therapeutic use

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15134535.001).
  • [ISSN] 1568-0096
  • [Journal-full-title] Current cancer drug targets
  • [ISO-abbreviation] Curr Cancer Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Retinoids; 0 / Transcription Factors
  • [Number-of-references] 85
  •  go-up   go-down


9. Bairati I, Meyer F, Gélinas M, Fortin A, Nabid A, Brochet F, Mercier JP, Têtu B, Harel F, Mâsse B, Vigneault E, Vass S, del Vecchio P, Roy J: A randomized trial of antioxidant vitamins to prevent second primary cancers in head and neck cancer patients. J Natl Cancer Inst; 2005 Apr 6;97(7):481-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A randomized trial of antioxidant vitamins to prevent second primary cancers in head and neck cancer patients.
  • BACKGROUND: Although low dietary intakes of antioxidant vitamins and minerals have been associated with higher risks of cancer, results of trials testing antioxidant supplementation for cancer chemoprevention have been equivocal.
  • We assessed whether supplementation with antioxidant vitamins could reduce the incidence of second primary cancers among patients with head and neck cancer.
  • METHODS: We conducted a multicenter, double-blind, placebo-controlled, randomized chemoprevention trial among 540 patients with stage I or II head and neck cancer treated by radiation therapy between October 1, 1994, and June 6, 2000.
  • Supplementation with alpha-tocopherol (400 IU/day) and beta-carotene (30 mg/day) or placebo began on the first day of radiation therapy and continued for 3 years after the end of radiation therapy.
  • Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs).
  • RESULTS: After a median follow-up of 52 months, second primary cancers and recurrences of the first tumor were diagnosed in 113 and 119 participants, respectively.
  • The effect of supplementation on the incidence of second primary cancers varied over time.
  • Similarly, the rate of having a recurrence or second primary cancer was higher during (HR = 1.86, 95% CI = 1.27 to 2.72) but lower after (HR = 0.71, 95% CI = 0.33 to 1.53) supplementation with alpha-tocopherol.
  • The proportion of participants free of second primary cancer overall after 8 years of follow-up was similar in both arms.
  • CONCLUSIONS: alpha-Tocopherol supplementation produced unexpected adverse effects on the occurrence of second primary cancers and on cancer-free survival.
  • [MeSH-minor] Adult. Aged. Anticarcinogenic Agents / administration & dosage. Anticarcinogenic Agents / adverse effects. Confounding Factors (Epidemiology). Double-Blind Method. Drug Administration Schedule. Female. Humans. Incidence. Male. Middle Aged. Neoplasm Recurrence, Local / prevention & control. Odds Ratio. Proportional Hazards Models. Radiotherapy / adverse effects. Survival Analysis. Treatment Failure

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • MedlinePlus Health Information. consumer health - Head and Neck Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. VITAMIN E .
  • Hazardous Substances Data Bank. BETA-CAROTENE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Natl Cancer Inst. 2005 Apr 6;97(7):468-70 [15812064.001]
  • (PMID = 15812073.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Antioxidants; 01YAE03M7J / beta Carotene; H4N855PNZ1 / alpha-Tocopherol
  •  go-up   go-down


10. Kassouf W, Kamat AM: Current state of immunotherapy for bladder cancer. Expert Rev Anticancer Ther; 2004 Dec;4(6):1037-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current state of immunotherapy for bladder cancer.
  • Bacillus Calmette-Guerin (BCG) has been shown to be the most effective agent for the treatment of superficial bladder cancer since its approval by the US Food and Drug Administration for the treatment of carcinoma in situ of the bladder in 1990.
  • Recently, augmentation of BCG immunotherapy with interferon-alpha2b and other agents is emerging as salvage therapy for those patients who fail initial treatment.
  • This review summarizes the role of various immunotherapeutic agents in the treatment of bladder cancer, with special emphasis on the appropriate administration and schedule of BCG therapy as well as salvage with the combination of BCG with interferon-alpha2b.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Antineoplastic Agents / therapeutic use. BCG Vaccine / therapeutic use. Interferon-alpha / therapeutic use. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / immunology
  • [MeSH-minor] Carcinoma in Situ / drug therapy. Carcinoma in Situ / immunology. Cytosine / analogs & derivatives. Cytosine / therapeutic use. Drug Administration Schedule. Garlic / chemistry. Humans. Interleukins / therapeutic use. Plant Extracts / therapeutic use. Prognosis. Recombinant Proteins. Salvage Therapy. Vitamins / therapeutic use

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15606331.001).
  • [ISSN] 1744-8328
  • [Journal-full-title] Expert review of anticancer therapy
  • [ISO-abbreviation] Expert Rev Anticancer Ther
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents; 0 / BCG Vaccine; 0 / Interferon-alpha; 0 / Interleukins; 0 / Plant Extracts; 0 / Recombinant Proteins; 0 / Vitamins; 8J337D1HZY / Cytosine; 99210-65-8 / interferon alfa-2b; J57CTF25XJ / bropirimine
  • [Number-of-references] 89
  •  go-up   go-down


11. Mitchell LA, Grant DF, Melchert RB, Petty NM, Kennedy RH: Linoleic acid metabolites act to increase contractility in isolated rat heart. Cardiovasc Toxicol; 2002;2(3):219-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Previous in vivo studies in dogs suggest that the 9,10-monoepoxide of linoleic acid (9,10-cis-epoxyoctadecenoic acid [9,10-EOA]) has toxic cardiovascular effects that result in death at higher doses.
  • More recent work with rabbit renal proximal tubule cells suggests that the 12,13-metabolites of linoleic acid are more toxic than the 9,10-isomers.
  • As indicated by peak left intraventricular pressure and/or +dP/dt(max), all three of the agents elicited moderate increases in contractile function that peaked within 10 20 min.
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Blood Pressure / physiology. Heart Rate / drug effects. Heart Rate / physiology. In Vitro Techniques. Male. Oleic Acids / metabolism. Oleic Acids / physiology. Rats. Rats, Sprague-Dawley

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. LINOLEIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12665667.001).
  • [ISSN] 1530-7905
  • [Journal-full-title] Cardiovascular toxicology
  • [ISO-abbreviation] Cardiovasc. Toxicol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 12,13-dihydroxyoctadecenoic acid; 0 / 12,13-epoxy-9-octadecenoic acid; 0 / Oleic Acids; 9KJL21T0QJ / Linoleic Acid
  •  go-up   go-down


12. Ivanov S, Ivanov S: [Chemoimmunoterapy in combination with radiotherapy for treatment of stage III B cervical cancer]. Akush Ginekol (Sofiia); 2005;44(2):17-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Chemoimmunoterapy in combination with radiotherapy for treatment of stage III B cervical cancer].
  • We wanted to examine the tolerability and the toxicity of the chemoimmunotherapy in combination with radiotherapy in patients with stage III B cervical cancer.
  • Sixteen patients were selected for examination and the experience of the Gynecological Cancer Center in Sidney was summarized as well.
  • We used cisplatin in dose from 10 to 20 mg/m2 intravenously weekly, 5-Fluoruracil/5 Fu/500 mg/m2--24 hours infusion, weekly, interferon-alpha--2a 3MU subcutaneously for 3 days course weekly and 13 cis-retinoic acid 0.5 mg/kg daily by month together with 8 weeks period of radiotherapy after the end of the radiotherapy these medicaments were given for another 4 weeks.
  • In conclusion from our small experience the cisplatin--15 mg/m2, 5-Fu-500 mg/m2 weekly, interferon alpha--2a 3MU subcutaneously for 3 days course weekly and 13-cis-retinoic acid 0.5 mg/kg daily in combination with radiotherapy for stage III B cervical cancer we can say that and the dose is tolerated extremely well.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Uterine Cervical Neoplasms / drug therapy. Uterine Cervical Neoplasms / radiotherapy
  • [MeSH-minor] Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents / administration & dosage. Cisplatin / administration & dosage. Combined Modality Therapy. Drug Administration Schedule. Female. Fluorouracil / administration & dosage. Humans. Infusions, Intravenous. Injections, Subcutaneous. Interferon-alpha / administration & dosage. Neoplasm Staging. Recombinant Proteins. Tretinoin / administration & dosage


13. Schwartz PE: The management of serous papillary uterine cancer. Curr Opin Oncol; 2006 Sep;18(5):494-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The management of serous papillary uterine cancer.
  • PURPOSE OF REVIEW: Uterine papillary serous cancer is an extremely aggressive cancer, the optimum management of which is still being determined.
  • It is important to understand advances that have been made in 2005 regarding the molecular biology, diagnosis, and management of this deadly disease.
  • RECENT FINDINGS: The main themes in the literature regarding uterine papillary serous cancer are that a potential precursor lesion, serous endometrial intraepithelial carcinoma, has been recognized as an early form of the disease.
  • A variety of molecular biologically important markers have now been identified, including p53, HER2/neu, IL-6, kallikrein 6, and claudin-4, some of which may be susceptible to molecularly targeted therapy.
  • Systematic surgical staging is necessary before additional therapy is recommended.
  • Stage I uterine papillary serous cancer requires aggressive treatment, including surgery, chemotherapy, and radiation therapy for successful treatment.
  • The most effective management of advanced stage disease remains to be resolved.
  • SUMMARY: Serous endometrial intraepithelial carcinoma should be treated as a form of uterine papillary serous cancer.
  • Multimodality therapy is required for the successful management of early stage uterine papillary serous cancer.
  • Advanced disease is often unresponsive to conventional therapy.
  • Molecularly targeted therapies are now being introduced into the management of this disease.
  • [MeSH-major] Carcinoma, Papillary / therapy. Endometrial Neoplasms / therapy. Uterine Neoplasms / therapy
  • [MeSH-minor] Biomarkers, Tumor / blood. Female. Humans. Prognosis


14. Farrell N, Povirk LF, Dange Y, DeMasters G, Gupta MS, Kohlhagen G, Khan QA, Pommier Y, Gewirtz DA: Cytotoxicity, DNA strand breakage and DNA-protein crosslinking by a novel transplatinum compound in human A2780 ovarian and MCF-7 breast carcinoma cells. Biochem Pharmacol; 2004 Sep 1;68(5):857-66
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytotoxicity, DNA strand breakage and DNA-protein crosslinking by a novel transplatinum compound in human A2780 ovarian and MCF-7 breast carcinoma cells.
  • Cisplatin, cis-[PtCl2(NH3)2], is commonly utilized in various combination chemotherapy protocols for the treatment of both ovarian and breast cancer while the corresponding trans isomer is therapeutically inactive.
  • This work describes efforts to elucidate the cellular mechanism of action of a novel trans-platinum compound, trans-(dichloroamminethiazole)platinum(II) (ATZ), which demonstrates antiproliferative and cytotoxic effects against both MCF-7 human breast and A2780 human ovarian carcinoma cells in culture.
  • Dye exclusion studies revealed a 50-70% loss in cell viability within the first 12 h of drug treatment in both cell lines.
  • Binding of ATZ to DNA, as estimated by atomic absorption spectroscopy, was similar for the two cell lines and was almost completely reversed 24 h after drug removal.
  • However, neither the extent of DNA strand breakage nor that of DNA protein crosslinking was sufficient to explain the different drug sensitivity in the two cell lines.
  • At 24 and 48 h after exposure of MCF-7 cells to high concentrations of ATZ, the formation of DNA-topoisomerase I complexes is detected, coincident with a high degree of apoptosis.
  • These studies suggest that ATZ has the capacity to interfere with topoisomerase I in the tumor cell, a function not evident in cis-platinum-based drugs.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. DNA Damage / drug effects. DNA, Neoplasm / drug effects. Organoplatinum Compounds / pharmacology
  • [MeSH-minor] Animals. Breast Neoplasms / pathology. Cell Aging / drug effects. Cell Division / drug effects. Cell Survival / drug effects. Cross-Linking Reagents / pharmacology. DNA Topoisomerases, Type I / metabolism. Female. Humans. Ovarian Neoplasms / pathology. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15294448.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA40615
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cross-Linking Reagents; 0 / DNA, Neoplasm; 0 / Organoplatinum Compounds; 0 / trans-(dichloroamminethiazole)platinum(II); EC 5.99.1.2 / DNA Topoisomerases, Type I
  •  go-up   go-down


15. Trias I, Algaba F, Condom E, Español I, Seguí J, Orsola I, Villavicencio H, García Del Muro X: Small cell carcinoma of the urinary bladder. Presentation of 23 cases and review of 134 published cases. Eur Urol; 2001 Jan;39(1):85-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell carcinoma of the urinary bladder. Presentation of 23 cases and review of 134 published cases.
  • OBJECTIVE: To investigate the morphological diagnostic criteria and biology of the urinary bladder small cell carcinoma (SCC).
  • METHODS: Study of 23 cases of bladder SCC, looking for the clinical presentation, pathological features and evolution, and review of 134 previously published cases.
  • RESULTS: The SCC is infrequent (0.48-1%), 50% of them have areas of transitional cell carcinoma, supporting the metaplastic theory.
  • The classic small cell morphology is the best diagnostic criterion.
  • An early metastatic incidence (56%) with a high mortality rate (68.7%), mostly before 2 years after the diagnosis, is the typical evolution.
  • Only the patients with additional cis-platinum-based chemotherapy have better prognosis.
  • CONCLUSION: The pathologist should watch out for the presence of SCC and the urologist should consider the possibility of combined treatment for these cases.
  • [MeSH-major] Carcinoma, Small Cell. Urinary Bladder Neoplasms


16. Van der Mey M, Boss H, Couwenberg D, Hatzelmann A, Sterk GJ, Goubitz K, Schenk H, Timmerman H: Novel selective phosphodiesterase (PDE4) inhibitors. 4. Resolution, absolute configuration, and PDE4 inhibitory activity of cis-tetra- and cis-hexahydrophthalazinones. J Med Chem; 2002 Jun 6;45(12):2526-33
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel selective phosphodiesterase (PDE4) inhibitors. 4. Resolution, absolute configuration, and PDE4 inhibitory activity of cis-tetra- and cis-hexahydrophthalazinones.
  • Recently, we reported that 4-catechol-substituted cis-(+/-)-4a,5,6,7,8,8a-hexa- and cis-(+/-)-4a,5,8,8a-tetrahydro-2H-phthalazin-1-ones show potent inhibition of phosphodiesterase (PDE4) activity, while the corresponding trans racemic mixtures exhibit only weak to moderate activity.
  • To determine the absolute configuration and PDE4 inhibitory activity of the individual cis-enantiomers, several optically active phthalazinones have been synthesized.
  • The enantiomers of the various gamma-keto acids, used as starting materials, were resolved in a classical way by the formation of diastereomeric salts, and each was converted to optically active phthalazinone in an enantioselective manner.
  • The absolute configuration of the (+)-enantiomer of cis-hexahydrophthalazinone (+)-12 was determined by X-ray crystallography.
  • In the present series of hexa- and tetrahydrophthalazinones, stereoselectivity for PDE4 inhibition is observed; the cis-(+)-enantiomers of the phthalazinones display high inhibitory activity, whereas their (-)-counterparts exhibit only weak to moderate activity.
  • It is likely that all cis-(+)-phthalazinones have a (4aS,8aR)-configuration and vice versa for the cis-(-)-analogues.
  • [MeSH-major] 3',5'-Cyclic-AMP Phosphodiesterases / antagonists & inhibitors. Adamantane / chemical synthesis. Anti-Inflammatory Agents, Non-Steroidal / chemical synthesis. Benzoates / chemical synthesis. Enzyme Inhibitors / chemical synthesis. Phthalazines / chemical synthesis
  • [MeSH-minor] Administration, Oral. Animals. Crystallography, X-Ray. Cyclic Nucleotide Phosphodiesterases, Type 4. Edema / drug therapy. Female. Humans. In Vitro Techniques. Mice. Molecular Conformation. Neutrophils / drug effects. Neutrophils / enzymology. Stereoisomerism. Structure-Activity Relationship

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12036361.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-adamantan-2-yl-4-(3,4-dimethoxyphenyl)-4a,5,8,8a-tetrahydro-2H-phthalazin-1-one; 0 / 4-(4-(3,4-diethoxyphenyl)-1oxo-4a,5,8,8a-tetrahydro-1H-phthalazin-2-yl)benzoic acid; 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Benzoates; 0 / Enzyme Inhibitors; 0 / Phthalazines; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4; PJY633525U / Adamantane
  •  go-up   go-down


17. Modok S, Scott R, Alderden RA, Hall MD, Mellor HR, Bohic S, Roose T, Hambley TW, Callaghan R: Transport kinetics of four- and six-coordinate platinum compounds in the multicell layer tumour model. Br J Cancer; 2007 Jul 16;97(2):194-200
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Transport kinetics of four- and six-coordinate platinum compounds in the multicell layer tumour model.
  • Four-coordinate (Pt(II)) platinum-based anticancer drugs are widely used in primary or palliative chemotherapy and produce considerable efficacy in certain clinical applications, for example testicular cancer.
  • However, in many cancers the Pt(II) drugs are beset by poor efficacy mainly due to suboptimal pharmacokinetic properties.
  • Consequently, the six-coordinate (Pt(IV)) class of Pt drugs were developed to improve platinum efficacy by (i) increasing stability, (ii) reducing reactivity, (iii) increasing lipophilicity, and (iv) nuclear targeting.
  • However, comparatively little information is available on the pharmacokinetic properties of these compounds within solid tumour tissue.
  • In the present study, the distribution and fluxes of [(14)C]-labelled [PtCl(2)(en)] (where en stands for ethane-1,2-diamine) and cis,trans-[PtCl(2)(OH)(2)(en)] drugs were determined in the multicell layer (MCL) tumour model comprising colon cancer cells.
  • Flux data were analysed by mathematical modelling of drug diffusion and cellular uptake in the transport system.
  • The flux of the Pt(IV) compound through the MCL was not significantly different to that of the Pt(II) drug nor were the diffusion coefficient or tissue uptake; the latter confirmed with elemental imaging analysis by synchrotron radiation induced X-ray emission.
  • However, the flux of the Pt(IV) through the MCL was increased by hydrostatic pressure, thereby demonstrating the potential to target cancer cells further away from the vessels with six-coordinate platinum drugs.
  • [MeSH-minor] Biological Transport. Cell Line, Tumor. Humans. Kinetics. Models, Biological

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Pharmacol. 1996 Jul 12;52(1):7-14 [8678910.001]
  • [Cites] Mol Biother. 1990 Dec;2(4):235-41 [2288724.001]
  • [Cites] Nat Rev Drug Discov. 2005 Apr;4(4):307-20 [15789122.001]
  • [Cites] Biochem Pharmacol. 2005 Oct 15;70(8):1137-46 [16139250.001]
  • [Cites] Curr Treat Options Oncol. 2005 Nov;6(6):519-30 [16242056.001]
  • [Cites] Eur J Cancer. 2006 Sep;42(14):2404-13 [16901688.001]
  • [Cites] Mutat Res. 2001 Jul 1;478(1-2):1-21 [11406166.001]
  • [Cites] Clin Cancer Res. 2002 Mar;8(3):878-84 [11895922.001]
  • [Cites] J Inorg Biochem. 2002 Feb;88(3-4):260-7 [11897339.001]
  • [Cites] Cancer Treat Res. 2002;112:263-84 [12481720.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1776-9 [12702562.001]
  • [Cites] J Am Chem Soc. 2003 Jun 25;125(25):7524-5 [12812486.001]
  • [Cites] Biochem Pharmacol. 2004 Jan 1;67(1):17-30 [14667925.001]
  • [Cites] Clin Cancer Res. 2004 Jul 1;10(13):4578-88 [15240550.001]
  • [Cites] J Inorg Biochem. 2004 Oct;98(10):1614-24 [15458824.001]
  • [Cites] Clin Cancer Res. 2004 Oct 1;10(19):6744-9 [15475465.001]
  • [Cites] Cancer Lett. 2004 Nov 25;215(2):167-77 [15488635.001]
  • [Cites] Nat Rev Cancer. 2004 Oct;4(10):806-13 [15510161.001]
  • [Cites] Br J Cancer. 1997;76(7):894-903 [9328149.001]
  • (PMID = 17579620.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds
  • [Other-IDs] NLM/ PMC2360296
  •  go-up   go-down


18. Bazarbashi S, Raja MA, El Sayed A, Ezzat A, Ibrahim E, Kattan S, Kardar A, Peracha A, Lindstedt E, Hanash K: Prospective phase II trial of alternating intravesical Bacillus Calmette-Guérin (BCG) and interferon alpha IIB in the treatment and prevention of superficial transitional cell carcinoma of the urinary bladder: preliminary results. J Surg Oncol; 2000 Jul;74(3):181-4
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective phase II trial of alternating intravesical Bacillus Calmette-Guérin (BCG) and interferon alpha IIB in the treatment and prevention of superficial transitional cell carcinoma of the urinary bladder: preliminary results.
  • BACKGROUND AND OBJECTIVE: Evaluate the efficacy and toxicity of alternating intravesical instillation of Bacillus Calmette-Guerin(BCG) and Interferon alpha2-b (IFN) in the treatment and prevention of recurrence of superficial transitional cell carcinoma (TCC) of the urinary bladder.
  • METHODS: Patients with Ta, T1 tumors and carcinoma in situ, either recurrent (TaG1, T1G1) or primary/recurrent TaG2 TaG3, T1G2, T1G3 and Tis (T: Tumor stage, G: grade) are eligible.
  • Cystoscopy performed 4 weeks after completion of therapy, and every 3 months thereafter.
  • With a median follow-up of 26.2 month, 22 patients (59%) failed above therapy.
  • Median time to treatment failure was 7 months.
  • Seven, 6 and 9 patients recurred at a higher, lower and same stage or grade respectively.
  • CONCLUSIONS: Alternating intravesical BCG and IFN is effective and well tolerated therapy for superficial TCC of urinary bladder.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Carcinoma, Transitional Cell / prevention & control. Neoplasm Recurrence, Local / drug therapy. Neoplasm Recurrence, Local / prevention & control. Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / prevention & control
  • [MeSH-minor] Administration, Intravesical. Adult. BCG Vaccine / administration & dosage. BCG Vaccine / adverse effects. Drug Administration Schedule. Female. Humans. Interferon-alpha / administration & dosage. Interferon-alpha / adverse effects. Male. Middle Aged. Neoplasm Staging. Prospective Studies. Recombinant Proteins

  • Genetic Alliance. consumer health - Transitional cell carcinoma.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10951412.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / BCG Connaught; 0 / BCG Vaccine; 0 / Interferon-alpha; 0 / Recombinant Proteins; 99210-65-8 / interferon alfa-2b
  •  go-up   go-down


19. Brenner BG, Roger M, Routy JP, Moisi D, Ntemgwa M, Matte C, Baril JG, Thomas R, Rouleau D, Bruneau J, Leblanc R, Legault M, Tremblay C, Charest H, Wainberg MA, Quebec Primary HIV Infection Study Group: High rates of forward transmission events after acute/early HIV-1 infection. J Infect Dis; 2007 Apr 1;195(7):951-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Clinical features, risk factors, and drug resistance for clustered and nonclustered transmission events were ascertained.
  • Coclustering of untreated and treated CIs with PHIs were infrequent (6.2% and 4.8%, respectively).
  • Low prevalence of drug resistance in PHI supported amplified transmissions at early stages.
  • Therapy at early stages of disease may prevent onward HIV transmission.
  • [MeSH-major] Disease Transmission, Infectious. Drug Resistance, Viral / genetics. Genes, pol. HIV Infections / epidemiology. HIV Infections / transmission. HIV-1 / genetics
  • [MeSH-minor] Adult. Anti-HIV Agents / therapeutic use. DNA, Viral / analysis. Female. Genetic Variation. Humans. Male. Phylogeny. Quebec / epidemiology. Risk Factors


20. de Csepel J, Tartter PI, Gajdos C: When not to give radiation therapy after breast conservation surgery for breast cancer. J Surg Oncol; 2000 Aug;74(4):273-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] When not to give radiation therapy after breast conservation surgery for breast cancer.
  • BACKGROUND AND OBJECTIVES: A significant proportion of breast cancer patients treated with breast conservation surgery do not receive adjuvant radiation therapy because of advanced age, severe intercurrent disease, or their own preference.
  • We studied patients for whom adjuvant radiation was not performed, to determine whether the rate of local recurrence was acceptable in particular clinical circumstances.
  • METHODS: Patients who had undergone breast conservation surgery for breast cancer were identified.
  • The charts of patients who did not receive adjuvant radiation therapy were reviewed to identify the reason for omitting radiation.
  • Local and distant recurrence rates were examined in relation to radiation and reason for omitting radiation.
  • RESULTS: Forty-three (9%, two bilateral) of the 487 patients did not receive radiation; 9 because of advanced age, 8 refused, 7 had severe intercurrent diseases, 6 developed stage IV disease while getting chemotherapy for stage III disease, 5 patients (1 bilateral) had two reasons for omission (3 cases: age + intercurrent disease; 2 cases: age + stage IV disease; and 1 case: age + small focus of ductal carcinoma in situ) and the remainder for miscellaneous reasons.
  • None of the 13 patients with intercurrent disease or progression to stage IV disease developed local recurrence in their life time; 5 (63%) of 8 patients who refused radiation recurred in the breast; 2 (22%) 9 of the elderly patients developed local recurrences and none of the 6 cases with more than one reason for omission developed local recurrences.
  • CONCLUSIONS: Omission of radiation therapy after breast conservation is appropriate for patients with intercurrent diseases, for those who develop metastases while receiving preoperative chemotherapy and for selected elderly patients.
  • Patients who refuse recommended adjuvant radiation therapy have unacceptably high rates of local recurrence.
  • Omission of radiation for advanced age alone is associated with local recurrence rates comparable to those for younger patients.
  • [MeSH-major] Breast Neoplasms / radiotherapy. Breast Neoplasms / surgery. Mastectomy, Segmental / methods. Neoplasm Recurrence, Local / epidemiology
  • [MeSH-minor] Aged. Aged, 80 and over. Disease-Free Survival. Female. Follow-Up Studies. Humans. Incidence. Middle Aged. Radiotherapy, Adjuvant. Registries. Risk Assessment. Severity of Illness Index. Survival Rate

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10962459.001).
  • [ISSN] 0022-4790
  • [Journal-full-title] Journal of surgical oncology
  • [ISO-abbreviation] J Surg Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  •  go-up   go-down


21. Hwang DY, Hwang MM, Kim HS, Kim KS: Genetically engineered dopamine beta-hydroxylase gene promoters with better PHOX2-binding sites drive significantly enhanced transgene expression in a noradrenergic cell-specific manner. Mol Ther; 2005 Jan;11(1):132-41
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetically engineered dopamine beta-hydroxylase gene promoters with better PHOX2-binding sites drive significantly enhanced transgene expression in a noradrenergic cell-specific manner.
  • A continuously growing body of evidence suggests that dysregulation of noradrenergic (NA) neurons is implicated in the etiology and pathophysiology of various human diseases such as depression, drug addiction, and autonomic dysfunction.
  • An efficient NA neuron-specific promoter is potentially valuable to investigate the precise role of NA neurons in normal as well as in diseased brain and to treat the associated disorders by gene therapy.
  • In this study, we tested a novel strategy to modify genetically the promoter of the human dopamine beta-hydroxylase (hDBH) gene to overcome its inherent weakness while maintaining its cell-type specificity.
  • More importantly, these modifications do not alter the level of transgene expression in non-NA cells either in vitro or in vivo, demonstrating tight cell-type specificity.
  • This work shows that a cellular gene promoter can be genetically modified to strengthen its promoter activity without losing cell-type specificity by optimizing critical cis-regulatory elements.
  • Our genetically engineered promoter may be useful for cell-type-specific gene targeting as well as for generating in vivo animal models with altered gene expression in a specific cell type.
  • [MeSH-minor] Animals. Base Sequence. Binding Sites. Brain / metabolism. Cell Line, Tumor. Genes, Reporter. Humans. Molecular Sequence Data. Nerve Tissue Proteins. Organ Specificity

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15585414.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Grant] United States / NIDCD NIH HHS / DC / DC006501; United States / NIMH NIH HHS / MH / MH48866; United States / NINDS NIH HHS / NS / NS044439
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / Nerve Tissue Proteins; 0 / PHOX2A protein, human; 0 / Transcription Factors; EC 1.14.17.1 / Dopamine beta-Hydroxylase
  •  go-up   go-down


22. Zylberberg B, Dormont D, Janklewicz S, Daraï E, Madelenat P, Antoine JM: [Secondary cytoreductions in the treatment of ovarian cancers]. Gynecol Obstet Fertil; 2000 Feb;28(2):127-36
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Secondary cytoreductions in the treatment of ovarian cancers].
  • [Transliterated title] Cytoréductions secondaires dans le traitement des cancers de l'ovaire.
  • The aim of this study was to investigate the potential benefit of secondary cytoreductive surgery for recurrent ovarian cancer.
  • METHODS: Between 1980 and 1993, 85 patients (11 stage Ic, 4 stage IIc, 70 stage III) with an epithelial ovarian cancer were treated after initial surgery with an intraperitoneal and intravenous Cis Platin-based immunochemotherapy.
  • RESULTS: Complete resection was achieved in 13 patients (65%) and was optimal with a < 0.5 cm residual disease left in one case.
  • All 21 patients who were not reoperated died with a median survival time from recurrence of eight months (10.5 months for the patients who refused to be reoperated and seven months for the patients rejected by the surgeons) against 29 for the 20 reoperated patients (P < 0.004).
  • CONCLUSION: This series is too small to enable us to draw definitive conclusions.
  • In our opinion, secondary surgical procedure should be proposed to relapsing patients to enhance efficacy of rescue chemotherapy, which is of limited value in bulky tumors.
  • [MeSH-major] Carcinoma / surgery. Neoplasm Recurrence, Local / surgery. Ovarian Neoplasms / surgery. Reoperation / methods
  • [MeSH-minor] Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chemotherapy, Adjuvant. Cisplatin / therapeutic use. Female. Follow-Up Studies. Humans. Middle Aged. Neoplasm Staging. Survival Analysis. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Ovarian Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10758587.001).
  • [ISSN] 1297-9589
  • [Journal-full-title] Gynécologie, obstétrique & fertilité
  • [ISO-abbreviation] Gynecol Obstet Fertil
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] FRANCE
  • [Chemical-registry-number] Q20Q21Q62J / Cisplatin
  •  go-up   go-down


23. Zajicek JP, Ingram WM, Vickery J, Creanor S, Wright DE, Hobart JC: Patient-orientated longitudinal study of multiple sclerosis in south west England (The South West Impact of Multiple Sclerosis Project, SWIMS) 1: protocol and baseline characteristics of cohort. BMC Neurol; 2010 Oct 07;10:88
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The South West Impact of MS Project (SWIMS) has been designed to improve understanding of disease impact using a patient-centred approach.
  • The purpose is to (1) develop improved measurement instruments for clinical trials, (2) evaluate longitudinal performance of a variety of patient-reported outcome measures, (3) develop prognostic predictors for use in individualising drug treatment for patients, particularly early on in the disease course.
  • METHODS: This is a patient-centred, prospective, longitudinal study of multiple sclerosis and clinically isolated syndrome (CIS) in south west England.
  • The study area comprises two counties with a population of approximately 1.7 million and an estimated 1,800 cases of MS.
  • Self-completion questionnaires are administered to participants every six months (for people with MS) or 12 months (CIS).
  • Average (standard deviation) age at time of entry to SWIMS was 51.6 (11.5) years (n = 961) and median (interquartile range) time since first symptom was 13.3 (6.8 to 24.5) years (n = 934).
  • Although medication use for symptom control was common, there was little evidence of effectiveness, particularly for fatigue.
  • Nineteen percent of participants were unable to classify their subtype of MS.
  • When patient-reported subtype was compared to neurologist assessment for a sample of participants (n = 396), agreement in disease sub-type was achieved in 63% of cases.
  • Twenty-three percent of the relapsing-remitting group and 12% of the total sample were receiving disease-modifying therapy at baseline.
  • Overall, the results broadly reflect clinical experience in confirming high symptom prevalence, with relatively little complete symptom relief.
  • Participants often had difficulty in defining MS relapses and their own MS type.

