[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 27 of about 27
1. Goss G, Ferry D, Wierzbicki R, Laurie SA, Thompson J, Biesma B, Hirsch FR, Varella-Garcia M, Duffield E, Ataman OU, Zarenda M, Armour AA: Randomized phase II study of gefitinib compared with placebo in chemotherapy-naive patients with advanced non-small-cell lung cancer and poor performance status. J Clin Oncol; 2009 May 01;27(13):2253-60
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Randomized phase II study of gefitinib compared with placebo in chemotherapy-naive patients with advanced non-small-cell lung cancer and poor performance status.
  • PURPOSE: To compare gefitinib with placebo in chemotherapy naïve patients with advanced non-small-cell lung cancer (NSCLC) and poor performance status.
  • PATIENTS AND METHODS: NSCLC patients (chemotherapy naïve, WHO performance status 2 or 3; unfit for chemotherapy; stage IIIB/IV) were randomly assigned to gefitinib (250 mg/d) plus best supportive care (BSC; n = 100) or placebo plus BSC (n = 101).
  • Secondary end points included overall survival (OS), objective response rate (ORR), quality of life (QOL), pulmonary symptom improvement (PSI), and safety.
  • Correlation of gefitinib efficacy with EGFR gene copy number (fluorescent in situ hybridization [FISH]) was explored.
  • CONCLUSION: There was no statistically significant difference in PFS, OS, and ORRs after treatment with gefitinib or placebo, in the overall population; improvements in QOL and symptoms were similar in both groups.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Double-Blind Method. Female. Humans. In Situ Hybridization, Fluorescence. Male. Middle Aged. Quality of Life

  • 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.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19289623.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P50 CA058187
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC4886538
  •  go-up   go-down


2. Krystal GW, Sulanke G, Litz J: Inhibition of phosphatidylinositol 3-kinase-Akt signaling blocks growth, promotes apoptosis, and enhances sensitivity of small cell lung cancer cells to chemotherapy. Mol Cancer Ther; 2002 Sep;1(11):913-22
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of phosphatidylinositol 3-kinase-Akt signaling blocks growth, promotes apoptosis, and enhances sensitivity of small cell lung cancer cells to chemotherapy.
  • A promising therapeutic alternative to inhibition of growth factor receptors is the inhibition of downstream signal transduction pathways.
  • Both stem cell factor (SCF) and insulin-like growth factor (IGF)-I, components of prominent small cell lung cancer (SCLC) autocrine loops, as well as FCS, can potently activate phosphatidylinositol 3-kinase (PI3K)-Akt signaling, albeit with different kinetics.
  • A panel of six SCLC cell lines grown in 10% FCS was also very sensitive to LY294002, with average IC50 and LD50 of 5 and 25 microM, respectively.
  • These drug concentrations suppressed the growth of the MRC-5 pulmonary fibroblast cell line and primary bronchial epithelial cells but did not induce significant cell death.
  • Taken together, these data demonstrate that PI3K-Akt signaling promotes SCLC growth, survival, and chemotherapy resistance.
  • Therefore, selective inhibitors of PI3K or Akt could potentially be useful as novel therapeutic agents in the treatment of SCLC.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis. Carcinoma, Small Cell / drug therapy. Carcinoma, Small Cell / pathology. Enzyme Inhibitors / pharmacology. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Phosphatidylinositol 3-Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases. Proto-Oncogene Proteins / metabolism
  • [MeSH-minor] Alleles. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Cell Death. Cell Division / drug effects. Cell Survival. Chromones / pharmacology. Doxycycline / pharmacology. Etoposide / pharmacology. Genes, Dominant. Genetic Vectors. Humans. In Situ Nick-End Labeling. Inhibitory Concentration 50. Insulin-Like Growth Factor I / metabolism. Morpholines / pharmacology. Mutation. Precipitin Tests. Proto-Oncogene Proteins c-akt. Signal Transduction. Stem Cell Factor / metabolism. Time Factors. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. DOXYCYCLINE .
  • 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
  • (PMID = 12481412.001).
  • [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; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / Proto-Oncogene Proteins; 0 / Stem Cell Factor; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; 67763-96-6 / Insulin-Like Growth Factor I; 6PLQ3CP4P3 / Etoposide; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; N12000U13O / Doxycycline
  •  go-up   go-down


3. Cherfils-Vicini J, Platonova S, Gillard M, Laurans L, Validire P, Caliandro R, Magdeleinat P, Mami-Chouaib F, Dieu-Nosjean MC, Fridman WH, Damotte D, Sautès-Fridman C, Cremer I: Triggering of TLR7 and TLR8 expressed by human lung cancer cells induces cell survival and chemoresistance. J Clin Invest; 2010 Apr;120(4):1285-97
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Triggering of TLR7 and TLR8 expressed by human lung cancer cells induces cell survival and chemoresistance.
  • Compelling evidence suggests that inflammation, cell survival, and cancer are linked, with a central role played by NF-kappaB.
  • Here we have demonstrated expression of TLR7 and TLR8, the natural receptors for single-stranded RNA, by tumor cells in human lung cancer in situ and in human lung tumor cell lines.
  • Stimulation with TLR7 or TLR8 agonists led to activated NF-kappaB, upregulated expression of the antiapoptotic protein Bcl-2, increased tumor cell survival, and chemoresistance.
  • Transcriptional analysis performed on human primary lung tumor cells and TLR7- or TLR8-stimulated human lung tumor cell lines revealed a gene expression signature suggestive of chronic stimulation of tumor cells by TLR ligands in situ.
  • Together, these data emphasize that TLR signaling can directly favor tumor development and further suggest that researchers developing anticancer immunotherapy using TLR7 or TLR8 agonists as adjuvants should take into account the expression of these TLRs in lung tumor cells.
  • [MeSH-major] Lung Neoplasms / drug therapy. Toll-Like Receptor 7 / physiology. Toll-Like Receptor 8 / physiology
  • [MeSH-minor] Cell Line, Tumor. Cell Survival. Drug Resistance, Neoplasm. Gene Expression Profiling. Guanosine / analogs & derivatives. Guanosine / pharmacology. Humans. Immunohistochemistry. Interleukin-1beta / pharmacology. Myeloid Differentiation Factor 88 / physiology. NF-kappa B / metabolism. Signal Transduction

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Immunity. 2007 Apr;26(4):461-75 [17398123.001]
  • [Cites] J Clin Invest. 2007 May;117(5):1137-46 [17476343.001]
  • [Cites] Nat Med. 2007 May;13(5):552-9 [17479101.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4346-52 [17483348.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 8;104(19):8047-52 [17463087.001]
  • [Cites] Cell. 2004 Sep 17;118(6):671-4 [15369667.001]
  • [Cites] Nature. 2004 Sep 23;431(7007):461-6 [15329734.001]
  • [Cites] Cancer Causes Control. 2004 Oct;15(8):819-27 [15456995.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1624-30 [15466979.001]
  • [Cites] J Clin Invest. 2004 Oct;114(7):898-907 [15467828.001]
  • [Cites] J Exp Med. 2007 Jun 11;204(6):1441-51 [17535975.001]
  • [Cites] Science. 2007 Jul 6;317(5834):124-7 [17615359.001]
  • [Cites] FEBS J. 2007 Jul;274(14):3655-68 [17608805.001]
  • [Cites] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4565-74 [17671143.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2007 Oct;16(10):1982-9 [17932345.001]
  • [Cites] Immunol Rev. 2007 Dec;220:60-81 [17979840.001]
  • [Cites] J Clin Invest. 2007 Dec;117(12):3846-56 [18060032.001]
  • [Cites] Oncogene. 2008 Jan 7;27(2):190-9 [18176600.001]
  • [Cites] Clin Cancer Res. 2008 Feb 1;14(3):856-64 [18245549.001]
  • [Cites] Trends Mol Med. 2008 Mar;14(3):109-19 [18261959.001]
  • [Cites] Front Biosci. 2008;13:5787-93 [18508622.001]
  • [Cites] Oncologist. 2008 Aug;13(8):859-75 [18701762.001]
  • [Cites] J Clin Oncol. 2008 Sep 20;26(27):4410-7 [18802153.001]
  • [Cites] J Cancer Res Clin Oncol. 2009 Mar;135(3):379-86 [18825409.001]
  • [Cites] Cancer. 2009 Apr 15;115(8):1701-12 [19197998.001]
  • [Cites] Semin Cancer Biol. 2004 Dec;14(6):433-9 [15489136.001]
  • [Cites] Br J Cancer. 2004 Nov 29;91(11):1970-6 [15545974.001]
  • [Cites] Lancet. 2001 Feb 17;357(9255):539-45 [11229684.001]
  • [Cites] J Cancer Res Clin Oncol. 2001;127(3):166-72 [11260861.001]
  • [Cites] Nat Immunol. 2002 Mar;3(3):221-7 [11875461.001]
  • [Cites] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959.001]
  • [Cites] J Biol Chem. 2004 Jan 23;279(4):2712-8 [14600154.001]
  • [Cites] N Engl J Med. 2004 Jan 22;350(4):379-92 [14736930.001]
  • [Cites] Respir Med. 2004 Feb;98(2):93-8 [14971870.001]
  • [Cites] J Biol Chem. 2004 Feb 27;279(9):7576-83 [14662759.001]
  • [Cites] Science. 2004 Mar 5;303(5663):1529-31 [14976261.001]
  • [Cites] Science. 2004 Mar 5;303(5663):1526-9 [14976262.001]
  • [Cites] Integr Cancer Ther. 2003 Sep;2(3):238-46 [15035887.001]
  • [Cites] J Immunol. 2004 Jul 15;173(2):1179-83 [15240708.001]
  • [Cites] Cell. 2004 Aug 6;118(3):285-96 [15294155.001]
  • [Cites] Respir Res. 2005;6:1 [15631627.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Apr;14(4):773-8 [15824142.001]
  • [Cites] J Biol Chem. 2005 May 27;280(21):20620-7 [15788393.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5009-14 [15958541.001]
  • [Cites] J Virol. 2005 Oct;79(20):12893-904 [16188991.001]
  • [Cites] J Clin Invest. 2005 Oct;115(10):2625-32 [16200195.001]
  • [Cites] Nat Rev Immunol. 2005 Oct;5(10):749-59 [16175180.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11771-8 [16357190.001]
  • [Cites] Semin Cancer Biol. 2006 Feb;16(1):32-7 [16153858.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2006 Mar;15(3):480-5 [16537705.001]
  • [Cites] Oncogene. 2006 Mar 13;25(11):1679-91 [16550168.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3859-68 [16585214.001]
  • [Cites] J Immunol. 2006 Apr 15;176(8):4894-901 [16585585.001]
  • [Cites] Blood. 2006 Apr 15;107(8):3295-302 [16380446.001]
  • [Cites] J Immunol. 2006 May 1;176(9):5529-37 [16622022.001]
  • [Cites] Respir Res. 2006;7:64 [16606450.001]
  • [Cites] Leukemia. 2006 Jun;20(6):1130-7 [16628189.001]
  • [Cites] Int J Mol Med. 2006 Aug;18(2):365-73 [16820947.001]
  • [Cites] J Biol Chem. 2006 Jul 28;281(30):21013-21 [16737960.001]
  • [Cites] Br J Cancer. 2006 Aug 7;95(3):247-52 [16892041.001]
  • [Cites] Clin Exp Metastasis. 2006;23(1):9-18 [16821125.001]
  • [Cites] Cancer Metastasis Rev. 2006 Sep;25(3):409-16 [16951987.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):2763-9 [17312119.001]
  • [Cites] J Immunol. 2007 Mar 1;178(5):3134-42 [17312161.001]
  • [Cites] Nat Rev Immunol. 2007 Mar;7(3):179-90 [17318230.001]
  • [Cites] Mol Immunol. 2007 Apr;44(11):2850-9 [17328955.001]
  • [Cites] Transgenic Res. 2007 Apr;16(2):193-201 [17206489.001]
  • [Cites] Nature. 2007 Apr 5;446(7136):690-4 [17377533.001]
  • [CommentIn] Immunotherapy. 2010 Sep;2(5):609 [20919443.001]
  • (PMID = 20237413.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Interleukin-1beta; 0 / MYD88 protein, human; 0 / Myeloid Differentiation Factor 88; 0 / NF-kappa B; 0 / TLR7 protein, human; 0 / TLR8 protein, human; 0 / Toll-Like Receptor 7; 0 / Toll-Like Receptor 8; 12133JR80S / Guanosine; 9CAS0V66OI / loxoribine
  • [Other-IDs] NLM/ PMC2846035
  •  go-up   go-down