  • Genetic Alliance. consumer health - Multiple Sclerosis.
  • MedlinePlus Health Information. consumer health - Multiple Sclerosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Neurology. 1996 Apr;46(4):907-11 [8780061.001]
  • [Cites] Neurology. 1996 Jul;47(1):129-39 [8710066.001]
  • [Cites] J Epidemiol Community Health. 1999 Jan;53(1):46-50 [10326053.001]
  • [Cites] Mult Scler. 1999 Aug;5(4):244-50 [10467383.001]
  • [Cites] Mov Disord. 2004 Dec;19(12):1482-5 [15390075.001]
  • [Cites] Brain. 2006 Jan;129(Pt 1):224-34 [16280352.001]
  • [Cites] Ann Neurol. 2007 Jan;61(1):14-24 [17262850.001]
  • [Cites] Eur J Health Econ. 2006 Sep;7 Suppl 2:S96-104 [17310341.001]
  • [Cites] Lancet Neurol. 2007 Oct;6(10):903-12 [17884680.001]
  • [Cites] Mult Scler. 2007 Sep;13(8):1033-7 [17468438.001]
  • [Cites] Health Qual Life Outcomes. 2008;6:100 [19014588.001]
  • [Cites] Clin J Pain. 2009 Mar-Apr;25(3):211-7 [19333171.001]
  • [Cites] Neurology. 2001 Aug 28;57(4):676-81 [11524478.001]
  • [Cites] Neurology. 2003 Jan 14;60(1):31-6 [12525714.001]
  • [Cites] Mult Scler. 2003 Feb;9(1):95-101 [12617275.001]
  • [Cites] J Neurol Neurosurg Psychiatry. 2004 Jan;75(1):56-60 [14707308.001]
  • [Cites] Health Technol Assess. 2004 Mar;8(9):iii, 1-48 [14982653.001]
  • [Cites] Ann Neurol. 1983 Mar;13(3):227-31 [6847134.001]
  • [Cites] Neurology. 1983 Nov;33(11):1444-52 [6685237.001]
  • [Cites] Neurology. 1988 Oct;38(10):1511-5 [3419593.001]
  • [Cites] Lancet. 1989 Jun 10;1(8650):1322-3 [2566844.001]
  • [Cites] Arch Neurol. 1989 Oct;46(10):1121-3 [2803071.001]
  • [Cites] Health Policy. 1990 Dec;16(3):199-208 [10109801.001]
  • [Cites] Ann Neurol. 1996 Mar;39(3):285-94 [8602746.001]
  • [Cites] Brain. 1999 Apr;122 ( Pt 4):625-39 [10219776.001]
  • (PMID = 20929556.001).
  • [ISSN] 1471-2377
  • [Journal-full-title] BMC neurology
  • [ISO-abbreviation] BMC Neurol
  • [Language] eng
  • [Grant] United Kingdom / Multiple Sclerosis Society / / 923
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2966453
  •  go-up   go-down


24. Fosså SD, Aass N, Heilo A, Daugaard G, E Skakkebaek N, Stenwig AE, Nesland JM, Looijenga LH, Oosterhuis JW: Testicular carcinoma in situ in patients with extragonadal germ-cell tumours: the clinical role of pretreatment biopsy. Ann Oncol; 2003 Sep;14(9):1412-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Testicular carcinoma in situ in patients with extragonadal germ-cell tumours: the clinical role of pretreatment biopsy.
  • BACKGROUND: The aim of this study was to determine the prevalence of testicular carcinoma in situ (CIS) in patients with a malignant extragonadal germ-cell tumour (EGGCT) and the incidence of metachronous invasive testicular cancer (TC) in relation to the pretreatment demonstration of CIS.
  • PATIENTS AND METHODS: Sixty-eight patients with EGGCT (53 retroperitoneal, 15 mediastinal) had pre-chemotherapy histological assessment of one (13) or both (55) testicle(s).
  • A total of 123 testicles were examined for the presence of CIS.
  • RESULTS: Testicular CIS was found in 21 patients (31%) (18 retroperitoneal EGGCT, three mediastinal EGGCT).
  • Two patients had bilateral CIS.
  • Five patients, four of them with proven pretreatment CIS, developed a metachronous TC.
  • The 10-year invasive-free TC survival rate for all 68 patients was 88%, but only 65% for those with proven pretreatment CIS.
  • CIS was demonstrated in seven of 48 trans-scrotal core biopsies, in 10 of 56 trans-scrotal surgical biopsies and in five of 11 orchiectomy specimens.
  • CONCLUSIONS: Approximately one-third of patients with EGGCT present with testicular CIS, predominantly those with a retroperitoneal tumour.
  • These patients have a considerable risk of metachronous TC development in spite of chemotherapy.
  • The pretreatment demonstration of testicular CIS in patients with EGGCT gives the possibility of individualised counselling and safe follow-up, and is therefore highly recommended.
  • The data are in agreement with a multi-site development of malignant germ-cell tumours, but do not exclude the possibility that the retroperitoneal EGGCTs in particular represent metastases from a burned-out TC.

  • MedlinePlus Health Information. consumer health - Biopsy.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12954581.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  •  go-up   go-down


25. Solomon DH, Avorn J, Katz JN, Weinblatt ME, Setoguchi S, Levin R, Schneeweiss S: Immunosuppressive medications and hospitalization for cardiovascular events in patients with rheumatoid arthritis. Arthritis Rheum; 2006 Dec;54(12):3790-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunosuppressive medications and hospitalization for cardiovascular events in patients with rheumatoid arthritis.
  • OBJECTIVE: The risk of cardiovascular disease (CVD) is increased in patients with rheumatoid arthritis (RA), most likely because of increased systemic inflammation.
  • Prior research suggests that immunosuppressive medications may reduce the risk of CVD among RA patients.
  • This study was undertaken to investigate the effects of various immunosuppressive medications on the risk of cardiovascular events among a group of older patients with RA.
  • METHODS: In this nested case-control study, the source cohort was derived from Medicare beneficiaries receiving a drug benefit from the state of Pennsylvania.
  • Cases were defined as those patients who were hospitalized for a cardiovascular event such as myocardial infarction or stroke, and 10 control subjects were matched to each case by age, sex, and calendar year of the index date (the time of the first cardiovascular event in each case).
  • Current use of an immunosuppressive medication was defined as having filled a prescription for these agents within the 90 days prior to the index date.
  • During followup of this cohort, 946 patients were hospitalized for a cardiovascular event.
  • Although the 95% confidence intervals (95% CIs) were wide in adjusted risk regression models with methotrexate (MTX) monotherapy as the reference group, biologic immunosuppressive agents showed neither protective nor deleterious effects (with biologics monotherapy, odds ratio [OR] 1.0, 95% CI 0.5-1.9; with biologics plus MTX combination therapy, OR 0.8, 95% CI 0.3-2.0; and with biologics plus other immunosuppressive agents, OR 1.2, 95% CI 0.7-2.2).
  • Monotherapy with oral glucocorticoids was associated with an increased risk of cardiovascular events (OR 1.5, 95% CI 1.1-2.1), and a similar trend in the direction of risk was seen with glucocorticoid combination therapy (OR 1.3, 95% CI 0.8-2.0).
  • Cytotoxic immunosuppressive agents other than MTX (azathioprine, cyclosporine, and leflunomide) were also associated with an increased risk of cardiovascular events (with both monotherapy and combination treatment, OR 1.8, 95% CI 1.1-3.0).
  • [MeSH-major] Antirheumatic Agents / therapeutic use. Arthritis, Rheumatoid / drug therapy. Arthritis, Rheumatoid / epidemiology. Cardiovascular Diseases / epidemiology. Hospitalization. Immunosuppressive Agents / therapeutic use

  • Genetic Alliance. consumer health - Arthritis.
  • Genetic Alliance. consumer health - Rheumatoid arthritis.
  • MedlinePlus Health Information. consumer health - Rheumatoid Arthritis.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17136752.001).
  • [ISSN] 0004-3591
  • [Journal-full-title] Arthritis and rheumatism
  • [ISO-abbreviation] Arthritis Rheum.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / K23-AR-48616; United States / PHS HHS / / K24-02123; United States / NIAMS NIH HHS / AR / P60-AR-47782
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antirheumatic Agents; 0 / Immunosuppressive Agents
  •  go-up   go-down


26. Noblía P, Vieites M, Parajón-Costa BS, Baran EJ, Cerecetto H, Draper P, González M, Piro OE, Castellano EE, Azqueta A, López de Ceráin A, Monge-Vega A, Gambino D: Vanadium(V) complexes with salicylaldehyde semicarbazone derivatives bearing in vitro anti-tumor activity toward kidney tumor cells (TK-10): crystal structure of [VVO2(5-bromosalicylaldehyde semicarbazone)]. J Inorg Biochem; 2005 Feb;99(2):443-51
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vanadium(V) complexes with salicylaldehyde semicarbazone derivatives bearing in vitro anti-tumor activity toward kidney tumor cells (TK-10): crystal structure of [VVO2(5-bromosalicylaldehyde semicarbazone)].
  • As a contribution to the development of novel vanadium complexes with pharmacologically interesting moieties, new dioxovanadium(V) semicarbazone complexes with the formula cis-VO(2)L, where L=5-bromosalicylaldehyde semicarbazone and 2-hydroxynaphtalen-1-carboxaldehyde semicarbazone have been synthesized and characterized by (1)H and (13)C NMR, Raman and FTIR spectroscopies.
  • The five complexes were tested in three different human tumor cell lines for bioactivity as potential anti-tumor agents, showing selective cytotoxicity on TK-10 cell line.
  • Results showed that structural modifications on the semicarbazone moiety could have a significant effect on the anti-tumor activity of the vanadium complexes.
  • No apparent correlation could be demonstrated between reduction potentials of the complexes and their anti-tumor activities.
  • The molecular structure of the novel [V(V)O(2)(5-bromosalicylaldehyde semicarbazone)] complex was solved by X-ray diffraction methods.
  • [MeSH-minor] Cell Line, Tumor. Crystallography, X-Ray. Drug Stability. HT29 Cells. Humans. Kidney Neoplasms / drug therapy. Molecular Structure. Nuclear Magnetic Resonance, Biomolecular. Spectroscopy, Fourier Transform Infrared. Spectrum Analysis, Raman

  • Hazardous Substances Data Bank. VANADIUM, ELEMENTAL .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15621276.001).
  • [ISSN] 0162-0134
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aldehydes; 0 / Antineoplastic Agents; 0 / Organometallic Compounds; 0 / Thiosemicarbazones; 00J9J9XKDE / Vanadium; 5351-90-6 / salicylaldehyde thiosemicarbazone
  •  go-up   go-down


27. Levin VA, Giglio P, Puduvalli VK, Jochec J, Groves MD, Yung WK, Hess K: Combination chemotherapy with 13-cis-retinoic acid and celecoxib in the treatment of glioblastoma multiforme. J Neurooncol; 2006 May;78(1):85-90
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combination chemotherapy with 13-cis-retinoic acid and celecoxib in the treatment of glioblastoma multiforme.
  • In a phase II clinical trial, we sought to determine if combining celecoxib with 13-cis-retinoic acid (13-cRA, Accutane) was efficacious in the treatment of recurrent (progressive) glioblastoma multiforme (GBM).
  • In parallel, we also sought to determine to what extent the outcomes from this clinical trial correlated with the findings from studies utilizing two murine intracerebral GBM models, U87MG and U251HF, to determine the predictive value of these murine models.
  • In the clinical trial, 25 patients were studied at recurrence.
  • Stable disease, which occurred in 44% of the patients, was the best response.
  • The median progression-free survival (PFS) was 8 weeks, with a PFS at 6 months of only 19%.
  • For the patients with stable disease, the median PFS was 24 weeks.
  • Thus, the combination of 13-cRA with celecoxib is not more effective than 13-cRA in the treatment of progressive GBM.
  • There was no evidence of synergism between the two drugs.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Brain Neoplasms / drug therapy. Disease Models, Animal. Glioblastoma / drug therapy
  • [MeSH-minor] Adult. Aged. Animals. Celecoxib. Disease-Free Survival. Female. Humans. Isotretinoin / administration & dosage. Male. Mice. Mice, Nude. Middle Aged. Pyrazoles / administration & dosage. Sensitivity and Specificity. Sulfonamides / administration & dosage. Survival Analysis

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CELECOXIB .
  • Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biochem. 1990 Feb;42(2):83-94 [2307713.001]
  • [Cites] Acta Neuropathol. 1999 Sep;98(3):240-4 [10483780.001]
  • [Cites] Neuro Oncol. 2004 Jul;6(3):253-8 [15279718.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):2230-5 [10473110.001]
  • [Cites] Cancer Res. 1988 Nov 15;48(22):6530-4 [2846152.001]
  • [Cites] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840.001]
  • [Cites] J Neurooncol. 1997 Sep;34(2):145-51 [9210061.001]
  • [Cites] Clin Cancer Res. 1996 Dec;2(12):1931-5 [9816151.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4375-81 [11389063.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4926-31 [10987308.001]
  • [Cites] Cancer Biol Ther. 2004 Jan;3(1):55-62 [14726653.001]
  • [Cites] J Neurooncol. 1989 Nov;7(4):329-38 [2555453.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2890-5 [9230197.001]
  • [Cites] Brain Res Mol Brain Res. 2001 Feb 19;87(1):100-8 [11223164.001]
  • [Cites] Cancer Res. 1989 Feb 15;49(4):1014-9 [2912547.001]
  • (PMID = 16391896.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Pyrazoles; 0 / Sulfonamides; EH28UP18IF / Isotretinoin; JCX84Q7J1L / Celecoxib
  •  go-up   go-down


28. Kenworthy T, Adams CE, Bilby C, Brooks-Gordon B, Fenton M: Psychological interventions for those who have sexually offended or are at risk of offending. Cochrane Database Syst Rev; 2004;(3):CD004858
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To date, no positive treatment effects have been found in quasi-experimental institutional treatment programmes.
  • SELECTION CRITERIA: Randomised controlled trials (RCTs) involving adults treated in institutional or community settings for sexual behaviours that have resulted in conviction or caution for sexual offences, or offences or violent behaviours with a sexual element.
  • Behavioural, cognitive-behavioural, psychodynamic, and psychoanalytic therapies were compared with each other, drug treatment, or standard care.
  • Where possible, number-needed-to-treat or harm statistics (NNT, NNH) and their 95% CIs were calculated.
  • MAIN RESULTS: We included nine RCTs with over 500 male offenders, 231 of whom have been followed up for a decade.
  • Cognitive behavioural therapy (CBT) in groups may reduce re-offence at one year for child molesters when compared with standard care (n=155, 1 RCT, RR any sexual/violent crime - 0.41 CI 0.2 to 0.82, NNT 6 CI 3 to 20).
  • However, when CBT was compared with a trans-theoretical counselling group therapy the former may have increased poor attitudes to treatment (corrected n=38, 1 RCT, RR 2.8 CI 1.26 to 6.22, NNH 2 CI 1 to 5).
  • The largest trial compared broadly psychodynamic group therapy with no treatment for 231 men guilty of paedophilia, exhibitionism or sexual assault.
  • Re-arrest over ten years was greater for those allocated to group therapy (result not statistically significant [n=231, 1 RCT, RR 1.87 CI 0.78 to 4.47]).
  • One study suggests that a cognitive approach results in a decline in re-offending after one year.
  • Another large study shows no benefit for group therapy and suggests the potential for harm at ten years.
  • The ethics of providing this still-experimental treatment to a vulnerable and potentially dangerous group of people outside of a well-designed evaluative study are debatable.
  • [MeSH-major] Paraphilic Disorders / therapy. Psychotherapy / methods. Sex Offenses / psychology

  • MedlinePlus Health Information. consumer health - Sexual Assault.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [UpdateIn] Cochrane Database Syst Rev. 2008;(4):CD004858 [18843670.001]
  • (PMID = 15266545.001).
  • [ISSN] 1469-493X
  • [Journal-full-title] The Cochrane database of systematic reviews
  • [ISO-abbreviation] Cochrane Database Syst Rev
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 127
  •  go-up   go-down


29. Kramer K, Kushner BH, Modak S, Pandit-Taskar N, Smith-Jones P, Zanzonico P, Humm JL, Xu H, Wolden SL, Souweidane MM, Larson SM, Cheung NK: Compartmental intrathecal radioimmunotherapy: results for treatment for metastatic CNS neuroblastoma. J Neurooncol; 2010 May;97(3):409-18
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Compartmental intrathecal radioimmunotherapy: results for treatment for metastatic CNS neuroblastoma.
  • We evaluated the addition of compartmental intrathecal antibody-based radioimmunotherapy (cRIT) in patients with recurrent metastatic central nervous system (CNS) neuroblastoma following surgery, craniospinal irradiation, and chemotherapy.
  • Most patients also received outpatient craniospinal irradiation, 3F8/GMCSF immunotherapy, 13-cis-retinoic acid and oral temozolomide for systemic control.
  • One patient died of infection at 22 months with no evidence of disease at autopsy, and one of lung and bone marrow metastases at 15 months, and one of progressive bone marrow disease at 30 months.
  • One patient with a 7-year history of metastatic neuroblastoma is in remission from MLL-associated secondary leukemia.
  • This is significantly improved to published results with non-cRIT based where relapsed CNS NB has a median time to death of approximately 6 months.
  • The cRIT-salvage regimen for CNS metastases was well tolerated by young patients, despite their prior history of intensive cytotoxic therapies.
  • [MeSH-minor] Adolescent. Adult. Aged. Antibodies, Monoclonal / therapeutic use. Child. Child, Preschool. Combined Modality Therapy. Drug Administration Schedule. Female. Granulocyte-Macrophage Colony-Stimulating Factor / therapeutic use. Humans. Injections, Spinal. Male. Middle Aged. Radiotherapy Dosage. Retrospective Studies. Time Factors. Tomography, Emission-Computed, Single-Photon / methods. Treatment Outcome. Young Adult

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Cancer. 1990 Oct;62(4):637-42 [2223581.001]
  • [Cites] J Natl Cancer Inst. 1986 Sep;77(3):739-45 [3091900.001]
  • [Cites] J Nucl Med. 1992 Nov;33(11):2020-3 [1432165.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1466-77 [8336186.001]
  • [Cites] J Neurooncol. 1997 Nov;35(2):101-11 [9266446.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2202-12 [9626222.001]
  • [Cites] J Clin Oncol. 1998 Sep;16(9):3053-60 [9738575.001]
  • [Cites] Cancer Res. 1998 Oct 1;58(19):4363-7 [9766665.001]
  • [Cites] Clin Cancer Res. 1996 Jun;2(6):963-72 [9816257.001]
  • [Cites] J Pediatr Hematol Oncol. 1999 May-Jun;21(3):181-9 [10363850.001]
  • [Cites] N Engl J Med. 1999 Oct 14;341(16):1165-73 [10519894.001]
  • [Cites] Pediatr Blood Cancer. 2005 Jul;45(1):68-71 [15770641.001]
  • [Cites] Cancer Biother Radiopharm. 2005 Oct;20(5):534-46 [16248769.001]
  • [Cites] Bone Marrow Transplant. 2006 Feb;37(3):271-6 [16400336.001]
  • [Cites] J Clin Oncol. 2006 Nov 20;24(33):5271-6 [17114661.001]
  • [Cites] J Clin Oncol. 2007 Dec 1;25(34):5465-70 [18048828.001]
  • [Cites] Neuro Oncol. 2008 Apr;10(2):182-9 [18287339.001]
  • [Cites] Clin Cancer Res. 1999 Oct;5(10 Suppl):3275s-3280s [10541375.001]
  • [Cites] Ann N Y Acad Sci. 2000 Jun;910:263-9; discussion 269-70 [10911919.001]
  • [Cites] Cancer. 2001 Apr 15;91(8):1510-9 [11301399.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):4048-54 [11358824.001]
  • [Cites] Med Pediatr Oncol. 2001 Jan;36(1):194-6 [11464881.001]
  • [Cites] Eur J Nucl Med Mol Imaging. 2003 Jun;30(6):895-906 [12721768.001]
  • [Cites] Cancer. 2003 Jul 1;98(1):155-65 [12833468.001]
  • [Cites] J Pediatr Hematol Oncol. 2003 Jul;25(7):515-9 [12847316.001]
  • [Cites] Eur J Cancer. 1992;28(2-3):511-3 [1591076.001]
  • (PMID = 19890606.001).
  • [ISSN] 1573-7373
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Grant] United States / PHS HHS / / FDA-KK-01A2; United States / NCI NIH HHS / CA / R21 CA117076-02; United States / NCI NIH HHS / CA / P01 CA033049-23; United States / NCI NIH HHS / CA / R21 CA089936-02; United States / FDA HHS / FD / FD003089; United States / NCI NIH HHS / CA / R21 CA089936; United States / FDA HHS / FD / R01 FD003089; United States / NCI NIH HHS / CA / P01 CA033049; United States / NCI NIH HHS / CA / CA106450; United States / NCI NIH HHS / CA / R21 CA117076; United States / NCI NIH HHS / CA / CA89935; United States / NCI NIH HHS / CA / CA117076; United States / NCI NIH HHS / CA / P01 CA106450; United States / NCI NIH HHS / CA / CA89936; United States / NCI NIH HHS / CA / R21 CA089935-02; United States / NCI NIH HHS / CA / P01 CA106450-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 83869-56-1 / Granulocyte-Macrophage Colony-Stimulating Factor
  • [Other-IDs] NLM/ NIHMS250577; NLM/ PMC3533371
  •  go-up   go-down


30. Lykkesfeldt AE, Henriksen KL, Rasmussen BB, Sasano H, Evans DB, Møller S, Ejlertsen B, Mouridsen HT: In situ aromatase expression in primary tumor is associated with estrogen receptor expression but is not predictive of response to endocrine therapy in advanced breast cancer. BMC Cancer; 2009;9:185
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In situ aromatase expression in primary tumor is associated with estrogen receptor expression but is not predictive of response to endocrine therapy in advanced breast cancer.
  • BACKGROUND: New, third-generation aromatase inhibitors (AIs) have proven comparable or superior to the anti-estrogen tamoxifen for treatment of estrogen receptor (ER) and/or progesterone receptor (PR) positive breast cancer.
  • It is unclear whether in situ carcinoma cell aromatization is the primary source of estrogen production for tumor growth and whether the aromatase expression is predictive of response to endocrine therapy.
  • METHODS: Primary tumor material was retrospectively collected from 88 patients who participated in a randomized clinical trial comparing the AI letrozole to the anti-estrogen tamoxifen for first-line treatment of advanced breast cancer.
  • Semi-quantitative immunohistochemical (IHC) analysis was performed for ER, PR, COX-2 and aromatase using Tissue Microarrays (TMAs).
  • Univariate Wilcoxon analysis and the Cox-analysis were performed to evaluate time to progression (TTP) in relation to marker expression.
  • RESULTS: Aromatase expression was associated with ER, but not with PR or COX-2 expression in carcinoma cells.
  • Expression of COX-2 and aromatase did not predict response to endocrine therapy.
  • Aromatase in combination with high PR expression may select letrozole treated patients with a longer TTP.
  • CONCLUSION: TMAs are not suitable for IHC analysis of in situ aromatase expression and we did not find COX-2 expression in carcinoma cells to be a surrogate marker for aromatase.
  • In situ aromatase expression in tumor cells is associated with ER expression and may thus point towards good prognosis.
  • Aromatase expression in cancer cells is not predictive of response to endocrine therapy, indicating that in situ estrogen synthesis may not be the major source of intratumoral estrogen.
  • However, aromatase expression in combination with high PR expression may select letrozole treated patients with longer TTP.
  • TRIAL REGISTRATION: Sub-study of trial P025 for advanced breast cancer.
  • [MeSH-major] Aromatase / biosynthesis. Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Nitriles / therapeutic use. Receptors, Estrogen / biosynthesis. Tamoxifen / therapeutic use. Triazoles / therapeutic use
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Aromatase Inhibitors / therapeutic use. Carcinoma in Situ / drug therapy. Carcinoma in Situ / enzymology. Carcinoma in Situ / metabolism. Cyclooxygenase 2 / biosynthesis. Female. Humans. Immunohistochemistry. Receptors, Progesterone / biosynthesis. Retrospective Studies. Tissue Array Analysis