Advertisement
4. Crinò L, Cappuzzo F, Zatloukal P, Reck M, Pesek M, Thompson JC, Ford HE, Hirsch FR, Varella-Garcia M, Ghiorghiu S, Duffield EL, Armour AA, Speake G, Cullen M: Gefitinib versus vinorelbine in chemotherapy-naive elderly patients with advanced non-small-cell lung cancer (INVITE): a randomized, phase II study. J Clin Oncol; 2008 Sep 10;26(26):4253-60
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gefitinib versus vinorelbine in chemotherapy-naive elderly patients with advanced non-small-cell lung cancer (INVITE): a randomized, phase II study.
  • PURPOSE: This phase II, open-label, parallel-group study compared gefitinib with vinorelbine in chemotherapy-naïve elderly patients with advanced non-small-cell lung cancer (NSCLC).
  • METHODS: Chemotherapy-naïve patients (age >or= 70 years) were randomly assigned to gefitinib (250 mg/d orally) or vinorelbine (30 mg/m(2) infusion on days 1 and 8 of a 21-day cycle).
  • Secondary end points were overall survival (OS), objective response rate (ORR), quality of life (QOL), pulmonary symptom improvement (PSI), and tolerability.
  • Exploratory end points included epidermal growth factor receptor (EGFR) gene copy number by fluorescent in situ hybridization (FISH).
  • There were fewer treatment-related grade 3 to 5 adverse events with gefitinib (12.8%) than with vinorelbine (41.7%).
  • CONCLUSION: There was no statistical difference between gefitinib and vinorelbine in efficacy in chemotherapy-naïve, unselected elderly patients with advanced NSCLC, but there was better tolerability with gefitinib.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinazolines / therapeutic use. Vinblastine / analogs & derivatives


5. Orikasa K, Namima T, Ota S, Miura M, Hama H, Kimura N, Ohnuma T: Acute eosinophilic pneumonia associated with intravesical bacillus Calmette-Guérin therapy of carcinoma in situ of the bladder. Int J Urol; 2003 Nov;10(11):622-4
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acute eosinophilic pneumonia associated with intravesical bacillus Calmette-Guérin therapy of carcinoma in situ of the bladder.
  • A 71-year-old man with a history of rheumatoid arthritis was treated with intravesical bacillus Calmette-Guérin (BCG) instillation of 80 mg once-a-week for carcinoma in situ.
  • He developed low-grade fever followed by dyspnea and severe hypoxemia.
  • From these findings, a pulmonary hypersensitivity reaction to immunotherapy was suspected, and therefore, methylprednisolone (500 mg per day) was started.
  • The present case is the first reported case of eosinophilic pneumonia following intravesical BCG therapy.
  • [MeSH-major] Adjuvants, Immunologic / administration & dosage. Adjuvants, Immunologic / adverse effects. BCG Vaccine / administration & dosage. BCG Vaccine / adverse effects. Pulmonary Eosinophilia / chemically induced. Urinary Bladder Neoplasms / drug therapy
  • [MeSH-minor] Acute Disease. Administration, Intravesical. Aged. Follow-Up Studies. Humans. Hypersensitivity / diagnosis. Hypersensitivity / etiology. Hypersensitivity / therapy. Male. Treatment Outcome

  • Genetic Alliance. consumer health - Pneumonia, eosinophilic.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14633091.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / BCG Vaccine
  •  go-up   go-down


6. Mańdziuk S, Dudzisz-Sledź M, Korszeń-Pilecka I, Milanowski J, Wojcierowski J, Korobowicz E: Expression of p53 gene in stage IIIA non-small cell lung cancer in patients after neoadjuvant chemotherapy with Vepesid and Cisplatin. Ann Univ Mariae Curie Sklodowska Med; 2003;58(1):154-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of p53 gene in stage IIIA non-small cell lung cancer in patients after neoadjuvant chemotherapy with Vepesid and Cisplatin.
  • Apoptosis (programmed cell death) plays a very important role in the development regulation, homeostasis maintenance as well as in the origin of many diseases, including neoplasms.
  • The process is considered to be of great significance in tumour originating and growth as well as in tumour cell response to chemotherapy.
  • Our study aimed at evaluating p53 gene expression in non-small-cell lung cancer patients after neoadjuvant chemotherapy.
  • We examined the tissue material from 35 patients after three-cycle inductive chemotherapy (Vepesid and Cisplatin).
  • The material was obtained before chemotherapy during bronchofiberoscopy and four weeks after drug treatment during surgery.
  • The control group comprised patients who had not undergone inductive chemotherapy.
  • After deparaffinising of tissue slides, gene p53 activity using in situ hybridisation technique was evaluated.
  • Our study revealed significantly higher percentage of cells undergoing apoptosis and increased gene p53 activity in tumour tissue slides of patients after neoadjuvant chemotherapy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Neoadjuvant Therapy. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Bronchoscopy. Chemotherapy, Adjuvant. Cisplatin / administration & dosage. Cytophotometry. Etoposide / administration & dosage. Female. Gene Expression Regulation, Neoplastic. Humans. Male. Neoplasm Staging

  • 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. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15314976.001).
  • [ISSN] 0066-2240
  • [Journal-full-title] Annales Universitatis Mariae Curie-Skłodowska. Sectio D: Medicina
  • [ISO-abbreviation] Ann Univ Mariae Curie Sklodowska Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Tumor Suppressor Protein p53; 6PLQ3CP4P3 / Etoposide; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


7. Karczmarek-Borowska B, Filip A, Wojcierowski J, Smoleń A, Pilecka I, Jabłonka A: Survivin antiapoptotic gene expression as a prognostic factor in non-small cell lung cancer: in situ hybridization study. Folia Histochem Cytobiol; 2005;43(4):237-42
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Survivin antiapoptotic gene expression as a prognostic factor in non-small cell lung cancer: in situ hybridization study.
  • Survivin is an inhibitor of apoptosis that plays a significant role in cell cycle regulation and is important for survival prognosis in many neoplasms.
  • Survivin expression was assessed by in situ hybridization (ISH) in 60 consecutive patients (54 males and 4 females) with NSCLC treated between 1993 and 1997.
  • The examined patients had IIB and IIIA stage according to TNM system.
  • In all cases the chemotherapy with cisplatin and etoposide (2 cycles) was administered prior the surgery; in patients responding to the therapy one more cycle was applied.
  • There was no correlation between survivin mRNA level and histological type of tumor, stage of cell differentiation, stage of disease according to TNM classification, performance status according to WHO and number of chemotherapy regimens administered (p > 0.05).
  • However, the correlation between survivin gene expression and response to the chemotherapy was statistically significant (p = 0.04).
  • Univariate analysis (log-rank test) showed that significant independent prognostic factors in NSCLC included: stage of the disease according to TNM classification (p = 0.006), response to chemotherapy (p = 0.005) and pattern of survivin gene expression (p = 0.00003).
  • Multivariate analysis utilizing Cox's model showed that for survival assessment the stage according to TNM, response to the chemotherapy and survivin expression estimated by means of ISH are of statistical significance (p=0.00001).
  • Our data show that survivin expression may be used as a prognostic factor and a target for therapy.