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • Hazardous Substances Data Bank. LETROZOLE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2007 Nov 20;25(33):5287-312 [17954709.001]
  • [Cites] J Surg Oncol. 2007 Oct 1;96(5):424-8 [17657731.001]
  • [Cites] Cancer. 2008 Feb 1;112(3 Suppl):689-94 [18072233.001]
  • [Cites] Breast Cancer Res Treat. 2008 May;109(2):189-98 [17624587.001]
  • [Cites] Breast. 2008 Jun;17(3):275-81 [18065223.001]
  • [Cites] Mol Endocrinol. 2008 Aug;22(8):1812-24 [18483177.001]
  • [Cites] J Natl Cancer Inst. 2008 Oct 1;100(19):1380-8 [18812550.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):6330-5 [18829517.001]
  • [Cites] J Clin Oncol. 2008 Oct 20;26(30):4883-90 [18794551.001]
  • [Cites] J Cell Biochem. 2008 Nov 1;105(4):956-64 [18821585.001]
  • [Cites] Acta Oncol. 2009;48(4):522-31 [19173092.001]
  • [Cites] Breast Cancer Res Treat. 2009 Jul;116(2):371-8 [18941892.001]
  • [Cites] J Clin Oncol. 2002 Feb 1;20(3):751-7 [11821457.001]
  • [Cites] Int J Cancer. 2000 Mar 20;89(2):111-7 [10754487.001]
  • [Cites] J Steroid Biochem Mol Biol. 2000 Apr;72(5):259-64 [10822015.001]
  • [Cites] J Clin Oncol. 2000 Nov 15;18(22):3758-67 [11078488.001]
  • [Cites] Clin Cancer Res. 2001 May;7(5):1230-6 [11350888.001]
  • [Cites] J Clin Oncol. 2001 May 15;19(10):2596-606 [11352951.001]
  • [Cites] Cancer. 2001 Nov 1;92(9):2247-58 [11745278.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):632-5 [11830510.001]
  • [Cites] J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):41-7 [11850206.001]
  • [Cites] Trends Endocrinol Metab. 2002 Apr;13(3):122-8 [11893526.001]
  • [Cites] J Steroid Biochem Mol Biol. 2002 Feb;80(2):203-12 [11897504.001]
  • [Cites] J Clin Oncol. 2003 May 15;21(10):1973-9 [12743151.001]
  • [Cites] J Clin Oncol. 2003 Jun 1;21(11):2101-9 [12775735.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):239-44 [14623517.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):245-53 [14623518.001]
  • [Cites] J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):413-21 [14623539.001]
  • [Cites] Cancer Res. 1975 Nov;35(11 Pt. 2):3362-4 [172222.001]
  • [Cites] Cancer. 1980 Dec 15;46(12 Suppl):2884-8 [7448733.001]
  • [Cites] Cancer Res. 1982 Aug;42(8 Suppl):3365s-3368s [7083201.001]
  • [Cites] J Clin Endocrinol Metab. 1984 Jul;59(1):29-33 [6725522.001]
  • [Cites] Int J Cancer. 1989 Aug 15;44(2):233-7 [2759729.001]
  • [Cites] J Steroid Biochem Mol Biol. 1990 Nov 20;37(3):317-25 [2257236.001]
  • [Cites] Am J Pathol. 1992 Feb;140(2):337-43 [1739127.001]
  • [Cites] J Endocrinol. 1992 Mar;132(3):R5-8 [1564416.001]
  • [Cites] Endocr Rev. 1994 Jun;15(3):342-55 [8076586.001]
  • [Cites] Mol Cell Endocrinol. 1994 Dec;106(1-2):17-21 [7895904.001]
  • [Cites] Mol Endocrinol. 1995 Mar;9(3):340-9 [7776980.001]
  • [Cites] Endocrinology. 1996 Dec;137(12):5739-42 [8940410.001]
  • [Cites] Cancer Res. 1997 Jun 1;57(11):2109-11 [9187104.001]
  • [Cites] Mod Pathol. 1998 Feb;11(2):155-68 [9504686.001]
  • [Cites] Breast Cancer Res Treat. 1998;49 Suppl 1:S23-6; discussion S33-7 [9797014.001]
  • [Cites] Breast Cancer Res Treat. 1998;49 Suppl 1:S79-84; discussion S109-19 [9797021.001]
  • [Cites] Breast Cancer Res Treat. 1998;49 Suppl 1:S93-9; discussion S109-19 [9797023.001]
  • [Cites] Breast Cancer Res Treat. 1998;49 Suppl 1:S101-7; discussion S109-19 [9797024.001]
  • [Cites] Clin Cancer Res. 2005 Apr 15;11(8):2809-21 [15837728.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Feb;94(1-3):167-72 [15862962.001]
  • [Cites] Lancet. 2005 May 14-20;365(9472):1687-717 [15894097.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 May;95(1-5):35-9 [16024247.001]
  • [Cites] Br J Cancer. 2006 Jan 30;94(2):253-8 [16421596.001]
  • [Cites] Breast Cancer Res Treat. 2006 Feb;95(3):235-41 [16322898.001]
  • [Cites] Oncol Rep. 2006 Aug;16(2):219-24 [16820896.001]
  • [Cites] J Clin Pathol. 2007 Apr;60(4):397-404 [16775123.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3945-54 [17440110.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3846-52 [17679725.001]
  • [Cites] J Steroid Biochem Mol Biol. 2007 Aug-Sep;106(1-5):16-23 [17616393.001]
  • [Cites] J Steroid Biochem Mol Biol. 2008 Feb;108(3-5):181-5 [17933521.001]
  • (PMID = 19531212.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Aromatase Inhibitors; 0 / Nitriles; 0 / Receptors, Estrogen; 0 / Receptors, Progesterone; 0 / Triazoles; 094ZI81Y45 / Tamoxifen; 7LKK855W8I / letrozole; EC 1.14.14.1 / Aromatase; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ PMC2702392
  •  go-up   go-down


31. Michelet N, Spenatto N, Viraben R, Cuny JF, Mazet J, Trechot P, Barbaud A, Schmutz JL: [BCG infection of the glans penis after intravesical BCG therapy]. Ann Dermatol Venereol; 2008 Jun-Jul;135(6-7):479-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [BCG infection of the glans penis after intravesical BCG therapy].
  • BACKGROUND: BCG therapy is an effective adjuvant treatment for superficial bladder tumors.
  • Therapy involves intravesical instillation of live attenuated Calmette-Guérin bacilli.
  • BCG infection of the glans is a rare local complication associated with this treatment, two cases of which are reported below.
  • PATIENTS AND METHODS: Case 1: A 77-year-old man presented relapsing urothelial bladder carcinoma treated by endoscopic resection and BCG therapy.
  • One week after the seventh instillation, severe balanitis developed.
  • Slow cure of the lesions was achieved within 12months using double antitubercular antibiotic therapy.
  • Case 2: In a 61-year-old man receiving BCG therapy for relapsing bladder carcinoma in situ, the sixth instillation was considered traumatic since it was highly painful.
  • One week later, papular nodules appeared on the glans with a sclerosing lesion of the balanopreputial sac, dark purple perimeatal papules and a mass beneath the mucosa of the glans.
  • Antibiotic treatment comprising ofloxacin followed by rifampicin for two months proved ineffective.
  • Triple antitubercular antibiotic therapy was initiated.
  • DISCUSSION: The first reported case of BCG infection of the glans in patients undergoing intravesical BCG therapy was published in 1992.
  • There is no stereotypical clinical presentation.
  • Diagnosis is based upon history and histological examination.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / adverse effects. BCG Vaccine / administration & dosage. BCG Vaccine / adverse effects. Balanitis / etiology. Carcinoma in Situ / therapy. Carcinoma, Transitional Cell / therapy. Tuberculosis / etiology. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Administration, Intravesical. Aged. Antibiotics, Antitubercular / administration & dosage. Antibiotics, Antitubercular / therapeutic use. Biopsy. Drug Therapy, Combination. Granuloma, Giant Cell / etiology. Granuloma, Giant Cell / pathology. Humans. Male. Penis / pathology

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • MedlinePlus Health Information. consumer health - Tuberculosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18598797.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antibiotics, Antitubercular; 0 / BCG Vaccine
  •  go-up   go-down


32. Douketis JD, Melo M, Bell CM, Mamdani MM: Does statin therapy decrease the risk for bleeding in patients who are receiving warfarin? Am J Med; 2007 Apr;120(4):369.e9-369.e14
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does statin therapy decrease the risk for bleeding in patients who are receiving warfarin?
  • PURPOSE: Recent observations in patients with atrial fibrillation who are receiving warfarin suggest that concomitant treatment with a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) decreases the risk for bleeding.
  • Logistic regression analysis was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between bleeding and statin use.
  • Long-term (>/=1 year) statin use was associated with a lower risk for any bleeding (OR=0.80; 95% CI, 0.66-0.97).
  • CONCLUSION: Long-term statin use may be associated with a decreased risk for bleeding in warfarin users with atrial fibrillation.
  • [MeSH-major] Atrial Fibrillation / drug therapy. Hemorrhage / epidemiology. Hydroxymethylglutaryl-CoA Reductase Inhibitors / therapeutic use. Warfarin / adverse effects
  • [MeSH-minor] Aged. Case-Control Studies. Cohort Studies. Comorbidity. Drug Interactions. Female. Humans. Male. Multivariate Analysis. Ontario / epidemiology. Risk Factors

  • MedlinePlus Health Information. consumer health - Atrial Fibrillation.
  • MedlinePlus Health Information. consumer health - Bleeding.
  • MedlinePlus Health Information. consumer health - Blood Thinners.
  • MedlinePlus Health Information. consumer health - Statins.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. WARFARIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17398234.001).
  • [ISSN] 1555-7162
  • [Journal-full-title] The American journal of medicine
  • [ISO-abbreviation] Am. J. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxymethylglutaryl-CoA Reductase Inhibitors; 5Q7ZVV76EI / Warfarin
  •  go-up   go-down


33. Crivera C, Suh DC, Huang ES, Cagliero E, Grant RW, Vo L, Shin HC, Meigs JB: The incremental costs of recommended therapy versus real world therapy in type 2 diabetes patients. Curr Med Res Opin; 2006 Nov;22(11):2301-11
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The incremental costs of recommended therapy versus real world therapy in type 2 diabetes patients.
  • Improved metabolic control is achieved through optimized medication regimens, but costs specifically associated with such optimization have not been examined.
  • OBJECTIVE: To estimate the incremental medication cost of providing optimal therapy to reach recommended goals versus actual therapy in patients with type 2 diabetes.
  • METHODS: We randomly selected the charts of 601 type 2 diabetes patients receiving care from the outpatient clinics of Massachusetts General Hospital March 1, 1996-August 31, 1997 and abstracted clinical and medication data.
  • We applied treatment algorithms based on 2004 clinical practice guidelines for hyperglycemia, hyperlipidemia, and hypertension to patients' current medication therapy to determine how current medication regimens could be improved to attain recommended treatment goals.
  • Four clinicians and three pharmacists independently applied the algorithms and reached consensus on recommended therapies.
  • Mean incremental medication costs, the cost differences between current and recommended therapies, per patient (expressed in 2004 dollars) were calculated with 95% bootstrap confidence intervals (CIs).
  • If treatment algorithm recommendations were applied, the average annual medication cost/patient would increase from 1525 to 2164 dollars.
  • Annual incremental costs/patient increased by 168 dollars (95% CI 133-206 dollars) for antihyperglycemic medications, 75 dollars (57-93 dollars) for antihypertensive medications, 392 dollars (354-434 dollars) for antihyperlipidemic medications, and 3 dollars (3-4 dollars) for aspirin prophylaxis.
  • LIMITATIONS: Although baseline data come from the clinics of a single academic institution, collected in 1997, the care of these diabetes patients was remarkably similar to care recently observed nationally.
  • CONCLUSION: Average yearly incremental cost of optimizing drug regimens to achieve recommended treatment goals for type 2 diabetes was approximately 600 dollars/patient.

  • Genetic Alliance. consumer health - Diabetes.
  • Genetic Alliance. consumer health - Diabetes, Type 2.
  • MedlinePlus Health Information. consumer health - Diabetes Type 2.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] South Med J. 2002 Jan;95(1):24-9 [11829012.001]
  • [Cites] Diabetes Care. 2000 Jan;23 Suppl 1:S32-42 [12017674.001]
  • [Cites] JAMA. 2002 May 15;287(19):2542-51 [12020335.001]
  • [Cites] Am J Med. 2002 Jun 1;112(8):603-9 [12034408.001]
  • [Cites] Health Econ. 2003 Jan;12(1):33-49 [12483759.001]
  • [Cites] Diabetes Care. 2003 Jan;26 Suppl 1:S33-50 [12502618.001]
  • [Cites] Arch Intern Med. 2003 Jan 13;163(1):33-40 [12523914.001]
  • [Cites] N Engl J Med. 2003 Jan 30;348(5):383-93 [12556541.001]
  • [Cites] Diabetes Care. 2003 Mar;26(3):917-32 [12610059.001]
  • [Cites] Diabetes Care. 2003 May;26(5):1408-12 [12716797.001]
  • [Cites] JAMA. 2003 May 21;289(19):2560-72 [12748199.001]
  • [Cites] Diabetes Care. 2003 Jun;26(6):1847-51 [12766121.001]
  • [Cites] Diabetes Care. 2004 Jan;27(1):17-20 [14693960.001]
  • [Cites] JAMA. 2004 Jan 21;291(3):335-42 [14734596.001]
  • [Cites] Am J Manag Care. 2004 Feb;10(2 Pt 2):118-23 [15005503.001]
  • [Cites] Diabetes Care. 1997 May;20(5):735-44 [9135935.001]
  • [Cites] Diabetes Care. 1998 Feb;21(2):296-309 [9539999.001]
  • [Cites] Lancet. 1998 Sep 12;352(9131):837-53 [9742976.001]
  • [Cites] JAMA. 1998 Nov 25;280(20):1757-63 [9842951.001]
  • [Cites] JAMA. 2005 Jan 26;293(4):485-8 [15671434.001]
  • [Cites] Endocrinol Metab Clin North Am. 2001 Dec;30(4):909-33 [11727405.001]
  • [Cites] Am J Med. 2001 Dec 1;111(8):633-42 [11755507.001]
  • (PMID = 17076990.001).
  • [ISSN] 1473-4877
  • [Journal-full-title] Current medical research and opinion
  • [ISO-abbreviation] Curr Med Res Opin
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / K23 DK067452-01A1; United States / NIA NIH HHS / AG / AG021963-01A1; United States / NIDDK NIH HHS / DK / K23 DK067452; United States / NIA NIH HHS / AG / K23 AG021963-01A1; United States / NIA NIH HHS / AG / K23 AG021963
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS44287; NLM/ PMC2291353
  •  go-up   go-down


34. Asif-Ullah M, Lévesque M, Robichaud G, Perreault JP: Development of ribozyme-based gene-inactivations; the example of the hepatitis delta virus ribozyme. Curr Gene Ther; 2007 Jun;7(3):205-16
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The development of gene-inactivation systems is an active and important field for both functional genomics and gene therapy.
  • However, the design and optimization of a ribozyme-based gene-inactivation system is not a straightforward procedure.
  • In this review we present the advances in this domain made available from work using the hepatitis delta virus (HDV) ribozyme as a cis-acting RNA motif in molecular biology, as well as a trans-acting molecular scissor for the development of a gene-inactivation system.
  • [MeSH-major] Genetic Therapy / methods. Hepatitis Delta Virus / enzymology. Hepatitis Delta Virus / genetics. RNA, Catalytic / metabolism. RNA, Catalytic / therapeutic use
  • [MeSH-minor] Base Sequence. Drug Design. Humans. Molecular Sequence Data. Nucleic Acid Conformation. RNA Interference

  • Genetic Alliance. consumer health - Hepatitis.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17584038.001).
  • [ISSN] 1566-5232
  • [Journal-full-title] Current gene therapy
  • [ISO-abbreviation] Curr Gene Ther
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / RNA, Catalytic
  • [Number-of-references] 130
  •  go-up   go-down


35. Tomita T, Hashimoto H, Yoshikawa H: Gene therapy for arthritis. Curr Drug Targets; 2003 Nov;4(8):609-12
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gene therapy for arthritis.
  • Two clinical trails using ex vivo retrovirus mediated delivery of interleukin -1 receptor antagonist gene for rheumatoid arthritis has begun in USA and Germany.
  • However, there are still many issues to be elucidated; one is the development of gene delivery system, and the other is the selection of therapeutic gene.
  • Arthritis is nonlethal disease, and safety is one of the important issues.
  • Currently viral mediated vectors are major even in clinical trials however, non viral efficient gene transfer system should be developed in future.
  • Recently the application of DNA technologies, such as antisense oligonucleotide (ODN) strategies to regulate the transcription of disease-related genes in vivo, has significant therapeutic potential.
  • Transfection of cis-clement double-stranded oligonucleotides (decoy ODN) for nuclear factor kappaB binding site has been reported as a new powerful tool in arthritis.
  • The concept of regulation the disease related gene expression at the level of transcriptional factor may be more therapeutic effects compared with monotherapy in arthritis.
  • [MeSH-major] Arthritis / genetics. Genetic Therapy / methods

  • Genetic Alliance. consumer health - Arthritis.
  • MedlinePlus Health Information. consumer health - Arthritis.
  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14577650.001).
  • [ISSN] 1389-4501
  • [Journal-full-title] Current drug targets
  • [ISO-abbreviation] Curr Drug Targets
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Oligodeoxyribonucleotides, Antisense
  • [Number-of-references] 41
  •  go-up   go-down


36. Stokes ME, Muehlenbein CE, Marciniak MD, Faries DE, Motabar S, Gillespie TW, Lipscomb J, Knopf KB, Buesching DP: Neutropenia-related costs in patients treated with first-line chemotherapy for advanced non-small cell lung cancer. J Manag Care Pharm; 2009 Oct;15(8):669-82
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Neutropenia-related costs in patients treated with first-line chemotherapy for advanced non-small cell lung cancer.
  • BACKGROUND: Neutropenia is a major adverse event often associated with chemotherapy administration.
  • Monitoring and treatment of neutropenia thus place an economic burden on the health care system.
  • OBJECTIVES: To evaluate (a) costs and medical resource use for chemotherapy- related afebrile and febrile neutropenia in an elderly population with Stage IIIB or Stage IV non-small cell lung cancer (NSCLC), and (b) costs unrelated to neutropenia and total all-cause health care costs during first-line chemotherapy.
  • METHODS: Study patients in this retrospective database analysis were aged 65 years or older with a diagnosis of Stage IIIB or Stage IV NSCLC in the Surveillance, Epidemiology and End Results (SEER) cancer registry from 1998 through 2002.
  • Neutropenia was identified by the presence of a primary or secondary diagnosis code for diseases of white blood cells (ICD-9-CM = 288.xx) during a period of first-line chemotherapy treatment.
  • Febrile neutropenia was defined by (a) an inpatient hospitalization with a primary or secondary diagnosis for neutropenia occurring at any time during first-line chemotherapy or (b) intravenous or intramuscular antibiotic administration occurring after the initial neutropenia diagnosis and during first-line chemotherapy.
  • Patients were followed in the SEER-Medicare database to evaluate costs (defined as all Medicare payments, primary insurer payments, and patient copayments and deductibles) and resource use associated with afebrile or febrile neutropenia while on first-line chemotherapy.
  • If a patient switched to second-line chemotherapy, the day prior to the switch was defined as the end of first-line treatment.
  • If a switch to second-line therapy did not occur, then first-line therapy was assumed to end 30 days following administration of the last first-line agent.
  • Costs were summed for 2 main types of cost measures: neutropenia-related costs, defined as costs for claims with either a primary or secondary diagnosis of neutropenia, and costs unrelated to neutropenia.
  • Costs were classified using ICD-9-CM diagnosis and procedure codes appearing on the claims, with confidence intervals [CIs] for cost measures estimated by using nonparametric bootstrapping methods.
  • The no neutropenia group was used as the reference category for comparisons involving patient characteristic, medical utilization, and total all-cause health care cost study measures.
  • RESULTS: Among elderly patients treated first-line for advanced NSCLC, 5,138 met inclusion criteria, of whom 1,228 (23.9%) developed afebrile (n = 740, 14.4%) or febrile neutropenia (n = 488, 9.5%) while on first-line chemotherapy.
  • Mean per patient costs for treating neutropenia during first-line chemotherapy were $12,148 (standard deviation [SD] = $15,432, 95% confidence interval [CI] = $10,915-$13,607) for patients with febrile neutropenia and $3,099 (SD = $4,541, 95% CI = $2,796-$3,431) for patients with afebrile neutropenia (P<0.001), with mean (SD) length of follow-up (duration of first-line chemotherapy) of 4.5 (4.8) and 5.5 (7.0) months, respectively.
  • Expressed as a percentage of total all-cause health care costs during first-line chemotherapy, neutropenia-related costs accounted for 32.2% of total costs for patients with febrile neutropenia (mean [SD] = $37,694 [$26,078]) and 9.1% of total costs for patients with afebrile neutropenia (mean [SD] = $34,204 [$26,317]).
  • Mean neutropenia-related costs per patient per month (PPPM) during first-line chemotherapy were $2,700 for patients with febrile neutropenia and $563 for patients with afebrile neutropenia.
  • In sensitivity analyses, results were highly sensitive to the definition of neutropenia (i.e., claims with primary diagnosis only vs. primary or secondary diagnosis) but insensitive to the type of chemotherapy regimen.
  • For elderly patients undergoing first-line chemotherapy for NSCLC, neutropenia, particularly febrile neutropenia, is associated with substantially higher total all-cause health care costs.
  • [MeSH-minor] Aged. Aged, 80 and over. Carcinoma, Non-Small-Cell Lung / drug therapy. Databases, Factual. Fever / chemically induced. Fever / economics. Humans. Lung Neoplasms / drug therapy. Medicare / economics. Neoplasm Staging. Retrospective Studies. SEER Program / statistics & numerical data. United States


37. Frey B, Buettiker V, Hug MI, Waldvogel K, Gessler P, Ghelfi D, Hodler C, Baenziger O: Does critical incident reporting contribute to medication error prevention? Eur J Pediatr; 2002 Nov;161(11):594-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Does critical incident reporting contribute to medication error prevention?
  • Medication-related critical incidents (CIs) comprise harmful and potentially harmful events.
  • In a prospective survey, we analysed our drug-related CIs of the year 2001 with an emphasis on how they contributed to system changes.
  • A voluntary, anonymous, non-punitive CI reporting was used.
  • The study was performed in a multidisciplinary, 23-bed, neonatal-paediatric intensive care unit (ICU).
  • CI severity was graded: minor (no interventions required), moderate (requiring routine therapy, available outside the ICU), major (need for therapeutic interventions specific to the ICU).
  • There were 284 drug-related CIs, 76% (95% confidence interval 71%-81%) of minor, 19% of moderate and 5% of major severity.
  • A total of 24 CIs were potentially life threatening (if not detected).
  • Some 27% of CIs were intercepted, 17% before preparation and 10% before administration of the drug to the patient.
  • There was a negative correlation between median delay (from CI to detection) and mean severity of the different drug classes involved (P = 0.027).
  • As to the impact on quality, 46 CIs were followed by system changes and 63% (95% confidence interval 49%-77%) of these CIs were of minor severity.
  • Examples of system changes are: double checking for potentially harmful drugs, standardised prescription form and contact to the national drug control agency regarding misleading drug labels.
  • CONCLUSION: most of the system changes were based on minor critical incidents which were often detected only after a longer period of time.
  • Repeated checks along the drug delivery process (prescription, preparation, administration) are an important means to reduce adverse drug events.
  • [MeSH-major] Disclosure. Intensive Care Units, Neonatal / standards. Intensive Care Units, Pediatric / standards. Medication Errors / prevention & control. Quality Assurance, Health Care / methods. Risk Management
  • [MeSH-minor] Child. Drug Monitoring. Drug Packaging. Humans. Infant, Newborn. Switzerland

  • MedlinePlus Health Information. consumer health - Medication Errors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12424584.001).
  • [ISSN] 0340-6199
  • [Journal-full-title] European journal of pediatrics
  • [ISO-abbreviation] Eur. J. Pediatr.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] Germany
  •  go-up   go-down


38. Yamashita H, Nakagawa K, Tago M, Igaki H, Nakamura N, Shiraishi K, Sasano N, Ohtomo K: Radiation therapy combined with cis-diammine-glycolatoplatinum (nedaplatin) and 5-fluorouracil for Japanese stage II-IV esophageal cancer compared with cisplatin plus 5-fluorouracil regimen: a retrospective study. Dis Esophagus; 2006;19(1):15-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiation therapy combined with cis-diammine-glycolatoplatinum (nedaplatin) and 5-fluorouracil for Japanese stage II-IV esophageal cancer compared with cisplatin plus 5-fluorouracil regimen: a retrospective study.
  • To evaluate the treatment outcome of radiotherapy combined with cis-diammine-glycolatoplatinum (nedaplatin) plus 5-fluorouracil (5-FU) for esophageal cancer.
  • From January 2000 to December 2004, a total of 12 esophageal cancer patients with locally advanced and metastatic esophageal cancer (stages II-IVB) were treated with radiation therapy (50.4 Gy) combined with nedaplatin (80 mg/m(2), bolus infusion) and 5-FU (800 mg/m(2)/24 h, continuous infusion for 4 days) (NDP group).
  • We compared the data with those of patients during the same period receiving a different chemotherapy regimen consisting of cisplatin (75 mg/m(2), bolus infusion) and 5-FU (1000 mg/m(2)/24 h, continuous infusion for 4 days) (n = 29, CDDP group) combined with the same radiation therapy.
  • Radiation combined with nedaplatin and 5-FU is a safe and effective method for treating esophageal cancer.