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16382892.001).
  • [ISSN] 0239-8508
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / RNA, Messenger
  •  go-up   go-down


8. Stănciulea O, Preda C, Herlea V, Popa M, Ulmeanu D, Vasilescu C: [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis]. Chirurgia (Bucur); 2007 Mar-Apr;102(2):215-20
MedlinePlus Health Information. consumer health - Intestinal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Rare indication of cephalic duodenopancreatectomy with total gastrectomy--periampullary carcinoma in moderate form of familial adenomatous polyposis].
  • [Transliterated title] Indicaţie rară de duodenopancreatectomie cefalică cu gastrectomie totală-- adenocarcinom periampular cu polipoză adenomatoasă familială forma atenuată.
  • The surgical procedure was followed by chemotherapy.
  • The patient underwent transverse colectomy (the histopathological exam--in situ carcinoma).
  • In 2005 was noted a pulmonary nodule, located in the postero-apical segment of upper left lobe, for which left superior lobe resection was performed (the histopathological exam: metastatic adenocarcinoma).
  • The surgical procedure recommended in patients with attenuated form of familial adenomatous polyposis and suspect periampullary lesions is duodenopancreatectomy.
  • [MeSH-major] Adenomatous Polyposis Coli / surgery. Carcinoma / surgery. Duodenal Neoplasms / surgery. Gastrectomy. Neoplasms, Multiple Primary / surgery. Pancreaticoduodenectomy / methods
  • [MeSH-minor] Ampulla of Vater. Humans. Male. Middle Aged. Stomach Neoplasms / surgery. Treatment Outcome

  • Genetic Alliance. consumer health - Familial Adenomatous Polyposis (FAP).
  • Genetic Alliance. consumer health - Familial Polyposis.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17615925.001).
  • [ISSN] 1221-9118
  • [Journal-full-title] Chirurgia (Bucharest, Romania : 1990)
  • [ISO-abbreviation] Chirurgia (Bucur)
  • [Language] rum
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Romania
  •  go-up   go-down


9. Chang YL, Wu CT, Shih JY, Lee YC: New aspects in clinicopathologic and oncogene studies of 23 pulmonary lymphoepithelioma-like carcinomas. Am J Surg Pathol; 2002 Jun;26(6):715-23
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New aspects in clinicopathologic and oncogene studies of 23 pulmonary lymphoepithelioma-like carcinomas.
  • Lymphoepithelioma-like carcinoma, an uncommon epithelial tumor, has been described as being closely associated with Epstein-Barr virus (EBV) infection in many organs, especially the nasopharynx.
  • We experienced 23 cases of lymphoepithelioma-like carcinoma arising in the lung from 2498 lung cancer patients in the Cancer Registry of our hospital.
  • EBV serology revealed prior infection in all 15 serum-available patients, all of whom were also found by in situ hybridization to have the virus genome.
  • EBV viral capsid antigen IgG level remained elevated despite response to therapy.
  • Nearly all cases had bcl-2 oncoprotein expression, but the detection rate of latent membrane protein-1, p53, and c-erb B-2 expression was extremely low.
  • The encouraging chemotherapy response for advanced stage disease is also discussed.
  • [MeSH-major] Capsid Proteins. Carcinoma / secondary. Lung Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antigens, Viral / analysis. CD8-Positive T-Lymphocytes / pathology. Cell Count. Female. Herpesviridae Infections / complications. Herpesviridae Infections / genetics. Herpesviridae Infections / pathology. Herpesvirus 4, Human / genetics. Herpesvirus 4, Human / immunology. Herpesvirus 4, Human / isolation & purification. Humans. Immunohistochemistry. In Situ Hybridization. Male. Middle Aged. Neoplasm Staging. Proto-Oncogene Proteins c-bcl-2 / genetics. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Viral / analysis. Tumor Suppressor Protein p53 / analysis

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12023575.001).
  • [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 / Antigens, Viral; 0 / Capsid Proteins; 0 / Epstein-Barr viral capsid antigen; 0 / Epstein-Barr virus encoded RNA 1; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Viral; 0 / Tumor Suppressor Protein p53
  •  go-up   go-down


10. Horita K, Inase N, Miyake S, Formby B, Toyoda H, Yoshizawa Y: Progesterone induces apoptosis in malignant mesothelioma cells. Anticancer Res; 2001 Nov-Dec;21(6A):3871-4
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Progesterone has been used in the treatment of patients with recurrent or metastatic progesterone receptor-positive endometrial carcinoma and breast cancer.
  • In vitro study using a breast cancer cell line, T47D, demonstrated an increase in p53 gene expression and induction of apoptosis by the administration of progesterone.
  • Therefore, we investigated the effect of progesterone administration on the proliferation and apoptosis in a mesothelioma cell line, 211H.
  • The expression of the progesterone receptor gene was detected in this cell line by a nested RT-PCR method.
  • The proliferation of the cell line was suppressed after a 10-day incubation with 30 microM progesterone.
  • These results clearly demonstrated that progesterone administration suppressed the cell proliferation and induced apoptosis in malignant mesothelioma cells.
  • [MeSH-major] Apoptosis / drug effects. Mesothelioma / drug therapy. Mesothelioma / pathology. Progesterone / pharmacology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Cell Division / drug effects. DNA Fragmentation / drug effects. Humans. In Situ Nick-End Labeling. Receptors, Progesterone / biosynthesis. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Mesothelioma, malignant.
  • MedlinePlus Health Information. consumer health - Mesothelioma.
  • Hazardous Substances Data Bank. PROGESTERONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11911261.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Receptors, Progesterone; 4G7DS2Q64Y / Progesterone
  •  go-up   go-down


11. Miyazu Y, Miyazawa T, Kurimoto N, Iwamoto Y, Kanoh K, Kohno N: Endobronchial ultrasonography in the assessment of centrally located early-stage lung cancer before photodynamic therapy. Am J Respir Crit Care Med; 2002 Mar 15;165(6):832-7
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Endobronchial ultrasonography in the assessment of centrally located early-stage lung cancer before photodynamic therapy.
  • To evaluate the utility of endobronchial ultrasonography (EBUS) in selecting appropriate candidates with centrally located early-stage lung cancer for photodynamic therapy (PDT) with curative intent, we performed EBUS before PDT in 18 biopsy-proven squamous cell carcinomas (including three carcinoma in situ) that had been considered to be appropriate candidates for PDT by conventional bronchoscopy and high-resolution computed tomography (HR-CT).
  • Long-term complete remission has been achieved in these patients with a median follow-up term after PDT of 32 months.
  • The remaining nine lesions were diagnosed as extracartilaginous by EBUS and were considered candidates for other therapies such as surgical resection, chemotherapy, and radiotherapy, although two were invisible by HR-CT, three were superficial, and five were < or = 1 cm in diameter on observation by bronchoscopy.
  • We conclude that EBUS is a useful technique that might be considered in addition to conventional bronchoscopy and HR-CT to improve the efficacy of PDT in patients with centrally located early-stage lung cancer.
  • [MeSH-major] Carcinoma, Squamous Cell / therapy. Carcinoma, Squamous Cell / ultrasonography. Endosonography. Lung Neoplasms / therapy. Lung Neoplasms / ultrasonography. Patient Selection. Photochemotherapy
  • [MeSH-minor] Aged. Carcinoma in Situ / pathology. Carcinoma in Situ / therapy. Carcinoma in Situ / ultrasonography. Female. Humans. Male. Middle Aged. Neoplasm Invasiveness. Prospective Studies