  • Genetic Alliance. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16364038.001).
  • [ISSN] 1120-8694
  • [Journal-full-title] Diseases of the esophagus : official journal of the International Society for Diseases of the Esophagus
  • [ISO-abbreviation] Dis. Esophagus
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Organoplatinum Compounds; 8UQ3W6JXAN / nedaplatin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


39. Feng WH, Cohen JI, Fischer S, Li L, Sneller M, Goldbach-Mansky R, Raab-Traub N, Delecluse HJ, Kenney SC: Reactivation of latent Epstein-Barr virus by methotrexate: a potential contributor to methotrexate-associated lymphomas. J Natl Cancer Inst; 2004 Nov 17;96(22):1691-702
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we determined whether MTX, in contrast to other commonly used medications for rheumatoid arthritis or polymyositis, is unique in its ability to induce the release of infectious EBV from latently infected cells.
  • METHODS: The effect of MTX and other immunosuppressant drugs on EBV replication in vitro was assessed using latently infected EBV-positive lymphoblastoid and gastric carcinoma cell lines.
  • Drug effects on transcription of the two EBV immediate-early promoters (BRLF1 and BZLF1) and on promoter constructs lacking cis-acting sequences required for activation by other effectors was examined using reporter gene assays.
  • EBV viral load in rheumatoid arthritis and polymyositis patients receiving MTX was compared with that in patients receiving other immunosuppressive medications.
  • RESULTS: MTX activated the release of infectious EBV from latently infected cell lines in vitro, and MTX treatment was associated with activation of the two viral immediate-early promoters in reporter gene assays.
  • Induction of lytic EBV infection by MTX required the p38 MAP kinase, PI3 kinase, and MEK pathways and specific cis-acting motifs in the two viral immediate-early promoters.
  • [MeSH-major] DNA, Viral / drug effects. Gene Expression Regulation, Viral / drug effects. Herpesvirus 4, Human / drug effects. Immunosuppressive Agents / adverse effects. Lymphoma / virology. Methotrexate / adverse effects
  • [MeSH-minor] Arthritis, Rheumatoid / drug therapy. Cell Line, Tumor. Epstein-Barr Virus Infections / complications. Epstein-Barr Virus Infections / diagnosis. Gene Expression Regulation, Neoplastic. Humans. MAP Kinase Kinase Kinases / metabolism. Phosphatidylinositol 3-Kinases / metabolism. Polymerase Chain Reaction. Polymyositis / drug therapy. Promoter Regions, Genetic. Signal Transduction / drug effects. Viral Load. p38 Mitogen-Activated Protein Kinases / metabolism

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • COS Scholar Universe. author profiles.
  • Nature Publishing Group. commentaries/discussion - Highlights from Nature Reviews Cancer .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15547182.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01-CA19014; United States / NHLBI NIH HHS / HL / R01 HL 64851; United States / NCI NIH HHS / CA / R01-CA 66519; United States / NCI NIH HHS / CA / R01-CA58853
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Viral; 0 / Immunosuppressive Agents; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 2.7.11.25 / MAP Kinase Kinase Kinases; YL5FZ2Y5U1 / Methotrexate
  •  go-up   go-down


40. Ott OJ, Rödel C, Weiss C, Wittlinger M, St Krause F, Dunst J, Fietkau R, Sauer R: Radiochemotherapy for bladder cancer. Clin Oncol (R Coll Radiol); 2009 Sep;21(7):557-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Radiochemotherapy for bladder cancer.
  • Standard treatment for muscle-invasive bladder cancer is cystectomy.
  • Multimodality treatment, including transurethral resection of the bladder tumour, radiation therapy, chemotherapy and deep regional hyperthermia, has been shown to produce survival rates comparable with those of cystectomy.
  • With these programmes, cystectomy has been reserved for patients with incomplete response or local relapse.
  • During the past two decades, organ preservation by multimodality treatment has been investigated in prospective series from single centres and co-operative groups, with more than 1000 patients included.
  • Clinical criteria helpful in determining patients for bladder preservation include such variables as small tumour size (<5 cm), early tumour stage, a visibly and microscopically complete transurethral resection, absence of ureteral obstruction, and no evidence of pelvic lymph node metastases.
  • On multivariate analysis, the completeness of transurethral resection of a bladder tumour was found to be one of the strongest prognostic factors for overall survival.
  • Patients at greater risk of new tumour development after initial complete response are those with multifocal disease and extensive associated carcinoma in situ at presentation.
  • Future investigations will focus on optimising radiation techniques, including all possibilities of radiosensitisation (e.g. concurrent radiochemotherapy, deep regional hyperthermia), and incorporating more effective systemic chemotherapy, and the proper selection of patients based on predictive molecular makers.
  • [MeSH-major] Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / radiotherapy
  • [MeSH-minor] Combined Modality Therapy. Developing Countries. Humans. Hyperthermia, Induced

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19564101.001).
  • [ISSN] 1433-2981
  • [Journal-full-title] Clinical oncology (Royal College of Radiologists (Great Britain))
  • [ISO-abbreviation] Clin Oncol (R Coll Radiol)
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 68
  •  go-up   go-down


41. Laitman CJ: DES exposure and the aging woman: mothers and daughters. Curr Womens Health Rep; 2002 Oct;2(5):390-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] DES exposure and the aging woman: mothers and daughters.
  • Diethylstilbestrol (DES), the first orally active artificial estrogen ever developed, was prescribed to several million pregnant women during the 1940s through the 1960s in the mistaken belief that it reduced the risk of miscarriage.
  • In 1971, the US Food and Drug Administration contraindicated its use in pregnancy when DES was associated with the development of vaginal clear cell adenocarcinoma (CCA) in daughters exposed in utero.
  • In daughters whose mothers took DES during pregnancy, the drug has been associated with congenital malformations of the reproductive tract, fertility problems, a possible increased risk of cervical carcinoma in situ, and a presumed lifetime risk of vaginal and cervical CCA.
  • DES mothers have an increased risk of breast cancer (RR = 1.3).
  • DES sons have an increased prevalence of urogenital anomalies, and a possible increased risk of testicular cancer.
  • [MeSH-minor] Adenocarcinoma / chemically induced. Breast Neoplasms / chemically induced. Carcinoma in Situ / chemically induced. Estrogen Replacement Therapy. Female. Genitalia, Female / abnormalities. Humans. Mothers. Nuclear Family. Pregnancy. Pregnancy Complications / prevention & control. Pregnancy, High-Risk. Risk Factors. Uterine Cervical Neoplasms / chemically induced. Vaginal Neoplasms / chemically induced

  • MedlinePlus Health Information. consumer health - Seniors' Health.
  • Hazardous Substances Data Bank. DIETHYLSTILBESTROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12215312.001).
  • [ISSN] 1534-5874
  • [Journal-full-title] Current women's health reports
  • [ISO-abbreviation] Curr Womens Health Rep
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 731DCA35BT / Diethylstilbestrol
  •  go-up   go-down


42. Paldino MJ, Barboriak D, Desjardins A, Friedman HS, Vredenburgh JJ: Repeatability of quantitative parameters derived from diffusion tensor imaging in patients with glioblastoma multiforme. J Magn Reson Imaging; 2009 May;29(5):1199-205
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Sixteen patients with glioblastoma multiforme underwent MR imaging at two time points without interval intervention.
  • Volumes of tumor-related enhancement (TRE) and FLAIR signal abnormality (FSA) were defined using a semiautomated segmentation technique.
  • Within TRE, repeatability coefficients and 95% confidence intervals (CIs) for change measured 0.104 x 10(-3) mm(2)S(-1) and 7.4% (ADC) and 0.0196 and 13.9% (FA), respectively.
  • CONCLUSION: Changes after therapy greater than the repeatability coefficient or 95% CI for change are unlikely to be related to variability in the measurement of ADC and FA.
  • [MeSH-major] Algorithms. Brain Neoplasms / diagnosis. Diffusion Magnetic Resonance Imaging / methods. Glioblastoma / diagnosis. Image Interpretation, Computer-Assisted / methods

  • Genetic Alliance. consumer health - Glioblastoma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19388113.001).
  • [ISSN] 1053-1807
  • [Journal-full-title] Journal of magnetic resonance imaging : JMRI
  • [ISO-abbreviation] J Magn Reson Imaging
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


43. Zhang JX, Fong WF, Wu JY, Yang M, Cheung HY: Pyranocoumarins isolated from Peucedanum praeruptorum as differentiation inducers in human leukemic HL-60 cells. Planta Med; 2003 Mar;69(3):223-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Differentiation therapy for myeloid leukemia offers great potential as a supplement to the current treatment modalities.
  • In the present report, we investigated if the pyranocoumarins, (+/-)-4'- O-acetyl-3'- O-angeloyl- cis-khellactone (or angular pyranocoumarin, APC) isolated from the medicinal plant Peucedanum praeruptorum Dunn, could induce human acute myeloid leukemic HL-60 cells to differentiate and elucidated the molecular mechanism(s) involved.
  • The ability of HL-60 cells to reduce nitroblue tetrazolium (NBT) was significantly increased after APC treatment for 72 h.
  • The differentiation inducing effect of APC was time- and dose-dependent.
  • Treatment with 20 microg/mL APC for 72 h inhibited cell growth by 90 % and cell cycle analysis revealed an increase in the proportion of G1 phase cells.
  • Pre-incubation of the cells with MEK1 inhibitor PD98059 blocked this APC-induced differentiation.
  • Our results suggest that APC are potent inducers of HL-60 cell differentiation along both the myelocytic and monocytic lineages and are potential agents for differentiation-treatment of leukemia.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apiaceae. Cell Differentiation / drug effects. Phytotherapy. Plant Preparations / pharmacology. Pyranocoumarins / pharmacology
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Cycle Proteins / metabolism. Cyclin-Dependent Kinase Inhibitor p27. Dose-Response Relationship, Drug. Flow Cytometry. Gene Expression Regulation, Leukemic. HL-60 Cells / drug effects. Humans. Leukemia, Myeloid / drug therapy. Leukemia, Myeloid / pathology. Tumor Suppressor Proteins / metabolism


44. Woźniak K, Walter Z: Immunospecific protein of 34.5 kDa from DNA-protein cross-links induced by cis- and trans-diamminedichloroplatinum. Cell Biol Int; 2002;26(6):495-503
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunospecific protein of 34.5 kDa from DNA-protein cross-links induced by cis- and trans-diamminedichloroplatinum.
  • Cis-diamminedichloroplatinum(II) (cis-DDP) is one of the most often used anticancer drugs.
  • It is generally accepted that the antitumor activity of the drug results from its interactions with DNA.
  • In the present work the lymphocyte nuclear proteins that participate in DNA-protein cross-links induced by cis- and trans-DDP are investigated.
  • It is shown that additional proteins of 28, 30, 34.5, 45 and 120 kDa are cross-linked with DNA in lymphocytes after 2-h incubation with cis-DDP at concentrations of 0.1 and 0.5 mM.
  • Trans-DDP does not bind additional proteins to DNA after the same incubation time.
  • Electrophoretic analysis shows that trans-DDP binds much more of the same nuclear proteins to DNA than cis-DDP after 12-h incubation.
  • This protein appears in the samples obtained after 12-h incubation of lymphocytes with cis- and trans-DDP at 0.5 and 1 mM, especially.
  • [MeSH-major] Cisplatin / pharmacology. Cross-Linking Reagents / pharmacology. DNA / drug effects. DNA-Binding Proteins / isolation & purification. Lymphocytes / drug effects. Nuclear Proteins / isolation & purification
  • [MeSH-minor] Antibody Specificity / immunology. Antineoplastic Agents / pharmacology. Cell Survival / drug effects. Cell Survival / immunology. Cells, Cultured. Dose-Response Relationship, Drug. Humans. Neoplasms / drug therapy

  • Hazardous Substances Data Bank. TRANS-DIAMMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12119176.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cross-Linking Reagents; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 14913-33-8 / transplatin; 9007-49-2 / DNA; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


45. Akbar Ali M, Mirza AH, Butcher RJ, Tarafder MT, Keat TB, Ali AM: Biological activity of palladium(II) and platinum(II) complexes of the acetone Schiff bases of S-methyl- and S-benzyldithiocarbazate and the X-ray crystal structure of the [Pd(asme)2] (asme=anionic form of the acetone Schiff base of S-methyldithiocarbazate) complex. J Inorg Biochem; 2002 Nov 25;92(3-4):141-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Biological activity of palladium(II) and platinum(II) complexes of the acetone Schiff bases of S-methyl- and S-benzyldithiocarbazate and the X-ray crystal structure of the [Pd(asme)2] (asme=anionic form of the acetone Schiff base of S-methyldithiocarbazate) complex.
  • Palladium(II) and platinum(II) complexes of general empirical formula, [M(NS)(2)] (NS=uninegatively charged acetone Schiff bases of S-methyl- and S-benzyldithiocarbazate; M=Pt(II) and Pd(II)) have been prepared and characterized by a variety of physicochemical techniques.
  • The crystal and molecular structure of the [Pd(asme)(2)] complex (asme=anionic form of the acetone Schiff base of S-methyldithiocarbazate) has been determined by X-ray diffraction.
  • The complex has a distorted cis-square planar structure with the ligands coordinated to the palladium(II) ions as uninegatively charged bidentate NS chelating agents via the azomethine nitrogen and the mercaptide sulfur atoms.
  • Antimicrobial tests indicate that the Schiff bases exhibit strong activities against the pathogenic bacteria, Bacillus subtilis (mutant defective DNA repair), methicillin-resistant Staphylococcus aureus, B. subtilis (wild type) and Pseudomonas aeruginosa and the fungi, Candida albicans (CA), Candida lypotica (2075), Saccharomyces cerevisiae (20341) and Aspergillus ochraceous (398)-the activities exhibited by these compounds being greater than that of the standard antibacterial and antifungal drugs, streptomycin and nystatin, respectively.
  • Screening of the compounds for their cytotoxicities against T-lymphoblastic leukemia cancer cells has shown that the acetone Schiff base of S-methyldithiocarbazate (Hasme) exhibits a very weak activity, whereas the S-benzyl derivative (Hasbz) is inactive.
  • However, the palladium(II) complexes exhibit strong cytotoxicities against this cancer; their activities being more than that of the standard anticancer drug, tamoxifen.
  • [MeSH-minor] Acetone. Anti-Bacterial Agents. Antineoplastic Agents / chemistry. Bacteria / drug effects. Candida / drug effects. Crystallography, X-Ray. Humans. Hydrazines / chemistry. Hydrazines / pharmacology. Leukemia / drug therapy. Leukemia / pathology. Microbial Sensitivity Tests. Molecular Structure. Schiff Bases. Tumor Cells, Cultured

  • Hazardous Substances Data Bank. ACETONE .
  • Hazardous Substances Data Bank. PALLADIUM, ELEMENTAL .
  • Hazardous Substances Data Bank. PLATINUM .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • Saccharomyces Genome Database. Saccharomyces Genome Database .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12433421.001).
  • [ISSN] 0162-0134
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Infective Agents; 0 / Antineoplastic Agents; 0 / Hydrazines; 0 / Organometallic Compounds; 0 / Schiff Bases; 1364PS73AF / Acetone; 471-31-8 / carbazic acid; 49DFR088MY / Platinum; 5TWQ1V240M / Palladium
  •  go-up   go-down


46. Haugnes HS, Aass N, Fosså SD, Dahl O, Brydøy M, Aasebø U, Wilsgaard T, Bremnes RM: Pulmonary function in long-term survivors of testicular cancer. J Clin Oncol; 2009 Jun 10;27(17):2779-86
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pulmonary function in long-term survivors of testicular cancer.
  • PURPOSE: Long-term toxicity after cancer treatment has gained increasing clinical attention.
  • We evaluated pulmonary function in long-term survivors of testicular cancer (TC).
  • The patients were categorized into five treatment groups, as follows: surgery only (n = 202); radiotherapy only (n = 449); chemotherapy (cisplatin < or = 850 mg; n = 306); chemotherapy (cisplatin > 850 mg [higher-dose group]; n = 62); and chemotherapy and pulmonary surgery (cis/pulmsurg; n = 30).
  • Restrictive lung disease was defined as FEV1/FVC > or = 70% and FVC%pred less than 80%.
  • RESULTS: Median observation time was 11.2 years (range, 5 to 21 years).
  • Compared with the surgery group, the higher-dose or cis/pulmsurg groups had considerably lower age-adjusted FVC (higher-dose: beta = -.37; P = .001; cis/pulmsurg: beta = -.58; P < .001), FEV1 (higher-dose: beta = -.24; P = .014; cis/pulmsurg: beta = -.55; P < .001), FVC%pred (higher-dose: beta = -8.3; cis/pulmsurg: beta = -10.5; bothP < .001), and FEV1%pred (higher-dose: beta = -6.8; P = .003; cis/pulmsurg: beta = -12.4; P < .001).
  • Eight percent of all patients had restrictive lung disease, and the highest prevalence was in the higher-dose group (17.7%) and the cis/pulmsurg (16.7%) group.
  • Compared with patients who underwent surgery only, these groups had odds ratio for restrictive disease of 3.1 (95% CI, 1.3 to 7.3) and 2.5 (95% CI, 0.8 to 7.6), respectively.
  • CONCLUSION: Large doses of cisplatin-based chemotherapy and combined chemotherapy/pulmonary surgery are significantly associated with decreased pulmonary function several years after TC treatment.
  • [MeSH-major] Lung / physiopathology. Lung Diseases / etiology. Testicular Neoplasms / complications
  • [MeSH-minor] Adolescent. Adult. Aged. Antineoplastic Combined Chemotherapy Protocols / adverse effects. Humans. Lung Neoplasms / etiology. Male. Middle Aged. Survivors. Young Adult

  • Genetic Alliance. consumer health - Testicular cancer.
  • MedlinePlus Health Information. consumer health - Lung Diseases.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19414680.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  •  go-up   go-down


47. Ocker M, Herold C, Ganslmayer M, Hahn EG, Schuppan D: The synthetic retinoid adapalene inhibits proliferation and induces apoptosis in colorectal cancer cells in vitro. Int J Cancer; 2003 Nov 10;107(3):453-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The synthetic retinoid adapalene inhibits proliferation and induces apoptosis in colorectal cancer cells in vitro.
  • Chemotherapy of advanced stages of colorectal carcinoma is unsatisfactory.
  • Retinoids inhibit cell growth and induce apoptosis in a variety of human malignancies.
  • We compared the effect of the synthetic retinoid adapalene (ADA) and 9-cis-retinoic acid (CRA) on carcinoma cell lines in vitro.
  • Colon carcinoma cell lines CC-531, HT-29 and LOVO as well as human foreskin fibroblasts were exposed to different concentrations of ADA and CRA for 3-72 hr.
  • Both retinoic derivatives suppressed DNA synthesis and induced apoptosis in all tested cell lines time- and dose-dependently.
  • ADA and CRA disrupt DeltaPsi(m) and induce caspase-3 activity in responsive tumor cells.
  • Therefore, we suggest that ADA may be far more suitable as an adjunctive therapeutic agent for treatment of colon cancer in vivo.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Colorectal Neoplasms / drug therapy. Naphthalenes / pharmacology
  • [MeSH-minor] Adapalene. Caspase 3. Caspases / metabolism. Cell Division / drug effects. Humans. Proto-Oncogene Proteins / physiology. Proto-Oncogene Proteins c-bcl-2 / physiology. Tretinoin / pharmacology. Tumor Cells, Cultured. bcl-2-Associated X Protein

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ALITRETINOIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2003 Wiley-Liss, Inc.
  • (PMID = 14506747.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Naphthalenes; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 1L4806J2QF / Adapalene; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases
  •  go-up   go-down


48. Cirenajwis H, Smiljanic S, Honeth G, Hegardt C, Marton LJ, Oredsson SM: Reduction of the putative CD44+CD24- breast cancer stem cell population by targeting the polyamine metabolic pathway with PG11047. Anticancer Drugs; 2010 Nov;21(10):897-906
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduction of the putative CD44+CD24- breast cancer stem cell population by targeting the polyamine metabolic pathway with PG11047.
  • Cancer stem cells (CSCs) are considered to be of particular concern in cancer as they possess inherent properties of self-renewal and differentiation, along with expressing certain genes related to a mesenchymal phenotype.
  • These features favour the promotion of tumour recurrence and metastasis in cancer patients.
  • Thus, the optimal chemotherapeutic treatment should target the CSC population, either by killing these cells and/or by inducing their transition to a more differentiated epithelial-like phenotype.
  • Experiments were carried out on the trastuzumab-resistant human epidermal growth factor receptor 2-overexpressing breast cancer cell line JIMT-1 to unravel the chemotherapeutic effects of the polyamine analogue [1N,12N]bis(ethyl)-cis-6,7-dehydrospermine (PG11047) and of the polyamine biosynthetic inhibitor 2-difluoromethylornithine (DFMO) on the CD44+CD24- CSC population.
  • Furthermore, effects on the properties of self-renewal and epithelial/mesenchymal markers were also investigated.
  • Treatment with PG11047 reduced the CD44+CD24- subpopulation of JIMT-1 cells by approximately 50%, inhibited and/or reduced self-renewal capability of the CSC population, decreased cell motility and induced expression of mesenchymal to epithelial transition-associated proteins that are involved in promoting an epithelial phenotype.
  • DFMO treatment reduced the self-renewal capability of the CSC population.
  • Our findings indicate that treatment with PG11047 targeted the CSC population by interfering with several stem cell-related properties, such as self-renewal, differentiation, motility and the mesenchymal phenotype.
  • [MeSH-major] Neoplastic Stem Cells / drug effects. Spermine / analogs & derivatives. Spermine / physiology
  • [MeSH-minor] Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD24 / immunology. Antigens, CD44 / immunology. Antineoplastic Agents / pharmacology. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Differentiation / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Drug Resistance, Neoplasm. Eflornithine / pharmacology. Epithelial-Mesenchymal Transition / drug effects. Female. Humans. Neoplasm Metastasis. Neoplasm Recurrence, Local / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / physiology. Trastuzumab


49. Orallo F: Comparative studies of the antioxidant effects of cis- and trans-resveratrol. Curr Med Chem; 2006;13(1):87-98
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparative studies of the antioxidant effects of cis- and trans-resveratrol.
  • Resveratrol (3,4',5-trihydroxystilbene, RESV) is a natural phenolic compound that exists as cis and trans isomers [c-RESV or (Z)-RESV and t-RESV or (E)-RESV, respectively].
  • RESV also exists in wines as a cis isomer, which (unlike t-RESV) is not currently available commercially; as a result, little is known about this isomer's pharmacological activity.
  • [MeSH-minor] Animals. Inflammation / drug therapy. Inflammation / metabolism. Interferon-gamma / pharmacology. Kluyveromyces / pathogenicity. Lipid Peroxidation / drug effects. Lipopolysaccharides / pharmacology. Macrophages, Peritoneal / drug effects. Macrophages, Peritoneal / metabolism. Mice. Rats. Reactive Oxygen Species / metabolism. Stereoisomerism

  • MedlinePlus Health Information. consumer health - Antioxidants.
  • Hazardous Substances Data Bank. RESVERATROL .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16457641.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Lipopolysaccharides; 0 / Reactive Oxygen Species; 0 / Stilbenes; 82115-62-6 / Interferon-gamma; Q369O8926L / resveratrol
  • [Number-of-references] 99
  •  go-up   go-down


50. Cossa G, Gatti L, Zunino F, Perego P: Strategies to improve the efficacy of platinum compounds. Curr Med Chem; 2009;16(19):2355-65
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Platinum drugs are widely used in antitumour therapy and are a cornerstone of the treatment of different solid tumours.
  • The pharmacological interest of cisplatin has led to the design of many analogues to broaden the spectrum of activity, reduce side effects, and overcome resistance.
  • Although the cis configuration was initially identified as the only active one, trans-platinum complexes have shown significant antitumour activity in preclinical models.
  • Since a major limitation to the clinical efficacy of platinum compounds is drug resistance, the most important feature of nonconventional platinum drugs should be the capability of overcoming cellular resistance.
  • However, due to the multifactorial nature of clinical resistance, which also involves pharmacological factors, the optimisation of current platinum-based therapy also includes the development of drug delivery approaches.
  • The present review focuses on recent studies on the molecular alterations of tumour cells that are associated with resistance to platinum drugs, the development of novel platinum drugs, and approaches that may contribute to improve the efficacy of platinum-based therapy.
  • [MeSH-minor] Cisplatin / pharmacology. DNA / metabolism. Drug Carriers. Humans. Neoplasms / drug therapy

  • Hazardous Substances Data Bank. PLATINUM COMPOUNDS .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19601785.001).
  • [ISSN] 1875-533X
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; 0 / Platinum Compounds; 9007-49-2 / DNA; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 97
  •  go-up   go-down


51. Simon D, Körber C, Krausch M, Segering J, Groth P, Görges R, Grünwald F, Müller-Gärtner HW, Schmutzler C, Köhrle J, Röher HD, Reiners C: Clinical impact of retinoids in redifferentiation therapy of advanced thyroid cancer: final results of a pilot study. Eur J Nucl Med Mol Imaging; 2002 Jun;29(6):775-82
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical impact of retinoids in redifferentiation therapy of advanced thyroid cancer: final results of a pilot study.
  • Differentiated thyroid cancer is a malignant tumour that has a fairly good prognosis, with patients surviving for many years.
  • Multimodal therapy with surgery, radioiodine therapy and TSH suppressive medication is of proven efficacy.
  • However, loss of differentiation is observed in up to one-third of patients with differentiated thyroid cancer, paralleled by an increase in tumour grading and loss of thyroid-specific functions (thyrotropin receptor, iodine accumulation).
  • Such tumours may no longer be amenable to standard treatment protocols, including TSH suppression and radioiodide therapy.
  • Patients with advanced thyroid cancer and without the therapeutic options of operation or radioiodide therapy were treated with 13- cis-retinoic acid at a dosage of 1.5 mg/kg body weight daily over 5 weeks.
  • Parameters for assessment of the therapeutic effect were serum thyroglobulin (TG) levels, radioiodine uptake, and tumour size prior to and after retinoid treatment.
  • Fifty patients were evaluated for response, classified as reduction in tumour size and TG levels, stable disease or disease progression.
  • Tumour size was assessable in 37 patients; tumour regression was observed in six, and there was no change in 22.
  • Response to retinoid therapy did not always correlate with increased radioiodine uptake, so other direct antiproliferative effects have to be assumed.
  • The encouraging results of the study and the low rate of side-effects with good tolerability of retinoids warrant further studies with altered inclusion criteria and employment of other redifferentiating drugs or combinations of agents.
  • [MeSH-major] Isotretinoin / therapeutic use. Thyroglobulin. Thyroid Neoplasms / diagnosis. Thyroid Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / drug therapy. Adenocarcinoma / radionuclide imaging. Adenocarcinoma / therapy. Adenocarcinoma, Follicular / diagnosis. Adenocarcinoma, Follicular / drug therapy. Adenocarcinoma, Follicular / radionuclide imaging. Adenocarcinoma, Follicular / therapy. Adult. Aged. Carcinoma, Papillary / diagnosis. Carcinoma, Papillary / drug therapy. Carcinoma, Papillary / radionuclide imaging. Carcinoma, Papillary / therapy. Carcinoma, Papillary, Follicular / diagnosis. Carcinoma, Papillary, Follicular / drug therapy. Carcinoma, Papillary, Follicular / radionuclide imaging. Carcinoma, Papillary, Follicular / therapy. Chemotherapy, Adjuvant. Disease Progression. Female. Follow-Up Studies. Germany. Humans. Iodine Radioisotopes / therapeutic use. Male. Middle Aged. Pilot Projects. Prospective Studies. Treatment Outcome

  • Genetic Alliance. consumer health - Thyroid Cancer.
  • MedlinePlus Health Information. consumer health - Thyroid Cancer.
  • Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .
  • Hazardous Substances Data Bank. THYROGLOBULIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12029551.001).
  • [ISSN] 1619-7070
  • [Journal-full-title] European journal of nuclear medicine and molecular imaging
  • [ISO-abbreviation] Eur. J. Nucl. Med. Mol. Imaging
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 9010-34-8 / Thyroglobulin; EH28UP18IF / Isotretinoin
  •  go-up   go-down


52. Kazanowska B, Reich A, Jelen M, Chybicka A: Chronic metastatic neuroblastoma. Pediatr Blood Cancer; 2008 Apr;50(4):898-900
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The diversity of neuroblastoma and its clinical course depends on histology, biology and clinical features.
  • The diagnosis was made by histological examination of a subcutaneous nodule and elevated urinary markers.
  • During that time no cytostatic treatment was given.
  • Attempt to treat with cis-retinoic acid 10 years later did not result in any significant change of the clinical course.
  • The patient has remained in good clinical condition for a 15-year observation period, having both progressing and regressing distant subcutaneous metastases.
  • Skin nodules are the hallmarks of the indolent clinical course of the disease.
  • We suggest the use of the "chronic neuroblastoma" as a term to describe patients with neuroblastoma showing indolent disease course over a very long period of time, but never achieving complete remission.
  • [MeSH-minor] Adolescent. Adrenal Gland Neoplasms / drug therapy. Adrenal Gland Neoplasms / secondary. Antineoplastic Agents / therapeutic use. Child. Child, Preschool. Chronic Disease. Humans. Immunohistochemistry. Infant. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary. Male. Tretinoin / therapeutic use

  • Genetic Alliance. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Neuroblastoma.
  • MedlinePlus Health Information. consumer health - Skin Cancer.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 17914736.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 5688UTC01R / Tretinoin
  •  go-up   go-down


53. Gwynn ES, Clark PE: Bladder cancer. Curr Opin Oncol; 2006 May;18(3):277-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bladder cancer.
  • PURPOSE OF REVIEW: This article will review the diagnosis and management of bladder cancer at each stage, from superficial to metastatic disease with an emphasis on recent developments over the last year.
  • RECENT FINDINGS: Bacille Calmette-Guerin is the most effective therapy for carcinoma in situ.
  • All patients who receive intravesical therapy with bacille Calmette-Guerin should be considered for ongoing maintenance therapy.
  • The management of muscle invasive disease in the United States centers on radical cystectomy with bilateral pelvic lymphadenectomy.
  • Areas of research include the optimal role for bladder preservation therapy, a growing experience in centers with laparoscopy, the effect of urinary diversion on quality of life, and the optimal standard for pelvic lymphadenectomy at surgery.
  • The role of combination chemotherapy for advanced bladder cancer continues to evolve.
  • Many questions remain unanswered including the relative value of neoadjuvant versus adjuvant chemotherapy for locally advanced disease and optimal chemotherapy regimen.
  • SUMMARY: The detection of bladder cancer continues to rely on direct visualization with cystoscopy.
  • The management of superficial bladder cancer is based on transurethral resection of the tumor with perioperative intravesical instillation of chemotherapy strongly suggested for most patients.
  • Risk stratifying patients with high-risk superficial bladder cancer remain a challenge and area of future research.
  • [MeSH-major] Carcinoma, Transitional Cell. Urinary Bladder Neoplasms
  • [MeSH-minor] Administration, Intravesical. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. BCG Vaccine / administration & dosage. BCG Vaccine / therapeutic use. Carcinoma in Situ / therapy. Combined Modality Therapy. Cystectomy. Disease Management. Humans. Immunotherapy. Lymph Node Excision. Neoadjuvant Therapy. Neoplasm Invasiveness. Neoplasm Metastasis

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16552241.001).
  • [ISSN] 1531-703X
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / BCG Vaccine
  • [Number-of-references] 73
  •  go-up   go-down


54. Shin SJ, DeLellis RA, Ying L, Rosen PP: Small cell carcinoma of the breast: a clinicopathologic and immunohistochemical study of nine patients. Am J Surg Pathol; 2000 Sep;24(9):1231-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Small cell carcinoma of the breast: a clinicopathologic and immunohistochemical study of nine patients.
  • Small cell carcinoma of the breast is an uncommon neoplasm that has been reported rarely in the literature.
  • Nine examples of mammary small cell carcinoma were retrieved from the authors' consultation files and reviewed.
  • Two patients had a previous history of cutaneous malignant melanoma and one had prior lobular carcinoma in situ and atypical duct hyperplasia in the same breast as the small cell carcinoma.
  • Eight patients presented with a mass in the breast; one patient had an axillary tumor.
  • Tumor size ranged from 1.3 to 5.0 cm (mean, 2.6 cm).
  • Histologically, the nine tumors had characteristics of small cell carcinoma with high mitotic activity and necrosis.
  • In one instance, this consisted of small cell carcinoma merging with invasive lobular carcinoma.
  • In three cases, small cell carcinoma was present together with invasive, poorly differentiated duct carcinoma; invasive carcinoma with "lobular and gland-forming elements"; and focal squamous differentiation, respectively.
  • Lymphatic tumor emboli were identified in four instances.
  • An in situ component was seen in seven tumors; five were of the small cell type in ducts and two were of the ductal type with high nuclear grade.
  • One tumor that was reactive for chromogranin and synaptophysin also contained calcitonin immunoreactive cells, whereas gastrin-releasing peptide was present in two other tumors that were also positive for chromogranin.
  • Eight underwent an axillary dissection that revealed metastatic carcinoma in four patients.
  • Seven patients received adjuvant chemotherapy and four patients received radiation.
  • Two patients also received tamoxifen treatment.
  • Metastases developed in two patients (22%) with a follow-up period of 11 and 32 months.
  • All patients were alive at last follow up 3 to 35 months after treatment.
  • When compared with published reports of mammary small cell carcinoma, our results show that the prognosis in these patients may not be as poor as previously suggested.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Small Cell / pathology
  • [MeSH-minor] Adult. Aged. Combined Modality Therapy. Female. Follow-Up Studies. Humans. Immunohistochemistry. Keratins / metabolism. Middle Aged. Receptors, Estrogen / metabolism

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Am J Surg Pathol. 2001 Jun;25(6):831-2 [11395567.001]
  • (PMID = 10976697.001).
  • [ISSN] 0147-5185
  • [Journal-full-title] The American journal of surgical pathology
  • [ISO-abbreviation] Am. J. Surg. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 68238-35-7 / Keratins
  •  go-up   go-down


55. Dalbagni G, Herr HW: Current use and questions concerning intravesical bladder cancer group for superficial bladder cancer. Urol Clin North Am; 2000 Feb;27(1):137-46,
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current use and questions concerning intravesical bladder cancer group for superficial bladder cancer.
  • Bacille Calmette-Guerin (BCG) is the most effective therapy for CIS of the bladder.
  • Although several series have shown a decrease in recurrence and progression of T1 tumor, this effect is temporary.
  • There is no definitive answer regarding the efficacy of maintenance therapy or the optimum dose of BCG.
  • Randomized trials are needed to address these issues in a more conclusive manner.
  • Phase III trials have shown that mitomycin C can be as effective as BCG in the management of papillary tumors; however, BCG is more effective in patients with CIS and high-risk superficial tumors.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. BCG Vaccine / administration & dosage. Cancer Vaccines / administration & dosage. Carcinoma in Situ / drug therapy. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Intravesical. Biomarkers, Tumor / metabolism. Disease Progression. Drug Administration Schedule. Humans. Neoplasm Recurrence, Local / prevention & control. Remission Induction

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10696252.001).
  • [ISSN] 0094-0143
  • [Journal-full-title] The Urologic clinics of North America
  • [ISO-abbreviation] Urol. Clin. North Am.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BCG Vaccine; 0 / Biomarkers, Tumor; 0 / Cancer Vaccines
  • [Number-of-references] 47
  •  go-up   go-down


56. de la Torre JC: Reverse genetics approaches to combat pathogenic arenaviruses. Antiviral Res; 2008 Dec;80(3):239-50
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Several arenaviruses cause hemorrhagic fever (HF) in humans, and evidence indicates that the worldwide-distributed prototypic arenavirus lymphocytic choriomeningitis virus (LCMV) is a neglected human pathogen of clinical significance.
  • No licensed anti-arenavirus vaccines are available, and current anti-arenavirus therapy is limited to the use of ribavirin, which is only partially effective and is associated with anemia and other side effects.
  • Therefore, it is important to develop effective vaccines and better antiviral drugs to combat the dual threats of naturally occurring and intentionally introduced arenavirus infections.
  • The development of arenavirus reverse genetic systems is allowing investigators to conduct a detailed molecular characterization of the viral cis-acting signals and trans-acting factors that control each of the steps of the arenavirus life cycle, including RNA synthesis, packaging and budding.
  • Knowledge derived from these studies is uncovering potential novel targets for therapeutic intervention, as well as facilitating the establishment of assays to identify and characterize candidate antiviral drugs capable of interfering with specific steps of the virus life cycle.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Antiviral Res. 2008 Apr;78(1):103-15 [18241935.001]
  • [Cites] Antiviral Res. 2008 Apr;78(1):9-25 [18313769.001]
  • [Cites] J Virol. 2008 Jun;82(12):6045-51 [18400865.001]
  • [Cites] J Biol Chem. 2008 Jul 4;283(27):18734-42 [18474596.001]
  • [Cites] Nature. 2004 Mar 25;428(6981):427-31 [15042091.001]
  • [Cites] Virology. 2003 Mar 30;308(1):37-47 [12706088.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7895-900 [12808132.001]
  • [Cites] J Virol. 2003 Aug;77(16):8640-9 [12885882.001]
  • [Cites] J Virol. 2004 Oct;78(20):11443-8 [15452271.001]
  • [Cites] J Virol. 1976 Oct;20(1):157-69 [185410.001]
  • [Cites] Lancet. 1979 Oct 6;2(8145):738 [90819.001]
  • [Cites] J Virol. 1985 Sep;55(3):704-9 [4020963.001]
  • [Cites] Virology. 1985 Apr 15;142(1):175-82 [4060570.001]
  • [Cites] N Engl J Med. 1986 Jan 2;314(1):20-6 [3940312.001]
  • [Cites] Antimicrob Agents Chemother. 1988 Sep;32(9):1304-9 [2848441.001]
  • [Cites] EMBO J. 1989 Dec 1;8(12):3867-74 [2555175.001]
  • [Cites] Cell. 1989 Dec 22;59(6):1107-13 [2598262.001]
  • [Cites] Nature. 1990 Mar 29;344(6265):467-8 [1690861.001]
  • [Cites] Science. 1990 Aug 3;249(4968):505-10 [2200121.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4663-8 [16537369.001]
  • [Cites] J Virol. 2006 Apr;80(8):4191-5 [16571837.001]
  • [Cites] N Engl J Med. 2006 May 25;354(21):2208-11 [16723613.001]
  • [Cites] N Engl J Med. 2006 May 25;354(21):2235-49 [16723615.001]
  • [Cites] PLoS Pathog. 2006 Jun;2(6):e51 [16751848.001]
  • [Cites] Virology. 2006 Jul 5;350(2):370-80 [16476461.001]
  • [Cites] J Biol Chem. 2006 Aug 18;281(33):23471-81 [16790437.001]
  • [Cites] J Virol Methods. 2006 Oct;137(1):115-9 [16837071.001]
  • [Cites] J Virol. 2006 Dec;80(24):12414-9 [17005649.001]
  • [Cites] Protein Expr Purif. 2007 Feb;51(2):308-19 [16973377.001]
  • [Cites] Virus Res. 2007 Mar;124(1-2):237-44 [17125871.001]
  • [Cites] J Virol. 2007 Sep;81(17):9451-60 [17581989.001]
  • [Cites] J Virol. 2007 Oct;81(20):10981-90 [17670839.001]
  • [Cites] J Virol. 2007 Oct;81(20):10849-60 [17686866.001]
  • [Cites] Antiviral Res. 2008 Apr;78(1):132-9 [18054395.001]
  • [Cites] Microbes Infect. 1999 Jul;1(8):609-14 [10611737.001]
  • [Cites] Curr Med Chem. 2000 Jan;7(1):73-98 [10637358.001]
  • [Cites] Antivir Chem Chemother. 2000 Jan;11(1):71-7 [10693656.001]
  • [Cites] J Virol. 2000 Apr;74(8):3470-7 [10729120.001]
  • [Cites] J Virol. 2000 Aug;74(15):6777-83 [10888616.001]
  • [Cites] Comb Chem High Throughput Screen. 2000 Jun;3(3):219-34 [10903381.001]
  • [Cites] Am J Ophthalmol. 2000 Aug;130(2):209-15 [11004296.001]
  • [Cites] Nat Med. 2000 Dec;6(12):1375-9 [11100123.001]
  • [Cites] Curr Opin Chem Biol. 2000 Dec;4(6):678-86 [11102874.001]
  • [Cites] Virus Res. 2001 Jan;73(1):41-55 [11163643.001]
  • [Cites] Mol Cell. 2000 Dec;6(6):1355-64 [11163209.001]
  • [Cites] Mol Cell. 2003 Sep;12(3):627-37 [14527409.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Oct 28;100(22):12978-83 [14563923.001]
  • [Cites] Biochem Soc Symp. 2003;(70):221-31 [14587295.001]
  • [Cites] EMBO Rep. 2003 Nov;4(11):1084-8 [14555961.001]
  • [Cites] J Virol. 2003 Dec;77(23):12617-29 [14610184.001]
  • [Cites] Virology. 2004 Jan 5;318(1):439-50 [14972569.001]
  • [Cites] J Virol. 2004 Mar;78(6):2979-83 [14990716.001]
  • [Cites] J Biol Chem. 2004 Mar 26;279(13):12293-9 [14709548.001]
  • [Cites] Nature. 2004 Mar 25;428(6981):431-7 [15042092.001]
  • [Cites] J Biol Chem. 2004 Apr 23;279(17):17338-47 [14970232.001]
  • [Cites] J Virol. 2004 May;78(10):5068-78 [15113888.001]
  • [Cites] J Biol Chem. 2004 Aug 6;279(32):33782-90 [15178688.001]
  • [Cites] Curr Top Microbiol Immunol. 2004;283:1-41 [15298166.001]
  • [Cites] FEBS Lett. 2004 Aug 27;573(1-3):186-94 [15327996.001]
  • [Cites] J Virol. 2004 Oct;78(19):10783-92 [15367645.001]
  • [Cites] Nature. 1990 Aug 30;346(6287):818-22 [1697402.001]
  • [Cites] J Exp Med. 1990 Oct 1;172(4):1043-8 [2212940.001]
  • [Cites] N Engl J Med. 1990 Oct 18;323(16):1120-3 [2215580.001]
  • [Cites] J Virol. 1991 Apr;65(4):1863-9 [1840619.001]
  • [Cites] Antiviral Res. 1990 Oct-Nov;14(4-5):287-99 [2088208.001]
  • [Cites] Arch Pathol Lab Med. 1992 May;116(5):486-8 [1316111.001]
  • [Cites] Virus Res. 1992 Mar;22(3):185-98 [1626415.001]
  • [Cites] Cell. 1993 Sep 24;74(6):969-78 [8402886.001]
  • [Cites] Antiviral Res. 1993 Sep;22(1):45-75 [8250543.001]
  • [Cites] Annu Rev Biochem. 1996;65:609-34 [8811191.001]
  • [Cites] Antiviral Res. 1996 Jul;31(3):149-58 [8811199.001]
  • [Cites] Clin Infect Dis. 1997 Apr;24(4):718-22 [9145749.001]
  • [Cites] Cell. 1997 May 2;89(3):331-40 [9150132.001]
  • [Cites] J Infect Dis. 1998 Feb;177(2):277-83 [9466512.001]
  • [Cites] J Biol Chem. 1998 Mar 6;273(10):5785-93 [9488713.001]
  • [Cites] Biochemistry. 1998 Apr 21;37(16):5549-57 [9548939.001]
  • [Cites] Bioorg Med Chem Lett. 1998 Sep 8;8(17):2339-44 [9873538.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1321-6 [9990022.001]
  • [Cites] Science. 1999 Apr 23;284(5414):611-5 [10213678.001]
  • [Cites] Pediatr Infect Dis J. 1999 Jun;18(6):540-1 [10391186.001]
  • [Cites] Med Clin North Am. 1999 Jul;83(4):865-83, v [10453254.001]
  • [Cites] J Virol. 2004 Dec;78(24):13793-803 [15564487.001]
  • [Cites] Nat Med. 2004 Dec;10(12 Suppl):S110-21 [15577929.001]
  • [Cites] Virus Res. 2005 Feb;107(2):165-71 [15649562.001]
  • [Cites] Mol Ther. 2005 Mar;11(3):435-43 [15727940.001]
  • [Cites] J Virol. 2005 Mar;79(6):3822-30 [15731275.001]
  • [Cites] J Virol. 2005 Apr;79(7):4519-26 [15767453.001]
  • [Cites] Virology. 2005 Apr 25;335(1):87-98 [15823608.001]
  • [Cites] J Virol. 2005 Jun;79(11):6890-9 [15890928.001]
  • [Cites] J Virol. 2005 Jun;79(11):7262-8 [15890965.001]
  • [Cites] Annu Rev Biochem. 2005;74:739-89 [15952902.001]
  • [Cites] PLoS Med. 2005 Jun;2(6):e183 [15971954.001]
  • [Cites] J Biomol Screen. 2005 Aug;10(5):476-84 [16093557.001]
  • [Cites] J Virol. 2005 Sep;79(17):11071-81 [16103158.001]
  • [Cites] J Virol. 2005 Nov;79(22):13934-42 [16254329.001]
  • [Cites] Neurology. 2006 Jan 24;66(2 Suppl 1):S102-9 [16432136.001]
  • [Cites] Antiviral Res. 2006 Feb;69(2):86-97 [16343651.001]
  • [Cites] Cell. 2006 Feb 10;124(3):587-99 [16469704.001]
  • [Cites] Science. 2001 Mar 23;291(5512):2344-50 [11269314.001]
  • [Cites] J Hum Virol. 2001 Mar-Apr;4(2):103-8 [11437313.001]
  • [Cites] Clin Infect Dis. 2001 Aug 1;33(3):370-4 [11438904.001]
  • [Cites] J Virol. 2001 Oct;75(19):9415-26 [11533204.001]
  • [Cites] Clin Infect Dis. 2001 Nov 15;33(10):1707-12 [11595975.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12701-5 [11606739.001]
  • [Cites] J Virol. 2001 Dec;75(23):11677-85 [11689649.001]
  • [Cites] J Virol. 2001 Dec;75(24):12241-51 [11711615.001]
  • [Cites] Curr Opin Drug Discov Devel. 2001 Jul;4(4):462-70 [11727311.001]
  • [Cites] Arch Biochem Biophys. 2002 Jan 15;397(2):139-48 [11795864.001]
  • [Cites] J Biol Chem. 2002 Mar 29;277(13):11265-75 [11756446.001]
  • [Cites] J Virol. 2002 May;76(9):4162-71 [11932381.001]
  • [Cites] Curr Opin Infect Dis. 2001 Dec;14(6):757-64 [11964896.001]
  • [Cites] Curr Med Chem. 2002 May;9(9):929-39 [11966454.001]
  • [Cites] J Virol. 2002 May;76(10):4679-87 [11967285.001]
  • [Cites] Curr Top Microbiol Immunol. 2002;262:65-74 [11987808.001]
  • [Cites] Curr Top Microbiol Immunol. 2002;262:111-37 [11987803.001]
  • [Cites] Curr Top Microbiol Immunol. 2002;263:1-5 [11987811.001]
  • [Cites] Curr Top Microbiol Immunol. 2002;263:83-117 [11987822.001]
  • [Cites] Curr Top Microbiol Immunol. 2002;263:239-61 [11987817.001]
  • [Cites] JAMA. 2002 May 8;287(18):2391-405 [11988060.001]
  • [Cites] J Virol. 2002 Jun;76(12):6393-7 [12021374.001]
  • [Cites] J Virol. 2002 Jul;76(13):6678-88 [12050381.001]
  • [Cites] J Virol. 2002 Jul;76(14):7263-75 [12072526.001]
  • [Cites] Adv Virus Res. 2002;58:125-55 [12205778.001]
  • [Cites] J Gen Virol. 2002 Nov;83(Pt 11):2635-62 [12388800.001]
  • [Cites] Trends Cell Biol. 2002 Dec;12(12):569-79 [12495845.001]
  • [Cites] Am J Obstet Gynecol. 2002 Dec;187(6):1715-6 [12501090.001]
  • [Cites] J Virol. 2003 Jan;77(2):1184-94 [12502835.001]
  • [Cites] Virology. 2002 Dec 20;304(2):235-45 [12504565.001]
  • [Cites] J Virol. 2003 Mar;77(5):2866-72 [12584310.001]
  • [Cites] J Virol. 2003 Mar;77(6):3578-85 [12610133.001]
  • [Cites] J Virol. 2003 Mar;77(6):3882-7 [12610166.001]
  • [Cites] Bioorg Med Chem. 2003 Apr 17;11(8):1607-13 [12659745.001]
  • [Cites] Nat Rev Mol Cell Biol. 2003 Aug;4(8):631-40 [12923525.001]
  • [Cites] J Virol. 2003 Oct;77(19):10700-5 [12970458.001]
  • [Cites] Angew Chem Int Ed Engl. 2003 Sep 15;42(35):4138-76 [14502729.001]
  • [Cites] Virology. 2003 Sep 15;314(1):168-78 [14517070.001]
  • (PMID = 18782590.001).
  • [ISSN] 1872-9096
  • [Journal-full-title] Antiviral research
  • [ISO-abbreviation] Antiviral Res.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R56 AI047140; United States / NIAID NIH HHS / AI / U54 AI065359-040007; United States / NIAID NIH HHS / AI / R01 AI047140-06A1; United States / NIAID NIH HHS / AI / AI-065359; United States / NIAID NIH HHS / AI / R01 AI047140; United States / NIAID NIH HHS / AI / U54 AI065359; United States / NIAID NIH HHS / AI / AI47140; United States / NIAID NIH HHS / AI / AI065359-040007
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Viral Vaccines
  • [Number-of-references] 144
  • [Other-IDs] NLM/ NIHMS82405; NLM/ PMC2628465
  •  go-up   go-down


57. Yu CS, Lin FC, Liu Y, Duan Y, Lei H, Li KC: Histogram analysis of diffusion measures in clinically isolated syndromes and relapsing-remitting multiple sclerosis. Eur J Radiol; 2008 Nov;68(2):328-34
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The purposes of our study were to employ diffusion tensor imaging (DTI)-based histogram analysis to determine the presence of occult damage in clinically isolated syndrome (CIS), to compare its severity with relapsing-remitting multiple sclerosis (RRMS), and to determine correlations between DTI histogram measures and clinical and MRI indices in these two diseases.
  • MATERIALS AND METHODS: DTI scans were performed in 19 CIS and 19 RRMS patients and 19 matched healthy volunteers.
  • Histogram analyses of mean diffusivity and fractional anisotropy were performed in normal-appearing brain tissue (NABT), normal-appearing white matter (NAWM) and gray matter (NAGM).
  • Correlations were analyzed between these measures and expanded disability status scale (EDSS) scores, T(2)WI lesion volumes (LV) and normalized brain tissue volumes (NBTV) in CIS and RRMS patients.
  • RESULTS: Significant differences were found among CIS, RRMS and control groups in the NBTV and most of the DTI histogram measures of the NABT, NAWM and NAGM.
  • In CIS patients, some DTI histogram measures showed significant correlations with LV and NBTV, but none of them with EDSS.
  • CONCLUSION: Occult damage occurs in both NAGM and NAWM in CIS, but the severity is milder than that in RRMS.
  • In CIS and RRMS, the occult damage might be related to both T2 lesion load and brain tissue atrophy.
  • Some DTI histogram measures might be useful for assessing the disease progression in RRMS patients.
  • [MeSH-major] Demyelinating Diseases / pathology. Diffusion Magnetic Resonance Imaging / methods. Multiple Sclerosis, Relapsing-Remitting / pathology

  • Genetic Alliance. consumer health - Multiple Sclerosis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17928182.001).
  • [ISSN] 0720-048X
  • [Journal-full-title] European journal of radiology
  • [ISO-abbreviation] Eur J Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  •  go-up   go-down


58. Sellers RS, Capen CC, Rosol TJ: Messenger RNA stability of parathyroid hormone-related protein regulated by transforming growth factor-beta1. Mol Cell Endocrinol; 2002 Feb 25;188(1-2):37-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Humoral hypercalcemia of malignancy (HHM), a paraneoplastic syndrome associated with epithelial cancers, including squamous cell carcinoma (SCC), is due to expression and secretion of parathyroid hormone-related protein (PTHrP).
  • In this study, oral squamous carcinoma cells (SCC2/88) had a two-fold increase in PTHrP mRNA stability (from 45 to 90 min) in response to treatment with TGFbeta1.
  • TGFbeta1 treatment resulting in decreased binding of 33, 31, 27, 20 and 18 kDa binding proteins to the terminal coding region.
  • These studies revealed that TGFbeta1-induced PTHrP mRNA stability might be, in part, the result of cis-acting sequences within the coding region of the PTHrP mRNA.
  • [MeSH-major] 3' Untranslated Regions / metabolism. Carcinoma, Squamous Cell / metabolism. Gene Expression / drug effects. Proteins / genetics. Proteins / metabolism. RNA, Messenger / metabolism. Transforming Growth Factor beta / pharmacology
  • [MeSH-minor] Animals. Cell-Free System. Cross-Linking Reagents. DNA Primers / chemistry. Dichlororibofuranosylbenzimidazole / pharmacology. Dogs. Enzyme Inhibitors / pharmacology. Humans. Mouth Neoplasms / drug therapy. Mouth Neoplasms / genetics. Mouth Neoplasms / metabolism. Mutagenesis, Site-Directed. Parathyroid Hormone-Related Protein. Polymerase Chain Reaction. Protein Biosynthesis. Tumor Cells, Cultured. Ultraviolet Rays

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11911944.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-77911; United States / NCI NIH HHS / CA / CA79110-01
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / Cross-Linking Reagents; 0 / DNA Primers; 0 / Enzyme Inhibitors; 0 / PTHLH protein, human; 0 / Parathyroid Hormone-Related Protein; 0 / Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 53-85-0 / Dichlororibofuranosylbenzimidazole
  •  go-up   go-down


59. Wei W, Guo RP, Li JQ, Xu L, Shi M, Zhang YQ: [Effects of cetuximab combined erlotinib on proliferation of human hepatocellular carcinoma cell lines HepG2 and Bel-7402]. Ai Zheng; 2008 Apr;27(4):386-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effects of cetuximab combined erlotinib on proliferation of human hepatocellular carcinoma cell lines HepG2 and Bel-7402].
  • BACKGROUND & OBJECTIVE: Several researches have reported that epidermal growth factor receptor (EGFR) is expressed frequently in hepatocellular carcinoma (HCC) and paratumor tissues, most likely to contribute to the biological characteristics of HCC, including invasion, metastasis, and resistance to chemotherapy and radiotherapy.
  • The inhibitory effects of the drugs on cell proliferation at different time points were observed; the combination index (CI) of these two agents was calculated.
  • The expression of key enzymes in EGFR signaling transduction pathway in HepG2 and Bel-7402 cells after different treatments was detected by Western blot.
  • RESULTS: The single agent of cetuximab and erlotinib inhibited the proliferation of HCC cells in a time-and dose-dependent manner; after 72-hour treatment, the proliferation inhibition rates of HepG2 cells were (43.1+/-1.9)% and (83.4+/-1.3)%, and those of Bel-7402 cells were (35.1+/-2.6)% and (73.9+/-1.2)%.
  • The CIs of different concentrations of these two agents at different time points were all less than 1, suggested that they have obvious synergistic activity.
  • The combined EGFR-targeting therapy on HCC xenografts in vivo and on HCC patients is worth of further exploration.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Quinazolines / administration & dosage
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Cell Line, Tumor. Cell Proliferation / drug effects. Cetuximab. Erlotinib Hydrochloride. Hep G2 Cells. Humans. Receptor, Epidermal Growth Factor / physiology. Signal Transduction / drug effects

  • Hazardous Substances Data Bank. CETUXIMAB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18423125.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Quinazolines; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
  •  go-up   go-down


60. Haydon RC, Zhou L, Feng T, Breyer B, Cheng H, Jiang W, Ishikawa A, Peabody T, Montag A, Simon MA, He TC: Nuclear receptor agonists as potential differentiation therapy agents for human osteosarcoma. Clin Cancer Res; 2002 May;8(5):1288-94
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nuclear receptor agonists as potential differentiation therapy agents for human osteosarcoma.
  • PURPOSE: This study was designed to investigate whether nuclear receptor agonists can be used as potential differentiation therapy agents for human osteosarcoma.
  • EXPERIMENTAL DESIGN: Four osteosarcoma cell lines (143B, MNNG/HOS, MG-63, and TE-85) were treated with proliferator-activated receptor (PPAR)gamma agonists, troglitazone and ciglitazone, and a retinoid X receptor (RXR) ligand, 9-cis retinoic acid.
  • On treatment with the PPARgamma and RXR ligands, all four osteosarcoma lines exhibited a significantly reduced proliferation rate and cell viability.
  • Of the three tested ligands, troglitazone was shown to be the most effective in inducing cell death, followed by 9-cis retinoic acid.
  • Moreover, a strong synergistic effect on the induction of cell death was observed when both troglitazone and 9-cis retinoic acid or ciglitazone and 9-cis retinoic acid were administered to osteosarcoma cells.
  • CONCLUSIONS: Our findings suggest that PPARgamma and/or RXR ligands may be used as efficacious adjuvant therapeutic agents for primary osteosarcoma, as well as potential chemopreventive agents for preventing the recurrence and metastasis of osteosarcoma after the surgical removal of the primary tumors.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Chromans / pharmacology. Thiazoles / pharmacology. Thiazolidinediones. Tretinoin / pharmacology
  • [MeSH-minor] Cell Differentiation / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Gene Expression Regulation, Neoplastic. HT29 Cells. Humans. Osteosarcoma / drug therapy. Osteosarcoma / genetics. Osteosarcoma / pathology. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. Receptors, Cytoplasmic and Nuclear / agonists. Receptors, Cytoplasmic and Nuclear / genetics. Receptors, Retinoic Acid / agonists. Retinoid X Receptors. Time Factors. Transcription Factors / agonists. Transcription Factors / genetics. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Osteosarcoma.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ALITRETINOIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12006550.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K12 DK083021
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Chromans; 0 / RNA, Neoplasm; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Retinoic Acid; 0 / Retinoid X Receptors; 0 / Thiazoles; 0 / Thiazolidinediones; 0 / Transcription Factors; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin; 74772-77-3 / ciglitazone; I66ZZ0ZN0E / troglitazone
  • [Other-IDs] NLM/ NIHMS595861; NLM/ PMC4527755
  •  go-up   go-down


61. Morales A, Phadke K, Steinhoff G: Intravesical mycobacterial cell wall-DNA complex in the treatment of carcinoma in situ of the bladder after standard intravesical therapy has failed. J Urol; 2009 Mar;181(3):1040-5
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Intravesical mycobacterial cell wall-DNA complex in the treatment of carcinoma in situ of the bladder after standard intravesical therapy has failed.
  • PURPOSE: We assessed the clinical efficacy and safety of mycobacterial cell wall-DNA complex after intravesical administration in patients with carcinoma in situ in whom prior therapy with bacillus Calmette-Guerin failed or in those who were treatment naïve.
  • Efficacy and safety were evaluated throughout the treatment phase and at months 12 and 18.
  • All patients were previously treated with bacillus Calmette-Guerin except for 8 who were treatment naïve and 2 who received chemotherapy.
  • CONCLUSIONS: Mycobacterial cell wall-DNA complex has shown antineoplastic activity in patients with bladder cancer with less toxicity than that associated with bacillus Calmette-Guerin administration.
  • The tolerance and efficacy of mycobacterial cell wall-DNA complex might hold promise for the treatment of carcinoma in situ of the bladder.
  • [MeSH-major] Carcinoma in Situ / therapy. Cell Wall. DNA, Bacterial / administration & dosage. Mycobacterium. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Administration, Intravesical. Aged. Aged, 80 and over. Female. Humans. Male. Middle Aged. Treatment Failure

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19150551.001).
  • [ISSN] 1527-3792
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Bacterial
  •  go-up   go-down


62. Villablanca EJ, Zhou D, Valentinis B, Negro A, Raccosta L, Mauri L, Prinetti A, Sonnino S, Bordignon C, Traversari C, Russo V: Selected natural and synthetic retinoids impair CCR7- and CXCR4-dependent cell migration in vitro and in vivo. J Leukoc Biol; 2008 Sep;84(3):871-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • This step requires the expression of a functional CCR7 chemokine receptor on DC undergoing maturation.
  • Here, we show that the natural retinoid 9-cis retinoic acid (9cRA) and the synthetic retinoid fenretinide (4-HPR) specifically inhibit the functional up-regulation of CCR7 on maturing human DCs, without affecting early steps of DC maturation.
  • Taken together, these data highlight a novel function of retinoids and suggest the possibility of using retinoids to treat inflammatory or autoimmune diseases.
  • [MeSH-major] Cell Movement / drug effects. Dendritic Cells / drug effects. Embryo, Nonmammalian / drug effects. Fenretinide / pharmacology. Receptors, CCR7 / physiology. Receptors, CXCR4 / physiology. Tretinoin / pharmacology. Zebrafish Proteins / physiology
  • [MeSH-minor] Animals. Bone Marrow / drug effects. Bone Marrow / metabolism. Cell Survival / drug effects. Cells, Cultured. Chemokine CXCL12 / metabolism. Chemotaxis. Enzyme-Linked Immunosorbent Assay. Flow Cytometry. Gene Expression Regulation, Developmental. Humans. In Situ Hybridization. In Vitro Techniques. Interleukin-6 / metabolism. Lymph Nodes / drug effects. Lymph Nodes / metabolism. Lymph Nodes / pathology. Mice. Mice, Inbred C57BL. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Zebrafish / physiology