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11897652.001).
  • [ISSN] 1073-449X
  • [Journal-full-title] American journal of respiratory and critical care medicine
  • [ISO-abbreviation] Am. J. Respir. Crit. Care Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


12. Darvishian F, Ginsberg MS, Klimstra DS, Brogi E: Carcinoid tumorlets simulate pulmonary metastases in women with breast cancer. Hum Pathol; 2006 Jul;37(7):839-44
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carcinoid tumorlets simulate pulmonary metastases in women with breast cancer.
  • A pulmonary carcinoid tumorlet (PCT) is a nodular proliferation of neuroendocrine cells smaller than 0.5 cm.
  • Cases of multiple PCTs diagnosed between 1992 and 2003 in patients with history of breast cancer were identified through a search of the pathology files.
  • We identified 12 women with a history of breast cancer and biopsy-proven PCTs, who were treated at our institution in a period of 12 years.
  • The mean age at diagnosis of the breast cancer was 62.8 years.
  • The breast cancer was invasive carcinoma in 10 cases (9 ductal and 1 lobular) and ductal carcinoma in situ and malignant phyllodes tumor in 1 case each.
  • Six women received radiotherapy; 5, chemotherapy; and 4, hormonal treatment, alone or in combination.
  • Pulmonary carcinoid tumorlets were identified within 5 months from diagnosis of the breast malignancy in 7 patients and at follow-up (range, 57-162 months) in the remaining 5.
  • In all cases, the PCTs consisted of multiple pulmonary nodules that were radiologically interpreted as suspicious for pulmonary metastases.
  • Misdiagnosis of metastatic carcinoma was rendered intraoperatively by frozen section analysis in 3 cases.
  • None of the patients had known metastatic disease at the time of diagnosis of PCTs.
  • Three patients subsequently developed recurrent disease, including 2 with extramammary spread.
  • Pulmonary carcinoid tumorlets are radiologic and histologic mimickers of pulmonary metastases in patients with a history of breast cancer.
  • Consideration should be given to the possibility of PCTs in patients with breast cancer with pulmonary nodules, even if multiple.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoid Tumor / pathology. Lung Neoplasms / pathology. Neoplasms, Multiple Primary / pathology
  • [MeSH-minor] Adult. Diagnosis, Differential. Female. Humans. Middle Aged. Tomography, X-Ray Computed


13. Hosaka Y: [Extratesticular germ cell tumor focusing on treatment and prognosis]. Gan To Kagaku Ryoho; 2000 Apr;27(4):536-41

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Extratesticular germ cell tumor focusing on treatment and prognosis].
  • About 3% to 5% of all germ cell tumors are thought to be primary extratesticular tumors, including a small group of benign tumors.
  • Developments in ultrasonography have enabled the detection of tiny testicular lesions, and ultrasonography is applied to determine the biopsy sites.
  • Nevertheless, burned-out tumor and carcinoma in situ are not always easy to find.
  • Extratesticular germ cell tumors are usually treated using methods similar to those for advanced testicular tumors; however, the results are discouraging.
  • Only limited cases are suitable for a monotherapy of surgery, so a combined treatment of cisplatin based chemotherapy and surgery is prevalent.
  • In addition to the advent of such pharmaceuticals as G-CSF and serotonin receptor antagonists, recent development of peripheral blood stem cell transplantation is expected to produce improved prognoses among patients burdened with this refractory disease.
  • A prognostic factor-based staging system developed by the International Germ Cell Cancer Collaborative Group is reasonable and useful.
  • Non-seminomas are classified as having good or intermediate prognoses if retroperitoneal tumors having no non-pulmonary visceral metastases show good or intermediate markers.
  • A poor prognosis is associated with extratesticular tumors with mediastinal primary or non-pulmonary visceral metastases or poor markers.
  • Seminomas with normal AFP are classified as having good or intermediate prognoses if no non-pulmonary visceral metastases are seen or discarded.
  • [MeSH-major] Germinoma / therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10790995.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] JAPAN
  • [Number-of-references] 34
  •  go-up   go-down


14. Gu Y, Zhu CF, Dai YL, Zhong Q, Sun B: Inhibitory effects of genistein on metastasis of human hepatocellular carcinoma. World J Gastroenterol; 2009 Oct 21;15(39):4952-7
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effects of genistein on metastasis of human hepatocellular carcinoma.
  • AIM: To investigate the inhibitory effects of genistein on metastasis of MHCC97-H hepatocellular carcinoma cells and to explore the underlying mechanism.
  • METHODS: MHCC97-H hepatocellular carcinoma cells were exposed to genistein.
  • A cell attachment assay was carried out in a microculture well pre-coated with fibronectin.
  • The invasive activity of tumor cells was assayed in a transwell cell culture chamber, and cell cycle and apoptosis were evaluated by a functional assay.
  • In situ xenograft transplantation of hepatocellular carcinoma was performed in 12 nude mice and lung metastasis of hepatocellular carcinoma was observed.
  • Genistein caused G(0)/G(1) cell cycle arrest, an S phase decrease, and increased apoptosis.
  • In situ xenograft transplantation of hepatocellular carcinoma was also significantly suppressed by genistein.
  • The number of pulmonary micrometastatic foci in the genistein group was significantly lower compared with the control group (12.3 +/- 1.8 vs 16.6 +/- 2.6, P < 0.05).
  • CONCLUSION: Genistein appears to be a promising agent in the inhibition of metastasis of hepatocellular carcinoma.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoma, Hepatocellular / drug therapy. Carcinoma, Hepatocellular / secondary. Genistein / pharmacology. Liver Neoplasms / pathology. Lung Neoplasms / drug therapy. Lung Neoplasms / secondary
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Adhesion / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Focal Adhesion Kinase 1 / metabolism. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Invasiveness. Phosphorylation. Time Factors. Tumor Burden / drug effects. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. GENISTEIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Int J Cancer. 2001 Mar 15;91(6):797-802 [11275982.001]
  • [Cites] Nat Clin Pract Oncol. 2008 Apr;5(4):206-19 [18253104.001]
  • [Cites] Phytochemistry. 2002 Jun;60(3):205-11 [12031439.001]
  • [Cites] J Nutr. 2002 Nov;132(11 Suppl):3482S-3489S [12421874.001]
  • [Cites] Cancer Invest. 2003;21(5):744-57 [14628433.001]
  • [Cites] Clin Exp Metastasis. 2003;20(7):585-92 [14669789.001]
  • [Cites] Cancer Lett. 2004 Jan 8;203(1):59-69 [14670618.001]
  • [Cites] Biochem Pharmacol. 2004 Feb 15;67(4):717-26 [14757171.001]
  • [Cites] Lancet Oncol. 2004 Apr;5(4):254-8 [15050959.001]
  • [Cites] Front Biosci. 2004 Sep 1;9:2714-24 [15353308.001]
  • [Cites] Int J Cancer. 1996 Apr 10;66(2):239-43 [8603818.001]
  • [Cites] Cancer Detect Prev. 1996;20(1):43-51 [8907202.001]
  • [Cites] Oncogene. 1999 Oct 7;18(41):5646-53 [10523844.001]
  • [Cites] Adv Exp Med Biol. 2004;546:121-65 [15584372.001]
  • [Cites] J Cancer Res Clin Oncol. 2004 Jul;130(7):375-82 [15133661.001]
  • [Cites] Cancer Gene Ther. 2005 Sep;12(9):769-77 [15877081.001]
  • [Cites] World J Gastroenterol. 2005 Nov 7;11(41):6512-7 [16425425.001]
  • [Cites] Biochem Pharmacol. 2007 Mar 15;73(6):782-92 [17188247.001]
  • [Cites] Mol Cell Biochem. 2007 Mar;297(1-2):73-80 [17006617.001]
  • [Cites] Curr Cancer Drug Targets. 2007 Aug;7(5):465-74 [17691906.001]
  • [Cites] Mol Biotechnol. 2008 Jan;38(1):33-40 [18095189.001]
  • [Cites] World J Gastroenterol. 2008 Jan 28;14(4):627-31 [18203299.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2008;11(1):6-12 [17923857.001]
  • [Cites] World J Gastroenterol. 2001 Oct;7(5):630-6 [11819844.001]
  • (PMID = 19842228.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; DH2M523P0H / Genistein; EC 2.7.10.2 / Focal Adhesion Kinase 1; EC 2.7.10.2 / PTK2 protein, human
  • [Other-IDs] NLM/ PMC2764975
  •  go-up   go-down


15. Shishido T, Itou T, Ono Y, Arai Y, Miki M: [Adenocarcinoma of the renal pelvis and transitional cell carcinoma of the ureter occurring 11 years after radical cystectomy for bladder cancer: a case report]. Hinyokika Kiyo; 2001 Mar;47(3):187-90
MedlinePlus Health Information. consumer health - Kidney Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Adenocarcinoma of the renal pelvis and transitional cell carcinoma of the ureter occurring 11 years after radical cystectomy for bladder cancer: a case report].
  • We report a case of upper urinary tract carcinoma which recurred 11 years after total cystectomy.
  • Carcinoma in situ was diagnosed pathologically.
  • The pathological diagnosis was transitional cell carcinoma, grade 3, pTis.
  • The right kidney was not visualized on IVP and computed tomography revealed a right renal irregular mass.
  • The pathologic diagnosis was renal pelvic adenocarcinoma and ureteral transitional cell carcinoma.
  • The patient was treated postoperatively with 3 cycles of systemic chemotherapy and radiotherapy.
  • He died of retroperitoneal lymph node, left adrenal gland and pulmonary metastases.
  • [MeSH-major] Adenocarcinoma / etiology. Carcinoma, Transitional Cell / etiology. Cystectomy. Kidney Neoplasms / etiology. Kidney Pelvis. Neoplasms, Second Primary / etiology. Postoperative Complications. Ureteral Neoplasms / etiology. Urinary Bladder Neoplasms / surgery
  • [MeSH-minor] Humans. Male. Middle Aged. Time Factors


16. Seward SM, Richardson DL, Leon ME, Zhao W, Cohn DE, Hitchcock CL: Metastatic squamous cell carcinoma of the vulva to the lung confirmed with allelotyping. Int J Gynecol Pathol; 2009 Sep;28(5):497-501
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metastatic squamous cell carcinoma of the vulva to the lung confirmed with allelotyping.
  • A squamous-cell carcinoma (SCC) of the lung can be indistinguishable from metastatic SCC of gynecologic origin using common histopathologic techniques; however, establishing tumor origin can be clinically relevant.
  • A patient with a Bartholin gland SCC was found to also have a pulmonary SCC, concerning for metastasis versus synchronous pulmonary primary.
  • Allelotyping for loss of heterozygosity established the pulmonary lesion as a rare event of vulvar pulmonary metastasis.
  • The patient received palliative chemotherapy instead of curative treatment.
  • [MeSH-major] Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / secondary. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Vulvar Neoplasms / genetics. Vulvar Neoplasms / pathology
  • [MeSH-minor] Aged. Alleles. Bartholin's Glands / pathology. Biomarkers, Tumor / genetics. Female. Humans. In Situ Hybridization. Loss of Heterozygosity. Microdissection. Palliative Care. Papillomavirus Infections / complications. Sarcoidosis / complications

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Vulvar Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19696623.001).
  • [ISSN] 1538-7151
  • [Journal-full-title] International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists
  • [ISO-abbreviation] Int. J. Gynecol. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor
  •  go-up   go-down


17. Krawczyk P, Chocholska S, Milanowski J: Anti-HER therapeutic agents in the treatment of non-small-cell lung cancer. Ann Univ Mariae Curie Sklodowska Med; 2003;58(1):113-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-HER therapeutic agents in the treatment of non-small-cell lung cancer.
  • Dimerised on binding with a number of ligands, including epidermal growth factor (EGF) and transforming growth factor alpha (TGFalpha), these proteins stimulate epithelial cell proliferation.
  • HER2 and EGFR overexpression is detected in the cells of many tumours, mainly in breast, lung and oral cancer and may be connected with HER2 gene amplification or point mutations as well as with the presence of overactive polymorphic forms of HER1 gene.
  • The first medication of a proved efficacy in breast cancer treatment was trastuzumab (Herceptin)--monoclonal antibody against HER2 protein.
  • Trastuzumab was effective only in the case of patients with high HER2 expression evaluated by immunohistochemical methods and with gene amplification ascertained by fluorescence in situ hybridisation assays.
  • In non-small-cell lung cancer (NSCLC), HER2 overexpression was detected only in a few cases.
  • Therefore, trastuzumab treatment seems to be problematic in NSCLC patients.
  • A small molecule quinazoline (erlotinib, Tarceva) is a promising therapeutic agent selectively blocking EGFR.
  • Phase III Tarceva clinical trail in NSCLC patients showed that their survival is prolonged and that the medication acts together with other chemotherapeutic agents like cisplatin and gemcitabine.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Erlotinib Hydrochloride. Gene Expression Regulation, Neoplastic. Genes, erbB-1 / drug effects. Genes, erbB-2 / drug effects. Humans. Quinazolines / therapeutic use. Receptor, Epidermal Growth Factor / drug effects. Receptor, ErbB-3 / drug effects. Receptor, ErbB-4. Trastuzumab