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ALITRETINOIN .
  • The Lens. Cited by Patents in .
  • ZFIN. ZFIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18515328.001).
  • [ISSN] 0741-5400
  • [Journal-full-title] Journal of leukocyte biology
  • [ISO-abbreviation] J. Leukoc. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ccr7 protein, zebrafish; 0 / Chemokine CXCL12; 0 / Interleukin-6; 0 / RNA, Messenger; 0 / Receptors, CCR7; 0 / Receptors, CXCR4; 0 / Zebrafish Proteins; 187EJ7QEXL / Fenretinide; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
  •  go-up   go-down


63. Nyazema NZ, Khoza S, Landman I, Sibanda E, Gael K: Antiretrovial (ARV) drug utilisation in Harare. Cent Afr J Med; 2000 Apr;46(4):89-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antiretrovial (ARV) drug utilisation in Harare.
  • OBJECTIVE: To investigate ARV utilisation in Harare in order to gather necessary data to help in the formulation of treatment guidelines to be used in Zimbabwe.
  • MAIN OUTCOME MEASURES: Number of physicians prescribing antiretroviral agents (ARVs) and pharmacists stocking ARvs. Type of ARV utilised, cost to the patient and information on ARV available.
  • About a quarter, 27.0%, of the retail pharmacists stocked ARvs. The majority, 82.0%, of the patients appeared to be on Zidovudine (AZT) mainly in combination with other drugs.
  • CONCLUSION: There appeared to be therapeutic anarchy in the private sector in Harare in the way ARVs were being used.
  • Patients need to be told that deciding to take one of the combinations means making a serious commitment to the drugs on schedule if they want to enjoy the benefit.
  • At the same time there is need to develop and publicize HIV/AIDS treatment guidelines and effective Information, Education and Communication (IEC) materials specific to Zimbabwe.
  • [MeSH-major] Anti-HIV Agents / therapeutic use. Urban Health / statistics & numerical data
  • [MeSH-minor] Cross-Sectional Studies. Drug Therapy, Combination. Drug Utilization. Family Practice / statistics & numerical data. Humans. Pharmacies / statistics & numerical data. Practice Guidelines as Topic. Prospective Studies. Surveys and Questionnaires. Zimbabwe

  • MedlinePlus Health Information. consumer health - HIV/AIDS Medicines.
  • HIV InSite. treatment guidelines - Adherence to HIV Antiretroviral Therapy .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11210341.001).
  • [ISSN] 0008-9176
  • [Journal-full-title] The Central African journal of medicine
  • [ISO-abbreviation] Cent Afr J Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Zimbabwe
  • [Chemical-registry-number] 0 / Anti-HIV Agents
  •  go-up   go-down


64. Svanborg C, Agerstam H, Aronson A, Bjerkvig R, Düringer C, Fischer W, Gustafsson L, Hallgren O, Leijonhuvud I, Linse S, Mossberg AK, Nilsson H, Pettersson J, Svensson M: HAMLET kills tumor cells by an apoptosis-like mechanism--cellular, molecular, and therapeutic aspects. Adv Cancer Res; 2003;88:1-29
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HAMLET kills tumor cells by an apoptosis-like mechanism--cellular, molecular, and therapeutic aspects.
  • HAMLET (human alpha-lactalbumin made lethal to tumor cells) is a protein-lipid complex that induces apoptosis-like death in tumor cells, but leaves fully differentiated cells unaffected.
  • This review summarizes the information on the in vivo effects of HAMLET in patients and tumor models on the tumor cell biology, and on the molecular characteristics of the complex.
  • HAMLET limits the progression of human glioblastomas in a xenograft model and removes skin papillomas in patients.
  • This broad anti-tumor activity includes >40 different lymphomas and carcinomas and apoptosis is independent of p53 or bcl-2.
  • In tumor cells HAMLET enters the cytoplasm, translocates to the perinuclear area, and enters the nuclei where it accumulates.
  • The formation of HAMLET relies on the propensity of alpha-lactalbumin to alter its conformation when the strongly bound Ca2+ ion is released and the protein adopts the apo-conformation that exposes a new fatty acid binding site.
  • Oleic acid (C18:1,9 cis) fits this site with high specificity, and stabilizes the altered protein conformation.
  • The results illustrate how protein folding variants may be beneficial, and how their formation in peripheral tissues may depend on the folding change and the availability of the lipid cofactor.
  • We propose that HAMLET should be explored as a novel approach to tumor therapy.
  • [MeSH-major] Apoptosis. Lactalbumin / therapeutic use. Oleic Acid / therapeutic use
  • [MeSH-minor] Active Transport, Cell Nucleus. Animals. Binding Sites. Calcium / metabolism. Cell Differentiation. Cytoplasm / metabolism. Dose-Response Relationship, Drug. Drug Therapy, Combination. Humans. Ions. Lipids. Neoplasm Transplantation. Protein Conformation. Protein Folding. Proto-Oncogene Proteins c-bcl-2 / metabolism. Time Factors. Tumor Cells, Cultured. Tumor Suppressor Protein p53 / metabolism

  • Hazardous Substances Data Bank. OLEIC ACID .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12665051.001).
  • [ISSN] 0065-230X
  • [Journal-full-title] Advances in cancer research
  • [ISO-abbreviation] Adv. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ions; 0 / Lipids; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53; 2UMI9U37CP / Oleic Acid; 9013-90-5 / Lactalbumin; SY7Q814VUP / Calcium
  • [Number-of-references] 90
  •  go-up   go-down


65. Liao Y, Wei Y, Zhou X, Yang JY, Dai C, Chen YJ, Agarwal NK, Sarbassov D, Shi D, Yu D, Hung MC: Peptidyl-prolyl cis/trans isomerase Pin1 is critical for the regulation of PKB/Akt stability and activation phosphorylation. Oncogene; 2009 Jul 2;28(26):2436-45
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Peptidyl-prolyl cis/trans isomerase Pin1 is critical for the regulation of PKB/Akt stability and activation phosphorylation.
  • Elevated expression of activated Akt has been detected in a wide variety of human cancers; however, the mechanism of Akt protein stability regulation remains unclear.
  • In this study, we showed a strong correlation between the expression levels of an oncogenic peptidyl-prolyl cis/trans isomerase Pin1 and levels of Akt phosphorylation at S473 in multiple cancer types (P<0.0001).
  • Akt-pS473 status combined with Pin1 expression levels predicted a poorer prognosis than did either one alone in patients with breast cancer (P=0.0052).
  • Our results show how Akt protein stability is regulated by the peptidyl-prolyl cis/trans isomerase Pin1 and highlight the importance of this oncogenic network in human disease pathogenesis.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Curr Cancer Drug Targets. 2008 May;8(3):223-9 [18473735.001]
  • [Cites] Curr Cancer Drug Targets. 2008 Feb;8(1):27-36 [18288941.001]
  • [Cites] EMBO J. 2008 Jul 23;27(14):1919-31 [18566587.001]
  • [Cites] J Mol Med (Berl). 1999 Sep;77(9):656-65 [10569203.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4262-6 [10759547.001]
  • [Cites] Annu Rev Biochem. 1999;68:965-1014 [10872470.001]
  • [Cites] Sci STKE. 2001 Jan 23;2001(66):pe1 [11752635.001]
  • [Cites] Nature. 2002 Oct 24;419(6909):853-7 [12397362.001]
  • [Cites] Biochem J. 2003 Mar 1;370(Pt 2):361-71 [12495431.001]
  • [Cites] J Leukoc Biol. 2003 Jun;73(6):689-701 [12773501.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6836-48 [12972603.001]
  • [Cites] Cancer Cell. 2003 Oct;4(4):257-62 [14585353.001]
  • [Cites] Biochem Soc Trans. 2004 Apr;32(Pt 2):350-4 [15046607.001]
  • [Cites] Nat Cell Biol. 2004 Apr;6(4):308-18 [15048125.001]
  • [Cites] Am J Pathol. 2004 May;164(5):1727-37 [15111319.001]
  • [Cites] Trends Biochem Sci. 2004 May;29(5):233-42 [15130559.001]
  • [Cites] Clin Cancer Res. 2004 Jun 1;10(11):3815-24 [15173090.001]
  • [Cites] EMBO J. 2004 Aug 18;23(16):3397-407 [15257284.001]
  • [Cites] EMBO J. 1996 Dec 2;15(23):6541-51 [8978681.001]
  • [Cites] Oncogene. 1998 Jul 23;17(3):313-25 [9690513.001]
  • [Cites] J Biol Chem. 1998 Nov 6;273(45):29864-72 [9792703.001]
  • [Cites] Science. 1999 Feb 26;283(5406):1325-8 [10037602.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):802-7 [15647370.001]
  • [Cites] Science. 2005 Feb 18;307(5712):1098-101 [15718470.001]
  • [Cites] Mol Cell. 2005 Apr 1;18(1):13-24 [15808505.001]
  • [Cites] Mol Cell. 2005 Apr 15;18(2):143-5 [15837416.001]
  • [Cites] Trends Mol Med. 2005 Aug;11(8):353-61 [16002336.001]
  • [Cites] Adv Cancer Res. 2005;94:29-86 [16095999.001]
  • [Cites] Science. 2005 Oct 14;310(5746):306-10 [16224021.001]
  • [Cites] Oncogene. 2005 Nov 14;24(50):7391-3 [16288285.001]
  • [Cites] Oncogene. 2005 Nov 14;24(50):7401-9 [16288287.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):184-92 [16453012.001]
  • [Cites] Mol Carcinog. 2006 Jun;45(6):397-402 [16652378.001]
  • [Cites] Oncology. 2006;70(4):285-9 [17047397.001]
  • [Cites] Cancer Res. 2007 Jan 1;67(1):167-77 [17210696.001]
  • [Cites] Oncogene. 2007 Feb 26;26(9):1338-45 [17322919.001]
  • [Cites] Biochem Soc Trans. 2007 Apr;35(Pt 2):231-5 [17371246.001]
  • [Cites] Mol Cell. 2007 Mar 23;25(6):917-31 [17386267.001]
  • [Cites] Dev Cell. 2007 Apr;12(4):487-502 [17419990.001]
  • [Cites] Nat Rev Cancer. 2007 May;7(5):381-8 [17410202.001]
  • [Cites] Cell. 2007 Jun 29;129(7):1261-74 [17604717.001]
  • [Cites] Nature. 2007 Jul 26;448(7152):439-44 [17611497.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Nov;8(11):904-16 [17878917.001]
  • [Cites] Cell Mol Life Sci. 2008 Feb;65(3):359-75 [17965833.001]
  • [Cites] EMBO J. 2008 Jul 23;27(14):1932-43 [18566586.001]
  • (PMID = 19448664.001).
  • [ISSN] 1476-5594
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA83639; United States / NCI NIH HHS / CA / R01 CA109311; United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P20 CA101936-05; United States / NCI NIH HHS / CA / CA099031-01; United States / NCI NIH HHS / CA / P50-CA83639-A01; United States / NCI NIH HHS / CA / P50 CA083639-090009; United States / NCI NIH HHS / CA / CA116199-04; United States / NCI NIH HHS / CA / P50 CA116199; United States / NCI NIH HHS / CA / P20 CA101936; United States / PHS HHS / / P01 099031; United States / NCI NIH HHS / CA / P50 CA083639; United States / NCI NIH HHS / CA / P01 CA099031-01; United States / NCI NIH HHS / CA / P01 CA099031; United States / NCI NIH HHS / CA / CA101936-05; United States / NCI NIH HHS / CA / P50 CA116199-04; United States / NCI NIH HHS / CA / CA083639-090009
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / NIMA-interacting peptidylprolyl isomerase; EC 2.5.1.18 / Glutathione Transferase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 5.2.1.8 / Peptidylprolyl Isomerase
  • [Other-IDs] NLM/ NIHMS125352; NLM/ PMC2748248
  •  go-up   go-down


66. Wang X, Lin J, Zhang X, Liu Q, Xu Q, Tan RX, Guo Z: 5-Fluorouracil-cisplatin adducts with potential antitumor activity. J Inorg Biochem; 2003 Feb 1;94(1-2):186-92
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Using 5-fluorouracil (5-FU) and cis-diamminedichloroplatinum(II) (cisplatin, CDDP) as starting compounds, 5-FU-cisplatin adducts cis-[Pt(NH(3))(2)(HFU)Cl] (1) and cis-[Pt(NH(3))(2)(HFU)(2)] (2) were prepared.
  • Complex 1 reacted with guanosine-5'-monophosphate (5'-GMP) and gave rise to a stable mixed-ligand complex cis-[Pt(NH(3))(2)(HFU)(GMP)] (3), whereas 2 did not undergo a similar reaction.
  • This work provides the basis for a potential alternative for the combinational use of 5-FU and CDDP in cancer therapy.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cisplatin / therapeutic use. Fluorouracil / therapeutic use
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Magnetic Resonance Spectroscopy. Melanoma, Experimental / pathology. Spectrometry, Mass, Electrospray Ionization. Spectrophotometry, Infrared. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12620690.001).
  • [ISSN] 0162-0134
  • [Journal-full-title] Journal of inorganic biochemistry
  • [ISO-abbreviation] J. Inorg. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


67. Costa V, McGregor M, Laneuville P, Brophy JM: The cost-effectiveness of stem cell transplantations from unrelated donors in adult patients with acute leukemia. Value Health; 2007 Jul-Aug;10(4):247-55
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: Hematopoietic stem cell transplantation is an accepted treatment of hematological malignancies, but the cost-effectiveness of this technology has not been fully explored.
  • This study aims to assess the cost-effectiveness of stem cell transplantation from either cord blood or bone marrow/peripheral blood compared with no transplantation in adult patients with acute leukemias not expected to be cured with chemotherapy.
  • A Markov decision analysis model using Monte Carlo simulations was used to calculate the incremental cost-effectiveness ratio (ICER) and 95% confidence intervals (CIs).
  • CONCLUSIONS: Although both types of stem cell transplantations are associated with a high short-term mortality and high cost, the cumulative gains in life-years of survivors can be substantial, resulting in ICERs compared with no transplantation that are usually considered acceptable.
  • [MeSH-major] Hematopoietic Stem Cell Transplantation / economics. Leukemia / therapy

  • MedlinePlus Health Information. consumer health - Childhood Leukemia.
  • MedlinePlus Health Information. consumer health - Leukemia.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17645679.001).
  • [ISSN] 1098-3015
  • [Journal-full-title] Value in health : the journal of the International Society for Pharmacoeconomics and Outcomes Research
  • [ISO-abbreviation] Value Health
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Number-of-references] 52
  •  go-up   go-down


68. Schouten HC, Qian W, Kvaloy S, Porcellini A, Hagberg H, Johnsen HE, Doorduijn JK, Sydes MR, Kvalheim G: High-dose therapy improves progression-free survival and survival in relapsed follicular non-Hodgkin's lymphoma: results from the randomized European CUP trial. J Clin Oncol; 2003 Nov 1;21(21):3918-27
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] High-dose therapy improves progression-free survival and survival in relapsed follicular non-Hodgkin's lymphoma: results from the randomized European CUP trial.
  • PURPOSE: To determine, in a randomized clinical trial, whether high-dose therapy (HDT) followed by autologous stem-cell transplantation is more effective than standard treatment with regard to progression-free survival (PFS) and overall survival (OS) in patients with relapsed follicular non-Hodgkin's lymphoma; and to assess the additional value of B-cell purging of the stem-cell graft with regards to PFS and OS.
  • PATIENTS AND METHODS: Patients received three cycles of chemotherapy.
  • Responding patients with limited bone marrow infiltration were eligible for random assignment to three further cycles of chemotherapy (C), unpurged HDT (U), or purged HDT (P).
  • Reasons for not randomizing included patient refusal, early progression, or death on induction therapy.
  • With a 69-month median follow-up, the log-rank P value for PFS and OS were.0037 and.079, respectively.
  • For PFS, the hazard ratios (95% CIs) for U versus C, P versus C, and P versus U were 0.33 (0.16 to 0.70), 0.38 (0.19 to 0.79), and 1.02 (0.51 to 2.05), respectively.
  • Hazard ratios (95% CIs) for OS were 0.43 (0.18 to 1.06), 0.43 (0.18 to 1.02), and 0.72 (0.32 to 1.63).
  • Kaplan-Meier estimates (95% CIs) of 2-year PFS for C, U, and P were 26% (8% to 44%), 58% (37% to 79%), and 55% (34% to 75%), respectively.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. B-Lymphocytes. Bone Marrow Purging. Lymphoma, Non-Hodgkin / therapy. Neoplasm Recurrence, Local / therapy. Stem Cell Transplantation
  • [MeSH-minor] Adult. Australia. Cyclophosphamide / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Europe. Female. Humans. Male. Middle Aged. Prednisone / administration & dosage. Survival Analysis. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Follicular Lymphoma.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. PREDNISONE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Clin Oncol. 2003 Nov 1;21(21):3894-6 [14517186.001]
  • (PMID = 14517188.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; VB0R961HZT / Prednisone; CHOP protocol
  •  go-up   go-down


69. Labialle S, Gayet L, Marthinet E, Rigal D, Baggetto LG: Transcriptional regulation of the human MDR1 gene at the level of the inverted MED-1 promoter region. Ann N Y Acad Sci; 2002 Nov;973:468-71
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The typical multidrug resistance phenotype (MDR), the major cause of failure of cancer chemotherapy, is the result of the overexpression of the human MDR1 gene, the regulation of which is still incompletely understood.
  • Using several EMSA experiments, we have identified a new regulatory sequence located from -103 to -98 bp relative to the +1 start site in the MDR1 promoter region.
  • This sequence, which we called inverted MED-1, acts as a cis-activator for this gene.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12485913.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Phosphoproteins; 0 / Transcription Factors; 0 / down-regulator of transcription 1; EC 3.1.- / Endodeoxyribonucleases; EC 3.1.- / MBD4 protein, human
  •  go-up   go-down


70. Goebell PJ, Vom Dorp F, Rödel C, Frohneberg D, Thüroff JW, Jocham D, Stief C, Roth S, Knüchel R, Schmidt KW, Kausch I, Zaak D, Wiesner C, Miller K, Sauer R, Rübben H: [Noninvasive and invasive bladder cancer: diagnostics and treatment]. Urologe A; 2006 Jul;45(7):873-84; quiz 885
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Noninvasive and invasive bladder cancer: diagnostics and treatment].
  • [Transliterated title] Nichtinvasives und invasives Harnblasenkarzinom: Diagnostik und Therapie.
  • Therapy of superficial bladder tumors is transurethral resection (TUR), and in cases of pT1 or high-grade tumors a re-TUR is indicated.
  • Patients with carcinoma in situ receive intravesical chemotherapy or BCG for at least 3 months.
  • Persistent carcinoma in situ may be treated by radical cystectomy.
  • With the provision of a functionally adequate urinary diversion, cystectomy represents an effective treatment for patients with muscle-invasive bladder cancer without metastatic spread.
  • Regional lymph node metastases can be found in up to 15% of stage T1 disease and are present in 33% of stage T3/4 lesions.
  • Thus, lymphadenectomy gains diagnostic and possibly also therapeutic importance.
  • After or prior to cystectomy systemic chemotherapy may become necessary for some patients to positively affect the course of the disease in cases of locally advanced or metastatic lesions.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Cystectomy / methods. Urinary Bladder Neoplasms / pathology. Urinary Bladder Neoplasms / therapy
  • [MeSH-minor] Humans. Neoplasm Invasiveness. Practice Guidelines as Topic. Practice Patterns, Physicians'. Treatment Outcome

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Radiat Oncol Biol Phys. 1994 Sep 30;30(2):261-6 [7928455.001]
  • [Cites] Am J Pathol. 1998 Nov;153(5):1615-21 [9811354.001]
  • [Cites] Semin Radiat Oncol. 2005 Jan;15(1):36-41 [15662605.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jan 1;40(1):121-7 [9422567.001]
  • [Cites] Urology. 1997 Sep;50(3):349-53 [9301696.001]
  • [Cites] BJU Int. 2001 Nov;88(7):692-701 [11890239.001]
  • [Cites] Semin Urol Oncol. 2001 Feb;19(1):45-50 [11246733.001]
  • [Cites] BJU Int. 2003 Apr;91(6):485-8 [12656899.001]
  • [Cites] Cochrane Database Syst Rev. 2005 Apr 18;(2):CD005246 [15846746.001]
  • [Cites] J Urol. 1992 Jul;148(1):44-6 [1613878.001]
  • [Cites] Clin Cancer Res. 1998 Oct;4(10):2511-20 [9796985.001]
  • [Cites] J Clin Oncol. 2002 Jul 15;20(14):3061-71 [12118019.001]
  • [Cites] J Clin Oncol. 2003 Feb 15;21(4):690-6 [12586807.001]
  • [Cites] Lancet. 2003 Jun 7;361(9373):1927-34 [12801735.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2005 Jun 1;62(2):309-17 [15890569.001]
  • [Cites] J Urol. 1995 Mar;153(3 Pt 2):934-41 [7853578.001]
  • [Cites] J Urol. 1987 Nov;138(5):1162-3 [3669160.001]
  • [Cites] Eur Urol. 2005 Aug;48(2):189-199; discussion 199-201 [15939530.001]
  • [Cites] J Urol. 2004 Sep;172(3):878-81 [15310988.001]
  • [Cites] Acta Cytol. 1993 Mar-Apr;37(2):163-9 [8465635.001]
  • [Cites] J Urol. 2002 Nov;168(5):1950-4 [12394683.001]
  • [Cites] J Clin Oncol. 1996 Nov;14(11):2901-7 [8918486.001]
  • [Cites] Eur Urol. 2003 Oct;44(4):429-34 [14499676.001]
  • [Cites] Urologe A. 1994 Jan;33(1):9-14 [8146940.001]
  • [Cites] Eur Urol. 2002 May;41(5):523-31 [12074794.001]
  • [Cites] J Urol. 2002 Sep;168(3):978-80 [12187203.001]
  • [Cites] J Urol. 2000 Apr;163(4):1124-9 [10737480.001]
  • [Cites] J Urol. 1988 Nov;140(5):964-7 [3172367.001]
  • [Cites] J Urol. 1996 Apr;155(4):1233-8 [8632538.001]
  • [Cites] J Urol. 2004 Sep;172(3):937-42 [15311003.001]
  • [Cites] J Urol. 2002 Oct;168(4 Pt 1):1442-5 [12352414.001]
  • [Cites] J Urol. 2004 Sep;172(3):882-4 [15310989.001]
  • [Cites] Urologe A. 2005 Apr;44(4):375-81 [15750678.001]
  • [Cites] Cancer Res. 1997 Jul 15;57(14):2860-4 [9230190.001]
  • [Cites] Urol Clin North Am. 1992 Aug;19(3):573-80 [1636241.001]
  • [Cites] J Urol. 1987 Oct;138(4):766-70 [3656529.001]
  • [Cites] J Urol. 1993 Apr;149(4):749-52 [8455236.001]
  • [Cites] J Clin Oncol. 2001 Feb 1;19(3):666-75 [11157016.001]
  • [Cites] Eur Urol. 1990;18(4):253-7 [2289517.001]
  • [Cites] Nat Med. 1997 Jun;3(6):621-4 [9176487.001]
  • [Cites] J Cell Biol. 1993 Feb;120(4):947-57 [8432734.001]
  • [Cites] Science. 1996 Feb 2;271(5249):659-62 [8571131.001]
  • [Cites] J Urol. 2001 Oct;166(4):1296-9 [11547061.001]
  • [Cites] J Urol. 1991 Jul;146(1):28-31 [2056599.001]
  • [Cites] Urol Res. 1979 Jun 22;7(2):83-91 [473447.001]
  • [Cites] J Clin Oncol. 1993 Nov;11(11):2150-7 [8229129.001]
  • [Cites] Eur Urol. 2005 Aug;48(2):202-5; discussion 205-6 [15939524.001]
  • [Cites] Front Biosci. 2002 Feb 01;7:e36-41 [11815300.001]
  • [Cites] J Pathol. 1998 Aug;185(4):345-51 [9828832.001]
  • [Cites] J Urol. 2003 Jun;169(6):1975-82 [12771702.001]
  • [Cites] J Urol. 1997 May;157(5):1660-4 [9112500.001]
  • [Cites] Radiother Oncol. 2002 Feb;62(2):215-25 [11937249.001]
  • [Cites] Eur Urol. 2002 Apr;41(4):440-8 [12074817.001]
  • [Cites] Ann Oncol. 2000 Jul;11(7):851-6 [10997813.001]
  • [Cites] J Urol. 1999 Dec;162(6):1963-6 [10569548.001]
  • [Cites] J Urol. 2004 Sep;172(3):1123-6 [15311054.001]
  • [Cites] Semin Radiat Oncol. 2005 Jan;15(1):28-35 [15662604.001]
  • [Cites] J Urol. 1998 Jan;159(1):95-8; discussion 98-9 [9400445.001]
  • (PMID = 16791629.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 66
  •  go-up   go-down


71. Fukushima Y, Nabe T, Mizutani N, Nakata K, Kohno S: Multiple cedar pollen challenge diminishes involvement of histamine in allergic conjunctivitis of Guinea pigs. Biol Pharm Bull; 2003 Dec;26(12):1696-700
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • It has been reported that antihistamines do not fully modify symptoms of allergic conjunctivitis in clinical settings, suggesting that histamine is not the only contributor to symptom generation in the disease.
  • In the present study, we used our recently developed guinea pig model of allergic conjunctivitis and evaluated whether involvement of histamine in the induction of symptoms of allergic conjunctivitis is altered by multiple antigen challenges.
  • The magnitude of the conjunctivitis intensity score (CIS), itch-associated scratching response and albumin leakage were found to increase with repeated challenges.
  • On the other hand, a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (10 mg/kg, i.v.
  • ), potently inhibited the increase of CIS and albumin leakage at the 15th challenge.
  • The allergic conjunctivitis at the chronic stage is partly mediated by nitric oxide (NO) derived from NOSs that may be activated by mediators other than histamine.
  • [MeSH-minor] Administration, Oral. Administration, Topical. Albumins / antagonists & inhibitors. Albumins / drug effects. Albumins / secretion. Animals. Disease Models, Animal. Drug Administration Schedule. Drug Evaluation, Preclinical. Drug Tolerance. Eye / drug effects. Guinea Pigs. Histamine H1 Antagonists. Injections, Intraperitoneal. Injections, Intravenous. Male. NG-Nitroarginine Methyl Ester / administration & dosage. NG-Nitroarginine Methyl Ester / pharmacokinetics. NG-Nitroarginine Methyl Ester / therapeutic use. Nitric Oxide / adverse effects. Nitric Oxide / biosynthesis. Plant Extracts / administration & dosage. Plant Extracts / adverse effects. Pruritus / chemically induced. Pruritus / drug therapy. Pruritus / prevention & control. Pyrilamine / administration & dosage. Pyrilamine / pharmacokinetics. Pyrilamine / therapeutic use. Time Factors

  • Hazardous Substances Data Bank. NITRIC OXIDE .
  • Hazardous Substances Data Bank. PYRILAMINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14646173.001).
  • [ISSN] 0918-6158
  • [Journal-full-title] Biological & pharmaceutical bulletin
  • [ISO-abbreviation] Biol. Pharm. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Albumins; 0 / Allergens; 0 / Histamine H1 Antagonists; 0 / Plant Extracts; 31C4KY9ESH / Nitric Oxide; HPE317O9TL / Pyrilamine; V55S2QJN2X / NG-Nitroarginine Methyl Ester
  •  go-up   go-down