18. Means-Markwell M, Linnoila RI, Williams J, Jänne PA, Kaye F, O'Neil K, Johnson BE: Prospective study of the airways and pulmonary parenchyma of patients at risk for a second lung cancer. Clin Cancer Res; 2003 Dec 1;9(16 Pt 1):5915-21
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prospective study of the airways and pulmonary parenchyma of patients at risk for a second lung cancer.
  • PURPOSE: We conducted our study to compare the number of preneoplastic lesions in the airways and nodules in the pulmonary parenchyma of patients with resected non-small cell lung cancer with the patients whose treatment included chest radiotherapy.
  • EXPERIMENTAL DESIGN: Patients were eligible if they had successfully resected stage I and II non-small cell lung cancer or advanced stage non-small cell or small cell lung cancer treated with chest radiotherapy with or without chemotherapy and were free of cancer for >2 years.
  • Patients underwent a history and physical examination, white light and fluorescence bronchoscopy, and computerized tomography of the chest.
  • The airway epithelium was examined for preneoplastic histological changes, and the pulmonary parenchyma was examined for the presence of nodules.
  • RESULTS: Twenty-nine patients at risk for lung cancer were studied between 1997 and 1999.
  • Two patients treated with chest radiotherapy had an area of moderate dysplasia (n=1) and carcinoma in situ (n=1), whereas one patient treated with surgical resection alone had an area of mild dysplasia.
  • Ten of the 13 patients treated with chest radiotherapy had pulmonary nodules compared with 5 of the 13 patients treated with surgical resection alone.
  • CONCLUSIONS: Mild dysplasia, moderate dysplasia, severe dysplasia, and carcinoma in situ are unusual in patients with resected lung cancer who have stopped smoking for an extended period of time.
  • Patients with lung cancer treated with chest irradiation may be at higher risk for preneoplastic lesions and pulmonary nodules than patients treated with surgical resection alone, but additional patients will need to be studied.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Small Cell / pathology. Lung Neoplasms / pathology. Neoplasms, Second Primary / pathology. Precancerous Conditions / pathology. Respiratory Mucosa / pathology

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 14676115.001).
  • [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
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


19. Martinez JM, Afshari CA, Bushel PR, Masuda A, Takahashi T, Walker NJ: Differential toxicogenomic responses to 2,3,7,8-tetrachlorodibenzo-p-dioxin in malignant and nonmalignant human airway epithelial cells. Toxicol Sci; 2002 Oct;69(2):409-23
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In humans, exposure to high levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with chronic obstructive pulmonary disease and lung cancer.
  • While several studies have shown that the lung is a target organ for TCDD toxicity, little is known on the specific biological pathways altered by TCDD.
  • Studies have shown that the transcriptional response of TCDD (in vivo and in vitro) is complex, and exhibits cell type and tissue specificity.
  • Thus, the purpose of this study was to look at global and concentration-dependent effects of TCDD on gene expression in human lung cells.
  • Gene expression profiling of both a nontumorigenic (HPL1A) and a malignant, tumorigenic lung cell line (A549) was performed by microarray dual fluorescence hybridizations in cells treated with increasing concentrations of TCDD (0, 0.1, 1, 10 nM) for 24 h.
  • Real time RT-PCR was used to verify alterations in specific genes.
  • Results showed that 68 out of 2091 genes were changed in each cell line, and 15 of those genes were found altered in both cell lines.
  • Common gene responses altered by TCDD were identified and included known xenobiotic metabolizing genes, genes known to alter cell cycle, as well as genes that are involved with cell signaling and that mediate cell motility or communication.
  • Cell line specific differences in gene expression were found that indicate the nonmalignant HPL1A cells are retinoic acid responsive.
  • These data show that TCDD alters multiple integrated networks of signaling pathways associated with pulmonary disease, particularly that of lung cancer.
  • [MeSH-major] Carcinogens / toxicity. Carcinoma / pathology. Epithelial Cells / drug effects. Gene Expression Regulation / drug effects. Gene Expression Regulation, Neoplastic / drug effects. Mutagens / toxicity. Tetrachlorodibenzodioxin / toxicity
  • [MeSH-minor] Algorithms. Cell Differentiation / drug effects. Cell Line. DNA, Complementary / metabolism. Fluorescent Dyes. Humans. Immune System / drug effects. In Situ Hybridization, Fluorescence. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Oligonucleotide Array Sequence Analysis. RNA / biosynthesis. RNA / isolation & purification. Receptors, Aryl Hydrocarbon / drug effects. Receptors, Aryl Hydrocarbon / genetics. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. Tumor Cells, Cultured

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12377990.001).
  • [ISSN] 1096-6080
  • [Journal-full-title] Toxicological sciences : an official journal of the Society of Toxicology
  • [ISO-abbreviation] Toxicol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / DNA, Complementary; 0 / Fluorescent Dyes; 0 / Mutagens; 0 / Receptors, Aryl Hydrocarbon; 63231-63-0 / RNA; DO80M48B6O / Tetrachlorodibenzodioxin
  •  go-up   go-down