72. Kato Y, Salumbides BC, Wang XF, Qian DZ, Williams S, Wei Y, Sanni TB, Atadja P, Pili R: Antitumor effect of the histone deacetylase inhibitor LAQ824 in combination with 13-cis-retinoic acid in human malignant melanoma. Mol Cancer Ther; 2007 Jan;6(1):70-81
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antitumor effect of the histone deacetylase inhibitor LAQ824 in combination with 13-cis-retinoic acid in human malignant melanoma.
  • Resistance to chemotherapy is a major hurdle in the treatment of malignant melanoma.
  • Histone deacetylase (HDAC) inhibitors have been shown to have antitumor activity in different tumor types, including melanoma, and to reverse epigenetic repression of tumor suppressor genes, such as retinoic acid receptor beta (RARbeta).
  • In this study, we tested the antitumor effect of the HDAC inhibitor LAQ824 in combination with 13-cis-retinoic acid (CRA) on two human melanoma cell lines both in vitro and in vivo.
  • Treatment of LAQ824 showed a dose-dependent inhibitory effect on A2058 and HMV-I cell lines in a clonogenic assay.
  • On treatment with combination of LAQ824 and CRA, a greater inhibitory effect (up to 98%) was achieved compared with single agents.
  • Treatment with LAQ824 restored retinoid sensitivity by reverting RARbeta2 epigenetic silencing.
  • Combination treatment showed 61% and 82% growth inhibition in A2058 and HMV-I tumors, respectively.
  • Greater induction of in vivo apoptosis was observed in the HMV-I but not in the A2058 tumors treated with combination therapy compared with single agents.
  • Combination of HDAC inhibitors and retinoids represents a novel therapeutic approach for malignant melanoma that warrants clinical testing.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Histone Deacetylase Inhibitors. Hydroxamic Acids / pharmacology. Isotretinoin / pharmacology. Melanoma / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. G2 Phase / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. Mice. Mice, Nude. Microfilament Proteins / genetics. Muscle Proteins / genetics. RNA, Messenger / genetics. RNA, Messenger / metabolism. Reactive Oxygen Species / metabolism. Receptors, Retinoic Acid / genetics

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Melanoma.
  • Hazardous Substances Data Bank. 13-CIS-RETINOIC ACID .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17237267.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / LAQ824; 0 / Microfilament Proteins; 0 / Muscle Proteins; 0 / RNA, Messenger; 0 / Reactive Oxygen Species; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta; 0 / transgelin; EH28UP18IF / Isotretinoin
  •  go-up   go-down


73. Miceli JJ, Tensfeldt TG, Shiovitz T, Anziano R, O'Gorman C, Harrigan RH: Effects of Oral Ziprasidone and Oral Haloperidol on QTc interval in patients with Schizophrenia or Schizoaffective disorder. Pharmacotherapy; 2010 Feb;30(2):127-35
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of Oral Ziprasidone and Oral Haloperidol on QTc interval in patients with Schizophrenia or Schizoaffective disorder.
  • SETTING: Inpatient clinical research facility.
  • Patients Fifty-nine adults (age range 25-59 yrs) with schizophrenia or schizoaffective disorder who had no clinically significant abnormality on electrocardiogram (ECG) at screening.
  • Intervention. During period 1 (days -10 to -4), antipsychotic and anticholinergic drugs were tapered.
  • On the first day (day -3) of period 2, the drugs were discontinued, and placebo was given for the next 3 days (days -2 to 0).
  • Period 4 (days 17-19) allowed for study drug washout and initiation of outpatient antipsychotic therapy; safety assessments were also performed during this period.
  • MEASUREMENTS AND RESULTS: At each steady-state dose level, three ECGs and a serum or plasma sample were collected at the predicted time of peak exposure to the administered drug.
  • Point estimates and 95% confidence intervals (CIs) were determined for the mean QTc interval at baseline and for the mean change from baseline in QTc at each steady-state dose level.
  • Although no patient in either treatment group experienced a QTc interval of 450 msec or greater, the QTc interval increased 30 msec or more in 11 and 17 ziprasidone-treated patients at 160 and 320 mg/day, respectively, and in 3 and 5 haloperidol-treated patients at 15 and 30 mg/day, respectively.
  • Most treatment-emergent adverse drug reactions were mild in intensity, and none were severe.
  • Treatment with high doses of ziprasidone or haloperidol did not result in any patient experiencing a QTc interval of 450 msec or greater.
  • [MeSH-major] Antipsychotic Agents / adverse effects. Electrocardiography / drug effects. Haloperidol / adverse effects. Piperazines / adverse effects. Psychotic Disorders / drug therapy. Schizophrenia / drug therapy. Thiazoles / adverse effects
  • [MeSH-minor] Administration, Oral. Adult. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Schizophrenia.
  • MedlinePlus Health Information. consumer health - Psychotic Disorders.
  • MedlinePlus Health Information. consumer health - Schizophrenia.
  • Hazardous Substances Data Bank. Ziprasidone .
  • Hazardous Substances Data Bank. HALOPERIDOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20099987.001).
  • [ISSN] 1875-9114
  • [Journal-full-title] Pharmacotherapy
  • [ISO-abbreviation] Pharmacotherapy
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Piperazines; 0 / Thiazoles; 6UKA5VEJ6X / ziprasidone; J6292F8L3D / Haloperidol
  •  go-up   go-down


74. Kelland L: Broadening the clinical use of platinum drug-based chemotherapy with new analogues. Satraplatin and picoplatin. Expert Opin Investig Drugs; 2007 Jul;16(7):1009-21
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Broadening the clinical use of platinum drug-based chemotherapy with new analogues. Satraplatin and picoplatin.
  • The three platinum-containing drugs that have been thus far approved by the FDA - cisplatin, carboplatin and oxaliplatin - have had a significant effect in the treatment of patients with some malignancies such as testicular, ovarian and colorectal cancer.
  • However, much more remains to be achieved to widen the therapeutic use of this important class of drug, either via further analogue development or by judicious use of combining the existing drugs with new molecularly targeted agents.
  • Two analogues arising from an academic (Institute of Cancer Research)/pharmaceutical (Johnson Matthey/AnorMed) collaboration - satraplatin (JM-216) and picoplatin (JM-/AMD-473) - have recently shown promising clinical activity; satraplatin (an orally available drug) in hormone-refractory prostate cancer and picoplatin in small-cell lung cancer.
  • There have also been advances in delivery vehicles for platinum drugs (e.g., the diaminocyclohexane [DACH]-based AP-5346 and aroplatin/liposomal cis-bis-neodecanoato-trans-(R,R)-1,2-diaminocyclohexane platinum (II) [L-NDDP] are in early clinical development).
  • Platinum-based drugs have also been successfully combined with molecularly targeted drugs (e.g., the recent approval of the vascular endothelial growth factor monoclonal antibody bevacizumab with carboplatin and paclitaxel in patients with NSCLC).
  • [MeSH-major] Drugs, Investigational. Neoplasms / drug therapy. Organoplatinum Compounds / administration & dosage. Platinum Compounds / administration & dosage
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Clinical Trials, Phase II as Topic. Clinical Trials, Phase III as Topic. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Male. Maximum Tolerated Dose. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Sensitivity and Specificity. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • Hazardous Substances Data Bank. PLATINUM COMPOUNDS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. DrugBank: Data: Chemical .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17594186.001).
  • [ISSN] 1744-7658
  • [Journal-full-title] Expert opinion on investigational drugs
  • [ISO-abbreviation] Expert Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drugs, Investigational; 0 / Organoplatinum Compounds; 0 / Platinum Compounds; 8D7B37T28G / satraplatin
  • [Number-of-references] 106
  •  go-up   go-down


75. Zhang MQ, Chen MZ: [Analysis of 174 cases with cervical cancer in women under 35 years old]. Zhonghua Fu Chan Ke Za Zhi; 2003 Nov;38(11):689-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Analysis of 174 cases with cervical cancer in women under 35 years old].
  • OBJECTIVE: To analyse the prevalence, etiology, presentation, preserving ovary and prognosis of cervical cancer in women under 35 years old.
  • METHODS: The clinical information of 174 patients were retrospectively analysed.
  • RESULTS: The percentage of new cervical cancer cases from 1991 to 2001 was 1.2%, 1.2%, 4.3%, 4.2%, 4.6%, 4.5%, 7.3%, 9.0%, 10.7%, 9.4%, 10.8%, respectively (P < 0.01).
  • The number of cases with carcinoma in situ, stage I, stage II, stage III was 22, 40, 94, 18, respectively.
  • The 5 year survival rate of stage I - III was 71.6%, 60.4% and 13.3%, respectively (P < 0.01).
  • COX regression analysis indicated that stage, lymph-vascular involvement and the depth of tumor infiltration were independently prognostic factors.
  • For patients with one risk factor after radical surgery, the survival of patients with adjuvant radiation therapy and chemotherapy or not was 100%, 88%, respectively (P > 0.05).
  • CONCLUSIONS: There is an increasing prevalence of cervical cancer in women under 35 years old, which is possibly related to the sexual transition.
  • The preserving ovary in young cervical cancer patients is safe and effective.
  • Patients with late stage, lymph-vascular involvement and deep infiltration of cervical stroma have poor prognosis.
  • Adjuvant treatment may be helpful for patients with 2 or more risk factors after radical surgery.
  • [MeSH-major] Uterine Cervical Neoplasms / therapy


76. Cordon-Cardo C, Cote RJ, Sauter G: Genetic and molecular markers of urothelial premalignancy and malignancy. Scand J Urol Nephrol Suppl; 2000;(205):82-93
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Primary molecular alterations may be defined as those directly related to the genesis of cancer.
  • These are frequently found as the sole abnormality and are often associated with particular tumors.
  • There are characteristic primary abnormalities involved in th production of low-grade/well-differentiated neoplasms, which destabilize cellular proliferation but have little effect on cellula "social" interactions or differentiation, as well as the rate of cell death or apoptosis.
  • A primary target leading to low-grade papillary superficial bladder tumors resides on chromosome 9, while p53 gene alterations are commonly seen in flat carcinoma in situ.
  • Other molecular alterations must be elucidated, as many non-invasive neoplasms have neither chromosome 9 nor p53 alterations.
  • Novel approaches utilizing tissue microdissection techniques an molecular genetic assays are needed to shed further light on this subject.
  • Secondary genetic or epigenetic abnormalities may be fortuitous, or may determine the biological behavior of the tumor.
  • These particular molecular aberrations may be especially important to evaluate for their use in the management of bladder cancer because of their commonality in progressive forms of the disease.
  • Thus, clinical trials are underway to explore their use in specific situations, particularly in the surgical management of locally advanced disease, and to determine whether adjuvant chemotherapy in such patients may be of benefit.
  • The use of molecular alterations in the management of non-invasive bladder neoplasms remains to be firmly established.
  • Our knowledge of molecular alterations important in bladder cancer progression is far from complete, and further study is necessary to further elucidate cruci pathways involved in progression and therapeutic response.
  • Nevertheless, molecular alterations involving chromosome 9q and the INK4A locus in papillary superficial tumors vs changes in chromosomes 14q and 8q, p53 and RB in flat carcinoma in situ lesions may indicate a molecular basis for early events that lead to varying pathways in urothelial tumorigenesis.
  • Studies aimed at revealing the clinical relevance of genet instability, as well as molecular or epigenetic alterations, in urothelium and preneoplastic lesions of otherwise morphologicall normal appearance are needed to further advance knowledge in the field.
  • Clinical advances in bladder cancer will be facilitated by novel animal models paralleling the human disease.
  • Molecular diagnostics, particularly specific antigen expression, fluorescence in situ hybridization and microsatellite analyses, have show great promise as screening and follow-up methodologies, and may supplement urine cytology in the diagnosis and characterization of new and recurrent disease.
  • In addition, the use of high-throughput genomic/proteomic assays, linked to comprehensive databases, and coupled with robust bioinformatics will be key elements in elucidating the components of regulatory and signaling pathways involved in bladder tumorigenesis and cancer progression.
  • [MeSH-major] Carcinoma in Situ / genetics. Carcinoma, Transitional Cell / genetics. Genetic Markers / genetics. Precancerous Conditions / genetics. Urinary Bladder Neoplasms / genetics
  • [MeSH-minor] Cell Transformation, Neoplastic / genetics. Cell Transformation, Neoplastic / pathology. Disease Progression. Humans. Urinary Bladder / pathology

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11144907.001).
  • [ISSN] 0300-8886
  • [Journal-full-title] Scandinavian journal of urology and nephrology. Supplementum
  • [ISO-abbreviation] Scand J Urol Nephrol Suppl
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Sweden
  • [Chemical-registry-number] 0 / Genetic Markers
  • [Number-of-references] 111
  •  go-up   go-down


77. Koizumi T, Nakanishi R, Taue R, Yamaguchi K, Nakatuji H, Kishimoto T, Izaki H, Oka N, Takahashi M, Fukumori T, Kanayama HO: [Case of tuberculous epididymitis caused by intravesical BCG therapy]. Hinyokika Kiyo; 2008 Sep;54(9):625-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Case of tuberculous epididymitis caused by intravesical BCG therapy].
  • Intravesical Bacillus Calmette-Guerin (BCG) therapy is commonly used against superficial urothelial carcinoma, especially carcinoma in situ (CIS).
  • We report a case of tuberculous epididymitis that occurred during a course of intravesical BCG therapy.
  • A 76-year-old man had received intravesical BCG therapy for multiple superficial bladder cancer and CIS in prostatic urethra after transurethral resection of bladder tumor (TUR-Bt).
  • He recognized hard nodules in the left scrotum after 4 times intravesical BCG therapy.
  • Histological diagnosis was tuberculous epididymitis.
  • Postoperatively, he was administered chemotherapy consisting of isoniazid, refampin and ethambutol.
  • [MeSH-minor] Administration, Intravesical. Aged. Antitubercular Agents / administration & dosage. Carcinoma in Situ / therapy. Cystectomy. Humans. Male. Orchiectomy. Urinary Bladder Neoplasms / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18975579.001).
  • [ISSN] 0018-1994
  • [Journal-full-title] Hinyokika kiyo. Acta urologica Japonica
  • [ISO-abbreviation] Hinyokika Kiyo
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antitubercular Agents; 0 / BCG Vaccine
  •  go-up   go-down


78. Quinn PG, Yeagley D: Insulin regulation of PEPCK gene expression: a model for rapid and reversible modulation. Curr Drug Targets Immune Endocr Metabol Disord; 2005 Dec;5(4):423-37
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Insulin and glucagon regulate the expression and/or activity of a variety of proteins to maintain blood glucose within normal limits.
  • The incomplete effectiveness of insulin action, whether due to intermittent insulin injection in type I diabetics or insulin resistance in type II diabetics, contributes to hyperglycemia and complications, resulting in damage to the eyes, nerves, kidneys and other organs over time.
  • Thus, defining a molecular mechanism for insulin inhibition of PEPCK gene transcription has been a major goal of research in several labs, because it would allow the development of drugs to prevent episodic increases in circulating glucose in diabetics.
  • Investigation of cis-acting elements in the PEPCK promoter has shed considerable light on the mechanisms of activation by cAMP and glucocorticoids but has failed to identify a regulatory element that mediates insulin inhibition of transcription.
  • Thus, we hypothesize that insulin-induced modification of a key transcription regulatory protein prevents an essential factor from participating in the induction process, leading to rapid but reversible inhibition, as is seen in animals.
  • The ability to alter the sensitivity of a key transcription factor to improve insulin-regulated control of blood glucose would be a major improvement in the treatment of diabetes, a growing problem in the industrialized world.
  • [MeSH-minor] Animals. Diabetes Mellitus / drug therapy. Diabetes Mellitus / enzymology. Diabetes Mellitus / genetics. Gluconeogenesis / drug effects. Gluconeogenesis / genetics. Humans. Hypoglycemic Agents / pharmacology. Hypoglycemic Agents / therapeutic use. Transcription, Genetic

  • MedlinePlus Health Information. consumer health - Diabetes Medicines.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16375695.001).
  • [ISSN] 1568-0088
  • [Journal-full-title] Current drug targets. Immune, endocrine and metabolic disorders
  • [ISO-abbreviation] Curr. Drug Targets Immune Endocr. Metabol. Disord.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK43871; United States / NIDDK NIH HHS / DK / DK49600
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Hypoglycemic Agents; 0 / Insulin; EC 4.1.1.32 / Phosphoenolpyruvate Carboxykinase (GTP)
  • [Number-of-references] 225
  •  go-up   go-down


79. Perera F, Yu E, Engel J, Holliday R, Scott L, Chisela F, Venkatesan V: Patterns of breast recurrence in a pilot study of brachytherapy confined to the lumpectomy site for early breast cancer with six years' minimum follow-up. Int J Radiat Oncol Biol Phys; 2003 Dec 1;57(5):1239-46
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patterns of breast recurrence in a pilot study of brachytherapy confined to the lumpectomy site for early breast cancer with six years' minimum follow-up.
  • PURPOSE: In this pilot study of high-dose-rate brachytherapy to the lumpectomy site as the sole radiation, ipsilateral and contralateral breast recurrences are documented with specific attention to the location of recurrence relative to the lumpectomy site.
  • METHODS: Between March 1992 and January 1996, 39 patients with T1 (32 patients) and T2 breast cancers received 37.2 Gy in 10 fractions (b.i.d.) over 1 week prescribed to a volume encompassing the surgical clips.
  • Thirteen received adjuvant tamoxifen, and 4 received chemotherapy.
  • Follow-up included annual bilateral mammograms and clinical breast examination every 3 to 6 months.
  • Whereas 13 patients had intraoperative implantation of the lumpectomy site, 26 had postoperative implantation.
  • The latter group and 7 of the former group had surgical clips marking the lumpectomy site, which allowed estimates of the distance of any ipsilateral breast recurrence from the lumpectomy site, using the mediolateral and cranio-caudad mammographic views.
  • RESULTS: At a median follow-up of 91 months, 33 women are alive, 4 have died of disease, and 2 have died of other causes.
  • Of 6 ipsilateral recurrences, 2 occurred within the lumpectomy site (in-field recurrences).
  • One of the 2 patients had a 1-mm microscopic margin at initial diagnosis; the recurrence was a 3.5-mm microscopic focus of duct carcinoma in situ.
  • The other patient had a 1.5-cm, high-grade infiltrating mammary carcinoma with no residual at wider resection at first diagnosis; the 5-mm invasive recurrence was also of high grade.
  • Four women developed invasive recurrences at least 1.6 cm or more from the lumpectomy site (out-of-field recurrences).
  • Two of these women had gross multifocal recurrences with two cancers in each patient; 1 of the 2 patients had an extensive intraductal component at initial diagnosis.
  • Among patients with any breast recurrence, 1 patient had a family history of prostate cancer; there was no family history of breast or ovarian cancer.
  • Of 17 patients who received adjuvant systemic therapy, only 1 had a breast recurrence.
  • CONCLUSIONS: In this pilot study, breast recurrences outside of the lumpectomy site were the predominant pattern of recurrence.
  • [MeSH-major] Brachytherapy / methods. Breast Neoplasms / radiotherapy. Breast Neoplasms / surgery. Carcinoma, Intraductal, Noninfiltrating / radiotherapy. Carcinoma, Intraductal, Noninfiltrating / surgery
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Carcinoma in Situ / pathology. Carcinoma in Situ / radiotherapy. Carcinoma in Situ / surgery. Chemotherapy, Adjuvant. Dose Fractionation. Female. Follow-Up Studies. Humans. Mastectomy, Segmental. Middle Aged. Neoplasm Recurrence, Local. Pilot Projects. Salvage Therapy. Treatment Failure

  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Int J Radiat Oncol Biol Phys. 2003 Dec 1;57(5):1214-6 [14630253.001]
  • [CommentIn] Int J Radiat Oncol Biol Phys. 2003 Dec 1;57(5):1210-3 [14630252.001]
  • (PMID = 14630257.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


80. Colombo R: Combined treatment with local thermo-chemotherapy for non muscle invasive bladder cancer. The present role in the light of acquired data and preliminary cumulative clinical experiences. Arch Ital Urol Androl; 2008 Dec;80(4):149-56
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Combined treatment with local thermo-chemotherapy for non muscle invasive bladder cancer. The present role in the light of acquired data and preliminary cumulative clinical experiences.
  • OBJECTIVES: During the last 15 years the endovesical administration of microwave-induced hyperthermia and chemotherapy as a combined regimen has been widely tested in many clinical trials for the treatment of patients suffering from non muscle invasive bladder cancer.
  • In this manuscript clinical results were assessed drawn from clinical prospective randomized or single arm studies already published.
  • In addition we collected and critically examined the most recent multicentric cumulative experiences still waiting for publication in the effort to update and define the clinical role of this procedure in both neo- and adjuvant settings.
  • METHODS: The rationale and some basic physical and biologic aspects concerning the clinical application of the combined treatment using local hyperthermia and chemotherapy are reported.
  • When used as ablative procedure (mono-therapy or complementary treatment to transurethral resection) the thermo-chemotherapy regimen has proved to be an effective treatment showing about 80% tumor complete response in many clinical studies.
  • Prospective, randomized as well as single arm studies also showed that thermo-chemotherapy procedure is consistently more effective than chemotherapy alone when treating both intermediate and high risk non muscle invasive bladder cancer.
  • Of particular interest, recent multicentric experiences showed that thermo-chemotherapy treatment is also effective in patients highly recurrent and failure after BCG.
  • In addition, patients with carcinoma in situ were tested with encouraging preliminary results.
  • CONCLUSION: Many clinical trials confirmed that endovesical thermo-chemotherapy is a safe and effective treatment when used for both ablative and prophylaxis approaches to non muscle invasive bladder cancer.
  • To date, patients suffering from multifocal and highly recurrent disease after chemotherapy and/or BCG seem to represent the most adequate indication.
  • Further multicentric studies are certainly needed in order to define clinical outcomes and to assess the cost/effectiveness analysis at long term follow-up.

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19235431.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 29
  •  go-up   go-down


81. Matsuyama H, Yamamoto Y, Nagao K, Ohmi C, Sakano S, Sasaki K: Cytogenetic analysis of false-positive mucosa by photodynamic diagnosis using 5-aminolevulinic acid - possible existence of premalignant genomic alterations examined by in vitro experiment. Oncology; 2009;76(2):118-25
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytogenetic analysis of false-positive mucosa by photodynamic diagnosis using 5-aminolevulinic acid - possible existence of premalignant genomic alterations examined by in vitro experiment.
  • OBJECTIVE: Although photodynamic diagnosis is a powerful tool for the detection of flat urothelial tumors, false-positive fluorescent mucosa still requires further elucidation.
  • METHODS: Sixty specimens of bladder mucosa were collected from 20 patients who were suspected of having carcinoma in situ by fluorescence cystoscopy with 5-aminolevulinic acid.
  • To detect the copy number aberrations, the multi-color fluorescence in situ hybridization technique was performed, and the variant fractions (total fractions other than those of the modal copy number) of chromosomes 7, 9 and 17 and the chromosomal instability were determined.
  • To delineate the relevant gene to the fluorescent mucosa, a comparative genomic hybridization technique was applied for 8 established bladder cancer cell lines, and these results were compared with the in vitro fluorescent expression experiment.
  • RESULTS: Fluorescent mucosa was detected in 33 of the 34 malignant tissue specimens (16 carcinoma in situ, 18 other transitional cell carcinomas) and in 11 of the 26 nonmalignant tissue specimens (6 dysplasia, 20 normal mucosa), with a false-positive rate of 42.3%.
  • The variant fraction of chromosome 9 was significantly higher in fluorescent than in non-fluorescent mucosa, not only for all tissues (33 vs. 17%; p = 0.0069), but also for nonmalignant tissues (28 vs. 15%; p = 0.0225).
  • [MeSH-minor] Aged. Aged, 80 and over. Carcinoma in Situ / drug therapy. Carcinoma in Situ / genetics. Chromosome Aberrations. False Positive Reactions. Female. Humans. In Vitro Techniques. Intestinal Mucosa / pathology. Male. Middle Aged. Photosensitizing Agents / pharmacology. Spectrometry, Fluorescence / methods

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19158444.001).
  • [ISSN] 1423-0232
  • [Journal-full-title] Oncology
  • [ISO-abbreviation] Oncology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 88755TAZ87 / Aminolevulinic Acid
  •  go-up   go-down


82. Klein R, Muehlenbein C, Liepa AM, Babineaux S, Wielage R, Schwartzberg L: Cost-effectiveness of pemetrexed plus cisplatin as first-line therapy for advanced nonsquamous non-small cell lung cancer. J Thorac Oncol; 2009 Nov;4(11):1404-14
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cost-effectiveness of pemetrexed plus cisplatin as first-line therapy for advanced nonsquamous non-small cell lung cancer.
  • INTRODUCTION: To estimate the cost-effectiveness of first-line cisplatin/pemetrexed (Cis/Pem) compared with cisplatin/gemcitabine (Cis/Gem), carboplatin/paclitaxel (Carb/Pac), and carboplatin/paclitaxel/bevacizumab (Carb/Pac/Bev) in patients with advanced non-small cell lung cancer (NSCLC), particularly in those with nonsquamous cell histology (i.e., adenocarcinoma, large cell carcinoma, or histology not otherwise specified).
  • METHODS: A semi-Markov model was developed to compare the 2-year impact of Cis/Pem to three other first-line regimens from the U.S. payer perspective.
  • Data from the randomized controlled clinical trial of Cis/Pem versus Cis/Gem and a mixed treatment comparison model (no head-to-head data were available for the Cis/Pem to Carb/Pac or Carb/Pac/Bev comparisons) provided clinical inputs.
  • Medicare reimbursement rates were used to determine drug costs.
  • RESULTS: In all patients with advanced NSCLC regardless of histologic subtype, using Cis/Pem as first-line chemotherapy led to an incremental cost per life-year gained (LYG) of $104,577 for Cis/Pem to Cis/Gem and $231,291 for Cis/Pem to Carb/Pac.
  • In the prespecified subset of patients with nonsquamous cell histology, the incremental cost per LYG was $83,537 for Cis/Pem to Cis/Gem and $178,613 for Cis/Pem to Carb/Pac.
  • The incremental cost per LYG for Carb/Pac/Bev to Cis/Pem was more than $300,000.
  • CONCLUSIONS: Compared with commonly used and reimbursed regimens for first-line chemotherapy in advanced NSCLC, Cis/Pem may be considered cost-effective, particularly in patients with nonsquamous cell histology.
  • This analysis emphasizes the importance of histology in identifying the appropriate patient for Cis/Pem first-line chemotherapy.
  • [MeSH-major] Antineoplastic Agents / economics. Carcinoma, Non-Small-Cell Lung / economics. Cisplatin / economics. Glutamates / economics. Guanine / analogs & derivatives. Lung Neoplasms / economics. Models, Economic
  • [MeSH-minor] Cost-Benefit Analysis. Drosophila Proteins. Drug Costs. Drug Therapy, Combination. Endopeptidases. Female. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Staging. Pemetrexed. Retrospective Studies. Thymidylate Synthase / antagonists & inhibitors. United States

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. PEMETREXED .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. GUANINE .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19786904.001).
  • [ISSN] 1556-1380
  • [Journal-full-title] Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
  • [ISO-abbreviation] J Thorac Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drosophila Proteins; 0 / Glutamates; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine; EC 2.1.1.45 / Thymidylate Synthase; EC 3.4.- / Endopeptidases; EC 3.4.99.- / RN-tre protein, Drosophila; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


83. Mugiya S, Ozono S, Nagata M, Takayama T, Ito T, Maruyama S, Hadano S, Nagae H: Long-term outcome of a low-dose intravesical bacillus Calmette-Guerin therapy for carcinoma in situ of the bladder: results after six successive instillations of 40 mg BCG. Jpn J Clin Oncol; 2005 Jul;35(7):395-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Long-term outcome of a low-dose intravesical bacillus Calmette-Guerin therapy for carcinoma in situ of the bladder: results after six successive instillations of 40 mg BCG.
  • We employed a dose of 40 mg once a week for six consecutive weeks in principle for carcinoma in situ (CIS) of the bladder, and retrospectively evaluated its effectiveness and safety.
  • METHODS: A total of 43 patients with CIS of the bladder were treated by this method and followed-up for a subsequent 12-79 months (median, 54 months).
  • Two patients underwent total cystectomy, but none died of bladder cancer.
  • There were no severe adverse effects requiring discontinuation of drug administration.
  • CONCLUSION: Our present study corroborated both the effectiveness and safety of low-dose BCG therapy for CIS of the bladder.
  • This therapy warrants further study by prospective randomized trials in the future.
  • [MeSH-major] BCG Vaccine / administration & dosage. Carcinoma in Situ / drug therapy. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Administration, Intravesical. Aged. Aged, 80 and over. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15976065.001).
  • [ISSN] 0368-2811
  • [Journal-full-title] Japanese journal of clinical oncology
  • [ISO-abbreviation] Jpn. J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / BCG Vaccine
  •  go-up   go-down


84. Eberhardt W, Doller A, Akool el-S, Pfeilschifter J: Modulation of mRNA stability as a novel therapeutic approach. Pharmacol Ther; 2007 Apr;114(1):56-73
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Modulation of mRNA stability as a novel therapeutic approach.
  • The functional relevance of posttranscriptional gene regulation is highlighted by many pathologies, wherein occurrence tightly correlates with a dysregulation in mRNA stability, including chronic inflammation, cardiovascular diseases and cancer.
  • Most commonly, the cis-regulatory elements of mRNA decay are represented by the adenylate- and uridylate (AU)-rich elements (ARE) which are specifically bound by trans-acting RNA binding proteins, which finally determine whether mRNA decay is delayed or facilitated.
  • The modulation of mRNA binding proteins, therefore, illuminates a promising approach for the pharmacotherapy of those key pathologies mentioned above and characterized by a posttranscriptional dysregulation.
  • In this review, we present timely examples of genes regulated by mRNA stability with a special focus on signaling pathways involved in the ARE-dependent mRNA decay.
  • A better understanding of these processes may form the basis for the development of novel therapeutics to treat major human diseases.

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17320967.001).
  • [ISSN] 0163-7258
  • [Journal-full-title] Pharmacology & therapeutics
  • [ISO-abbreviation] Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / RNA, Messenger
  • [Number-of-references] 213
  •  go-up   go-down


85. Yuan P, Miao XP, Zhang XM, Wang ZH, Tan W, Zhang XR, Sun Y, Xu BH, Lin DX: [Association of the responsiveness of advanced non-small cell lung cancer to platinum-based chemotherapy with p53 and p73 polymorphisms]. Zhonghua Zhong Liu Za Zhi; 2006 Feb;28(2):107-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Association of the responsiveness of advanced non-small cell lung cancer to platinum-based chemotherapy with p53 and p73 polymorphisms].
  • OBJECTIVE: It has been proposed that genetic polymorphisms in apoptosis-related genes might be associated with sensitivity of cancer cells to platinum-based chemotherapy.
  • This study examined the relationship between p53 and p73 genetic polymorphisms and the response to platinum-based chemotherapy in patients with advanced non-small cell lung cancer (NSCLC).
  • METHODS: A total of 165 patients with advanced NSCLC treated with platinum-based chemotherapy were genotyped for the p53 codon 72 Pro-->Arg and p73 exon 2 G4C14-->A4T14 polymorphisms using PCR-RFLP and ARMS-PCR assays.
  • Clinical response to the chemotherapy was obtained after 2 to 3 cycles.
  • The adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using unconditional logistic regression model.
  • RESULTS: The p53 Pro allele carriers had higher response rate than non-carriers (OR = 2.46; 95% CI = 1.11 - 5.45).
  • When these two polymorphisms were combined to be analyzed, it was found that the response rate in those carrying the wild-type genotypes at both genes was only 7.7%, whereas the response rates in patients carrying 1, 2, or more than 2 variant alleles of p53 and p73 were 34.8%, 42.2% and 40.7%, respectively.
  • CONCLUSION: Those results suggest that p53 and p73 polymorphisms may be associated with clinical responsiveness to platinum-based chemotherapy in advanced NSCLC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / genetics. DNA-Binding Proteins / genetics. Lung Neoplasms / genetics. Nuclear Proteins / genetics. Polymorphism, Genetic. Tumor Suppressor Protein p53 / genetics. Tumor Suppressor Proteins / genetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16750013.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA-Binding Proteins; 0 / Nuclear Proteins; 0 / Tumor Suppressor Protein p53; 0 / Tumor Suppressor Proteins; 0 / tumor suppressor protein p73; BG3F62OND5 / Carboplatin; P88XT4IS4D / Paclitaxel; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


86. Lehmann MH, Yang H: Sexual dimorphism in the electrocardiographic dynamics of human ventricular repolarization: characterization in true time domain. Circulation; 2001 Jul 3;104(1):32-8
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Sexual dimorphism in the electrocardiographic dynamics of human ventricular repolarization: characterization in true time domain.
  • BACKGROUND: Previous characterizations of sex differences in ST-T waveform voltages have largely focused on amplitudes at selected time points during repolarization, subject to potential distortions from variations in heart rate (HR) or reliance on a JT-normalized time scale.
  • METHODS AND RESULTS: Using digitized 12-lead ECGs from 553 normal adults (426 males) with HRs confined to 60+/-1, 70+/-1, or 80+/-1 bpm, we derived X, Y, and Z lead voltages and then generated, for each HR category by sex, summary (population mean) resultant spatial vector amplitudes (ST-T(XYZ)) and instantaneous slopes (dV/dt(XYZ)) at successive 4-ms intervals following the J point.
  • Within each HR category, there was an early intersex divergence of ST-T(XYZ) trajectories (95% CIs nonoverlapping), with men exhibiting 2- to 3-fold greater dV/dt(XYZ) values during the ST segment and achieving greater maximum T(XYZ) and dV/dt(XYZ) values than women; descending T(XYZ) limbs were relatively more concordant between sexes but still steeper in men.
  • In men, absolute values of extrema of T(XYZ) and dV/dt(XYZ) varied inversely with HR.
  • CONCLUSIONS: At physiological resting HRs, the spatial ST-T vector voltage time trajectory is steeper in men than in women, beginning virtually from the J point.
  • In addition to its mechanistic implications, the demonstration of marked sensitivity of ST-T(XYZ) and especially dV/dt(XYZ) to sex raises the possibility that these time-based, ECG-derived parameters might be informative in pathophysiological studies of ventricular repolarization.

  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11435334.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


87. Kuroda I, Ueno M, Mitsuhashi T, Nakagawa K, Yanaihara H, Tsukamoto T, Deguchi N: Testicular seminoma after the complete remission of extragonadal yolk sac tumor : a case report. BMC Urol; 2004 Nov 16;4:13
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Testicular seminoma after the complete remission of extragonadal yolk sac tumor : a case report.
  • BACKGROUND: Between 2% and 5% of malignant germ-cell tumors in men arise at extragonadal sites.
  • Of extragonadal germ cell tumors, testicular carcinoma in situ (CIS) are present in 31-42% of cases, and CIS are reported to have low sensitivity to chemotherapy in spite of the various morphology and to have a high likelihood of developing into testicular tumors.
  • A testicular biopsy may thus be highly advisable when evaluating an extragonadal germ cell tumor.
  • CASE PRESENTATION: A 36-year-old man was diagnosed as having an extragonadal non-seminomatous germ cell tumor, that was treated by cisplatin-based chemotherapy, leading to a complete remission.
  • About 4 years later, a right testicular tumor was found, and orchiectomy was carried out.
  • Microscopically, the tumor was composed of seminoma.
  • CONCLUSIONS: We herein report a case of metachronous occurrence of an extragonadal and gonadal germ cell tumor.
  • In the evaluation of an extragonadal germ cell tumor, a histological examination should be included since ultrasonography is not sufficient to detect CIS or minute lesions of the testis.
  • [MeSH-major] Endodermal Sinus Tumor / drug therapy. Neoplasms, Second Primary / etiology. Seminoma / etiology. Testicular Neoplasms / drug therapy. Testicular Neoplasms / etiology
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Bleomycin / administration & dosage. Cisplatin / administration & dosage. Etoposide / administration & dosage. Humans. Male. Orchiectomy. Remission Induction

  • Genetic Alliance. consumer health - Seminoma.
  • Genetic Alliance. consumer health - Yolk sac tumor.
  • MedlinePlus Health Information. consumer health - Testicular Cancer.
  • Hazardous Substances Data Bank. BLEOMYCIN .
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Histopathology. 1978 May;2(3):157-70 [27442.001]
  • [Cites] Ann Oncol. 2003 Sep;14(9):1412-8 [12954581.001]
  • [Cites] Hinyokika Kiyo. 2003 May;49(5):291-5 [12822460.001]
  • [Cites] APMIS. 2003 Jan;111(1):49-59; discussion 59-63 [12752235.001]
  • [Cites] Ann Oncol. 2002 Jan;13(1):121-4 [11863093.001]
  • [Cites] J Urol. 1989 Aug;142(2 Pt 1):243-7 [2545927.001]
  • [Cites] Urology. 1990 Aug;36(2):181-2 [2385889.001]
  • [Cites] Nihon Hinyokika Gakkai Zasshi. 1995 Sep;86(9):1497-500 [7474641.001]
  • [Cites] J Urol. 1995 Oct;154(4):1367-9 [7658540.001]
  • [Cites] Lancet. 1994 May 7;343(8906):1130-2 [7910232.001]
  • [Cites] Cancer Res. 1994 Mar 15;54(6):1542-4 [8137260.001]
  • [Cites] Eur Urol. 1993;23(1):115-8; discussion 119 [8477771.001]
  • [Cites] Eur Urol. 1993;23(1):104-10; discussion 111-4 [8477770.001]
  • [Cites] Ann Oncol. 1992 Apr;3(4):283-9 [1327076.001]
  • [Cites] Urol Int. 1992;48(2):162-6 [1374974.001]
  • [Cites] Br J Cancer. 1998;77(2):329-35 [9461006.001]
  • (PMID = 15546481.001).
  • [ISSN] 1471-2490
  • [Journal-full-title] BMC urology
  • [ISO-abbreviation] BMC Urol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ PMC535804
  •  go-up   go-down


88. Edwards MR, Haas J, Panettieri RA Jr, Johnson M, Johnston SL: Corticosteroids and beta2 agonists differentially regulate rhinovirus-induced interleukin-6 via distinct Cis-acting elements. J Biol Chem; 2007 May 25;282(21):15366-75
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Corticosteroids and beta2 agonists differentially regulate rhinovirus-induced interleukin-6 via distinct Cis-acting elements.
  • Interleukin-6 (IL-6) is a proinflammatory cytokine up-regulated by rhinovirus infection during acute exacerbations of asthma and chronic obstructive pulmonary disease.
  • In this study we investigate the effects of common asthma treatments fluticasone propionate and beta(2) agonists salmeterol and salbutamol on IL-6 production in BEAS-2B and primary bronchial epithelial cells.
  • Salmeterol and salbutamol enhanced rhinovirus- and IL-1beta-induced IL-6 production; however, fluticasone treatment caused a reduction of IL-6 protein and mRNA.
  • Salmeterol caused an augmentation of rhinovirus-induced promoter activation via a mechanism dependent upon the c/EBP and/or CRE (cyclic AMP response element) cis-acting sites.
  • The suppressive effect of FP was dependent upon distinct glucocorticoid response element sequences proximal to the transcriptional start site within the IL-6 promoter.
  • [MeSH-minor] Adrenal Cortex Hormones / pharmacology. Adrenal Cortex Hormones / therapeutic use. Asthma / complications. Asthma / drug therapy. Asthma / metabolism. Asthma / pathology. Asthma / virology. Bronchi / metabolism. Bronchi / pathology. Bronchi / virology. CCAAT-Enhancer-Binding Proteins / metabolism. Colforsin / pharmacology. Cyclic AMP / agonists. Cyclic AMP / metabolism. Epithelial Cells / metabolism. Epithelial Cells / pathology. Epithelial Cells / virology. Fluticasone. Gene Expression Regulation / drug effects. HeLa Cells. Humans. Interleukin-1beta / metabolism. NF-kappa B / metabolism. Phosphodiesterase Inhibitors / pharmacology. Pulmonary Disease, Chronic Obstructive / complications. Pulmonary Disease, Chronic Obstructive / drug therapy. Pulmonary Disease, Chronic Obstructive / metabolism. Pulmonary Disease, Chronic Obstructive / pathology. Pulmonary Disease, Chronic Obstructive / virology. Rolipram / pharmacology. Salmeterol Xinafoate. Transcription, Genetic / drug effects

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALBUTEROL .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17395587.001).
  • [ISSN] 0021-9258
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Adrenergic beta-Agonists; 0 / Androstadienes; 0 / Anti-Inflammatory Agents; 0 / CCAAT-Enhancer-Binding Proteins; 0 / IL6 protein, human; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / NF-kappa B; 0 / Phosphodiesterase Inhibitors; 1F7A44V6OU / Colforsin; 6EW8Q962A5 / Salmeterol Xinafoate; CUT2W21N7U / Fluticasone; E0399OZS9N / Cyclic AMP; K676NL63N7 / Rolipram; QF8SVZ843E / Albuterol
  •  go-up   go-down


89. Goldberg SL, Chiang L, Selina N, Hamarman S: Patient perceptions about chemotherapy-induced oral mucositis: implications for primary/secondary prophylaxis strategies. Support Care Cancer; 2004 Jul;12(7):526-30
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Patient perceptions about chemotherapy-induced oral mucositis: implications for primary/secondary prophylaxis strategies.
  • GOALS: Oral mucositis (OM), the painful inflammation of oropharyngeal tissues, is an economically costly chemotherapy toxicity.
  • Several agents to prevent chemotherapy-induced OM are in development, with most studies conducted among transplantation subjects with a brief well-defined risk period.
  • The potential value of these preventative agents among hematology-oncology populations receiving cyclic standard-dose therapy is unknown.
  • PATIENTS AND METHODS: Patients receiving standard-dose chemotherapy at an outpatient oncology center over a 2-week time-frame were invited to participate in an anonymous unprompted survey.
  • The survey instrument consisted of six demographic questions and six questions regarding toxicities of chemotherapy.
  • Factors associated with developing OM included number of chemotherapy cycles ( P=0.001), hematologic malignancy ( P=0.02), female gender ( P=0.03), age ( P=0.05), and treatment with anthracyclines ( P=0.001), vinca alkaloids ( P=0.001), cyclophosphamide ( P=0.001), fludarabine ( P=0.01), cis/carboplatin ( P=0.05) and radiotherapy ( P=0.005).
  • CONCLUSIONS: OM represents a common toxicity of standard-dose chemotherapy occurring in approximately one-third of patients.
  • However, since OM was self-reported by only one-third of patients receiving standard-dose chemotherapy, but over half of those experiencing OM developed recurrent episodes, secondary prophylaxis strategies targeting recurrent OM episodes may be more appropriate.
  • [MeSH-major] Antineoplastic Agents / adverse effects. Mouth Mucosa / drug effects. Stomatitis / chemically induced. Stomatitis / psychology. Stress, Psychological / etiology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Female. Humans. Male. Middle Aged. Neoplasms / complications. Neoplasms / drug therapy. Retrospective Studies. Risk Factors. Severity of Illness Index. Surveys and Questionnaires. Time Factors

  • MedlinePlus Health Information. consumer health - Stress.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer. 2003 Oct 1;98(7):1531-9 [14508842.001]
  • [Cites] Oral Surg Oral Med Oral Pathol. 1989 Dec;68(6):711-6 [2594318.001]
  • [Cites] Support Care Cancer. 2000 Jan;8(1):33-9 [10650895.001]
  • [Cites] J Clin Oncol. 2001 Apr 15;19(8):2201-5 [11304772.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2446-53 [10561308.001]
  • [Cites] Cochrane Database Syst Rev. 2002;(1):CD001973 [11869616.001]
  • [Cites] J Dent Educ. 2002 Aug;66(8):903-11 [12214838.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1999 Sep;88(3):273-6 [10503852.001]
  • [Cites] Bone Marrow Transplant. 2001 May;27 Suppl 2:S3-S11 [11436115.001]
  • [Cites] J Pain Symptom Manage. 2001 Jun;21(6):498-505 [11397608.001]
  • [Cites] Cancer. 1998 Jun 1;82(11):2275-81 [9610710.001]
  • (PMID = 15150704.001).
  • [ISSN] 0941-4355
  • [Journal-full-title] Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer
  • [ISO-abbreviation] Support Care Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


90. Lavignac N, Nicholls JL, Ferruti P, Duncan R: Poly(amidoamine) conjugates containing doxorubicin bound via an acid-sensitive linker. Macromol Biosci; 2009 May 13;9(5):480-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Poly(amidoamine)s with amino pendant groups were prepared by hydrogen-transfer polyaddition of primary and secondary amines to bis-acrylamines.
  • Dansyl cadaverine (DC) doxorubicin (Dox) were bound to the polymers via a cis-aconityl spacer to give conjugates containing 3 microg of DC per mg of polymer and 28 to 35 microg of Dox per mg of polymer.
  • [MeSH-major] Antibiotics, Antineoplastic / chemistry. Doxorubicin / chemistry. Drug Carriers / chemistry. Polymers / chemistry
  • [MeSH-minor] Animals. Biocompatible Materials / chemistry. Biocompatible Materials / pharmacology. Cadaverine / analogs & derivatives. Cadaverine / chemistry. Cell Line, Tumor / drug effects. Drug Screening Assays, Antitumor. Humans. Hydrogen-Ion Concentration. Materials Testing. Mice. Molecular Structure. Neoplasms / drug therapy

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. Cadaverine .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19016501.001).
  • [ISSN] 1616-5195
  • [Journal-full-title] Macromolecular bioscience
  • [ISO-abbreviation] Macromol Biosci
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / /
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Biocompatible Materials; 0 / Drug Carriers; 0 / Polymers; 80168379AG / Doxorubicin; I9N81SC5HD / monodansylcadaverine; L90BEN6OLL / Cadaverine
  •  go-up   go-down


91. Lee MS, Choi TY, Park JE, Lee SS, Ernst E: Moxibustion for cancer care: a systematic review and meta-analysis. BMC Cancer; 2010;10:130
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Moxibustion for cancer care: a systematic review and meta-analysis.
  • Considering moxibustion is closely related to acupuncture, it seems pertinent to evaluate the effectiveness of moxibustion as a treatment of symptoms of cancer.
  • The objective of this review was to systematically assess the effectiveness of moxibustion for supportive cancer care.
  • We included randomised clinical trials (RCTs) in which moxibustion was employed as an adjuvant treatment for conventional medicine in patients with any type of cancer.
  • RESULTS: Five RCTs compared the effects of moxibustion with conventional therapy.
  • Four RCTs failed to show favourable effects of moxibustion for response rate compared with chemotherapy (n = 229, RR, 1.04, 95% CI 0.94 to 1.15, P = 0.43).
  • Two RCTs assessed the occurrence of side effects of chemotherapy and showed favourable effects of moxibustion.
  • A meta-analysis showed significant less frequency of nausea and vomiting from chemotherapy for moxibustion group (n = 80, RR, 0.38, 95% CIs 0.22 to 0.65, P = 0.0005, heterogeneity: chi2 = 0.18, P = 0.67, I2 = 0%).
  • CONCLUSION: The evidence is limited to suggest moxibustion is an effective supportive cancer care in nausea and vomiting.
  • Further research is required to investigate whether there are specific benefits of moxibustion for supportive cancer care.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Moxibustion. Neoplasms / therapy
  • [MeSH-minor] Combined Modality Therapy. Evidence-Based Medicine. Humans. Nausea / chemically induced. Nausea / prevention & control. Quality of Life. Randomized Controlled Trials as Topic. Treatment Outcome. Vomiting / chemically induced. Vomiting / prevention & control

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • PubMed Health. DARE review .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Hum Brain Mapp. 2000;9(1):13-25 [10643726.001]
  • [Cites] Prim Care. 2010 Mar;37(1):105-17 [20189001.001]
  • [Cites] J Clin Oncol. 2000 Jul;18(13):2505-14 [10893280.001]
  • [Cites] Cancer Treat Rev. 2001 Aug;27(4):235-46 [11545543.001]
  • [Cites] Zhongguo Zhong Xi Yi Jie He Za Zhi. 2000 Oct;20(10):733-5 [11938806.001]
  • [Cites] Trends Neurosci. 2003 Jan;26(1):17-22 [12495858.001]
  • [Cites] J R Soc Med. 2003 Jan;96(1):17-22 [12519797.001]
  • [Cites] Zhongguo Zhong Xi Yi Jie He Za Zhi. 2001 Apr;21(4):262-4 [12577352.001]
  • [Cites] J Tradit Chin Med. 2004 Mar;24(1):56-8 [15119180.001]
  • [Cites] J Tradit Chin Med. 1993 Dec;13(4):266-7 [8139276.001]
  • [Cites] Nature. 1997 Feb 6;385(6616):480 [9020351.001]
  • [Cites] Control Clin Trials. 1998 Apr;19(2):159-66 [9551280.001]
  • [Cites] J Altern Complement Med. 1999 Jun;5(3):229-36 [10381246.001]
  • [Cites] J Clin Oncol. 2004 Dec 1;22(23):4810-5 [15570083.001]
  • [Cites] Hum Brain Mapp. 2005 Mar;24(3):193-205 [15499576.001]
  • [Cites] South Med J. 2005 Mar;98(3):289-94 [15813155.001]
  • [Cites] Neuroimage. 2005 Sep;27(3):479-96 [16046146.001]
  • [Cites] J Intern Med. 2006 Feb;259(2):125-37 [16420542.001]
  • [Cites] Annu Rev Public Health. 2006;27:81-102 [16533110.001]
  • [Cites] J Soc Integr Oncol. 2006 Winter;4(1):13-5 [16737667.001]
  • [Cites] World J Gastroenterol. 2007 Apr 21;13(15):2174-8 [17465496.001]
  • [Cites] J Altern Complement Med. 2007 Jul-Aug;13(6):603-16 [17718643.001]
  • [Cites] Zhong Xi Yi Jie He Xue Bao. 2008 Feb;6(2):197-202 [18241659.001]
  • [Cites] Hematol Oncol Clin North Am. 2008 Aug;22(4):631-48, viii [18638692.001]
  • [Cites] Zhongguo Zhen Jiu. 2008 May;28(5):392-4 [18652337.001]
  • [Cites] J Altern Complement Med. 2008 Sep;14(7):861-9 [18803495.001]
  • [Cites] J Altern Complement Med. 2008 Dec;14(10):1231-3 [19040374.001]
  • [Cites] Natl Health Stat Report. 2008 Dec 10;(12):1-23 [19361005.001]
  • [Cites] Acupunct Med. 2009 Mar;27(1):16-20 [19369189.001]
  • [Cites] J Soc Integr Oncol. 2006 Spring;4(2):86-92 [19449505.001]
  • [Cites] J Clin Epidemiol. 2000 May;53(5):485-9 [10812320.001]
  • (PMID = 20374659.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Meta-Analysis; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 51
  • [Other-IDs] NLM/ PMC2873382
  •  go-up   go-down


92. Suda S, Akiyama S, Sekiguchi H, Kasai Y, Ito K, Nakao A: Evaluation of the histoculture drug response assay as a sensitivity test for anticancer agents. Surg Today; 2002;32(6):477-81
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Evaluation of the histoculture drug response assay as a sensitivity test for anticancer agents.
  • PURPOSE: To investigate whether the effects of anticancer agents are able to be predicted, the results of sensitivity tests on anticancer agents were compared with the results of preoperative chemotherapy.
  • METHODS: Biopsies were taken from 25 patients with esophageal cancer and 10 with gastric cancer, before chemotherapy, and the drug sensitivity was determined after culturing for 1 week.
  • The chemotherapy consisted of low-dose cis-diamino-dichloroplatinum + 5-fluorouracil, and its clinical effect was determined after 3 or 5 weeks.
  • RESULTS: Sensitivity was determined in 20 of the esophageal cancer patients and 8 of the gastric cancer patients, accounting for 80% of all the patients.
  • Of the 11 patients judged to have sensitivity by the histoculture drug response assay (HDRA), 7 had a partial response, and of the 17 judged to have no sensitivity, 16 had a minor response or no change (NC).
  • From the viewpoint of both medical costs and patient quality of life, treatments other than preoperative chemotherapy should be selected for patients assessed to have NC.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Drug Screening Assays, Antitumor. Esophageal Neoplasms / drug therapy. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Biopsy. Cell Culture Techniques / methods. Chi-Square Distribution. Drug Resistance, Neoplasm. Female. Humans. Male. Middle Aged. Sensitivity and Specificity. Tumor Cells, Cultured

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Esophageal Cancer.
  • MedlinePlus Health Information. consumer health - Stomach Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12107769.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


93. Fischetti G, Barrese F, Cuzari S, Marino C, Mariani S, Morello P: [Neoadjuvant chemotherapy and conservative surgery in invasive bladder cancer. Personal experience]. Minerva Urol Nefrol; 2001 Sep;53(3):119-23
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Neoadjuvant chemotherapy and conservative surgery in invasive bladder cancer. Personal experience].
  • [Transliterated title] Chemioterapia neoadiuvante e chirurgia conservativa nel carcinoma infiltrante della vescica. Nostr esperienza.
  • BACKGROUND: To evacuate the efficacy of conservative treatment in invasive stage T2 bladder tumours by means of deep transurethral resection of the bladder (TURB) followed by three cycles of chemotherapy with methotrexate, vinblastin, adriamycin and cisplatin (M-VAC).
  • Following histological confirmation of muscle involvement (stage T2), all patients were assigned to the M-VAC chemotherapy protocol after having established clinical stage with chest, abdominal and pelvic computed tomography (CT) and bone scintiscan.
  • Patients were evaluated by means of diagnostic cystoscopy, TURB and bladder mapping, 4 weeks after completing treatment.
  • RESULTS: Of these patients, 4 (80%) completed the treatment protocol.
  • Of these 5 patients 3 (60%) were tumour-free at the follow-up observation 4 weeks after chemotherapy, one patient (20%) still presented with involvement of the bladder wall, and one (20%) presented both with a superficial stage (Ta) and carcinoma in situ (Cis).
  • CONCLUSIONS: Deep TURB followed by three cycles of chemotherapy according to the M-VAC protocol, could be an effective alternative to conservative treatment of stage T2 bladder tumours.
  • [MeSH-major] Urinary Bladder Neoplasms / drug therapy. Urinary Bladder Neoplasms / surgery
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Female. Humans. Male. Middle Aged

  • Genetic Alliance. consumer health - Bladder cancer.
  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11723435.001).
  • [ISSN] 0393-2249
  • [Journal-full-title] Minerva urologica e nefrologica = The Italian journal of urology and nephrology
  • [ISO-abbreviation] Minerva Urol Nefrol
  • [Language] ita
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Italy
  •  go-up   go-down


94. Corey SJ, Elopre M, Weitman S, Rytting ME, Robinson LJ, Rumelhart S, Goldman FD: Complete remission following clofarabine treatment in refractory juvenile myelomonocytic leukemia. J Pediatr Hematol Oncol; 2005 Mar;27(3):166-8
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Complete remission following clofarabine treatment in refractory juvenile myelomonocytic leukemia.
  • Juvenile myelomonocytic leukemia (JMML) is the most common myeloproliferative/myelodysplastic disorder seen in children.
  • The treatment of choice, allogeneic stem cell transplantation, provides the only known cure for the disease, but relapse after transplant is common.
  • Initial treatment consisted of fludarabine and cis-retinoic acid therapy, followed by a matched sibling bone marrow transplant.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arabinonucleosides / therapeutic use. Drug Resistance, Neoplasm. Leukemia, Myelomonocytic, Chronic / drug therapy
  • [MeSH-minor] Adenine Nucleotides. Bone Marrow Transplantation. Child. Humans. Male. Neoplasm Recurrence, Local / drug therapy. Remission Induction. Treatment Outcome

  • Genetic Alliance. consumer health - Juvenile Myelomonocytic Leukemia (JMML).
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15750451.001).
  • [ISSN] 1077-4114
  • [Journal-full-title] Journal of pediatric hematology/oncology
  • [ISO-abbreviation] J. Pediatr. Hematol. Oncol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adenine Nucleotides; 0 / Antineoplastic Agents; 0 / Arabinonucleosides; 762RDY0Y2H / clofarabine
  •  go-up   go-down


95. Reif S, Kingreen D, Kloft C, Grimm J, Siegert W, Schunack W, Jaehde U: Bioequivalence investigation of high-dose etoposide and etoposide phosphate in lymphoma patients. Cancer Chemother Pharmacol; 2001 Aug;48(2):134-40
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bioequivalence was assessed using a two-treatment randomized crossover design.
  • METHODS: Ten patients with high-risk or relapsed lymphoma were treated with a sequential high-dose chemotherapy.
  • They were randomized to receive either 3 x 400 mg/m2 etoposide or an equimolar amount of etoposide phosphate (as 1-h infusions on three consecutive days) in the first course and the alternative drug in the second course.
  • Serial plasma and ultrafiltered plasma samples were collected and analysed for etoposide by a reversed-phase HPLC method with UV and electrochemical detection.
  • RESULTS: Pharmacokinetic parameters of etoposide were comparable in both treatment arms except that terminal half-life was significantly shorter and apparent Vss in ultrafiltered plasma was significantly larger following administration of the prodrug.
  • The 90% CIs were in the range from 80% to 125% where bioequivalence can be assumed.
  • The point estimates of Cmax on day 3 of chemotherapy were 96.5% and 81.7% in plasma and ultrafiltrate with the 90% CI in ultrafiltered plasma being out of the range from 80% to 125%.
  • CONCLUSION: With respect to total drug exposure, represented by AUC(0-infinity), high-dose etoposide phosphate is bioequivalent to high-dose etoposide.
  • [MeSH-minor] Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Cross-Over Studies. Dexamethasone / administration & dosage. Dose-Response Relationship, Drug. Doxorubicin / administration & dosage. Humans. Ifosfamide / administration & dosage. Infusions, Intravenous. Middle Aged.