20. Miyazu YM, Miyazawa T, Hiyama K, Kurimoto N, Iwamoto Y, Matsuura H, Kanoh K, Kohno N, Nishiyama M, Hiyama E: Telomerase expression in noncancerous bronchial epithelia is a possible marker of early development of lung cancer. Cancer Res; 2005 Nov 1;65(21):9623-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Telomerase expression in noncancerous bronchial epithelia is a possible marker of early development of lung cancer.
  • Centrally located lung cancers in smokers frequently associated with subsequent primary tumors.
  • We evaluated the telomerase expression chronologically in noncancerous epithelia as a risk factor of susceptibility to lung cancer development.
  • Telomerase protein expression was examined in situ by immunohistochemistry in 26 noncancerous bronchial epithelia adjacent to centrally located early-stage lung cancers in sequential 23 patients treated by photodynamic therapy or surgery among 206 patients who underwent autofluorescence bronchoscopy from 1997 to 2003.
  • Among the 15 lesions in 12 patients treated by photodynamic therapy alone, 11 lesions achieved complete remission after photodynamic therapy, and none of their noncancerous bronchial epithelia was telomerase positive.
  • On the contrary, in the remaining four lesions, either recurrence or secondary lung cancer developed adjacent to the successfully treated primary cancer within 26 months, and the telomerase protein expression in noncancerous epithelia was detected before the secondary cancer development (P < 0.001).
  • The overall relationship of human telomerase reverse transcriptase positivity in noncancerous epithelia and subsequent lung cancer development, including patients treated by radiation or surgery, showed higher significance (P < 0.0001).
  • Histologically "normal" bronchial epithelia in smokers may unphysiologically express telomerase as a field, and such epithelia are likely susceptible to develop lung cancer.
  • We propose that ectopic expression of telomerase in bronchial epithelia may precede transformation in human lung cancer development and that detection of telomerase protein in noncancerous bronchial epithelia will become a useful marker detecting high-risk patients for lung cancer development.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Bronchi / enzymology. Cell Transformation, Neoplastic / metabolism. Lung Neoplasms / enzymology. Telomerase / biosynthesis
  • [MeSH-minor] Carcinoma in Situ / drug therapy. Carcinoma in Situ / enzymology. Carcinoma in Situ / radiotherapy. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / enzymology. Carcinoma, Squamous Cell / radiotherapy. DNA-Binding Proteins / biosynthesis. Epithelial Cells / enzymology. Humans. Immunohistochemistry. Photochemotherapy

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16266979.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase
  •  go-up   go-down


21. Regalado JJ: Mixed micropapillary and trophoblastic carcinoma of bladder: report of a first case with new immunohistochemical evidence of urothelial origin. Hum Pathol; 2004 Mar;35(3):382-4
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mixed micropapillary and trophoblastic carcinoma of bladder: report of a first case with new immunohistochemical evidence of urothelial origin.
  • The micropapillary variant of urothelial carcinoma has a reported incidence of 0.7%.
  • Trophoblastic urinary carcinoma is very rare, with roughly 30 cases reported during the last century.
  • This is the first report of mixed micropapillary and trophoblastic bladder carcinoma.
  • His tumor contained choriocarcinomatoid areas with syncytiotrophoblasts, classic micropapillary carcinoma, conventional high-grade urothelial carcinoma, and flat carcinoma in situ.
  • He underwent radical surgery; tumor stage was T4N2M0.
  • Despite postoperative combination chemotherapy, he developed pulmonary and retroperitoneal metastases and died 20 months after presentation.
  • Because high-molecular-weight cytokeratin is expressed by urothelium but is rarely found in placental trophoblast or germ-cell choriocarcinoma, its presence in trophoblastic bladder carcinoma is new evidence that the latter is a transformed neoplasm of urothelial origin.
  • [MeSH-major] Carcinoma, Papillary / pathology. Carcinoma, Transitional Cell / pathology. Mixed Tumor, Malignant / pathology. Trophoblasts / pathology. Urinary Bladder Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chorionic Gonadotropin, beta Subunit, Human / analysis. Cisplatin / therapeutic use. Combined Modality Therapy. Doxorubicin / therapeutic use. Fatal Outcome. Humans. Lymph Nodes / pathology. Male. Methotrexate / therapeutic use. Middle Aged. Salvage Therapy. Urologic Surgical Procedures, Male. Urothelium / pathology. Vinblastine / therapeutic use

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. METHOTREXATE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15017598.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chorionic Gonadotropin, beta Subunit, Human; 5V9KLZ54CY / Vinblastine; 80168379AG / Doxorubicin; Q20Q21Q62J / Cisplatin; YL5FZ2Y5U1 / Methotrexate; M-VAC protocol
  •  go-up   go-down


22. Salajka F, Pokorny A, Vomela J, Pacík D, Krpensky A, Hrazdirovà A: Severe complications following intravesical BCG instillation. Monaldi Arch Chest Dis; 2002 Oct-Dec;57(5-6):321-4
MedlinePlus Health Information. consumer health - Pneumonia.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • In patients with urinary bladder carcinoma, the intravesical BCG instillation is widely used.
  • We present two cases of severe pulmonary afflictions developed during this treatment.
  • The possible mechanisms of etiology are discussed and the classification of the intravesical BCG treatment side effects is suggested.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12814051.001).
  • [ISSN] 1122-0643
  • [Journal-full-title] Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace
  • [ISO-abbreviation] Monaldi Arch Chest Dis
  • [Language] ENG
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / BCG Vaccine
  •  go-up   go-down


23. Piso RJ, Toniolo M: [Urothelial carcinoma--fever and weight loss after intravesical instillation of BCG]. Praxis (Bern 1994); 2008 Aug 13;97(16):901-4
MedlinePlus Health Information. consumer health - Weight Control.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Urothelial carcinoma--fever and weight loss after intravesical instillation of BCG].
  • We report the case of a patient, who suffered from an acute BCG-pneumonitis after the fourth treatment of his bladder cancer with intravesical instillation of BCG.
  • Under treatment with Rifampicine, Isoniazid and Ethambutol the patient recovered within a short time and the follow up chest-x-ray became normal.
  • A supplementary steroid therapy was not needed.
  • [MeSH-major] BCG Vaccine / adverse effects. Carcinoma in Situ / drug therapy. Carcinoma, Transitional Cell / drug therapy. Fever of Unknown Origin / etiology. Mycobacterium bovis. Neoplasm Recurrence, Local / drug therapy. Tuberculosis, Pulmonary / radiography. Urinary Bladder Neoplasms / drug therapy. Weight Loss
  • [MeSH-minor] Administration, Intravesical. Aged. Combined Modality Therapy. Humans. Male

  • MedlinePlus Health Information. consumer health - Bladder Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18777719.001).
  • [ISSN] 1661-8157
  • [Journal-full-title] Praxis
  • [ISO-abbreviation] Praxis (Bern 1994)
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / BCG Vaccine
  •  go-up   go-down


24. Noro R, Gemma A, Kosaihira S, Kokubo Y, Chen M, Seike M, Kataoka K, Matsuda K, Okano T, Minegishi Y, Yoshimura A, Kudoh S: Gefitinib (IRESSA) sensitive lung cancer cell lines show phosphorylation of Akt without ligand stimulation. BMC Cancer; 2006;6:277
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Gefitinib (IRESSA) sensitive lung cancer cell lines show phosphorylation of Akt without ligand stimulation.
  • BACKGROUND: Phase III trials evaluating the efficacy of gefitinib (IRESSA) in non-small cell lung cancer (NSCLC) lend support to the need for improved patient selection in terms of gefitinib use.
  • METHODS: To identify other key factors involved in gefitinib sensitivity, we analyzed the protein expression of molecules within the EGFR family, PI3K-Akt and Ras/MEK/Erk pathways and examined the sensitivity to gefitinib using the MTT cell proliferation assay in 23 lung cancer cell lines.
  • RESULTS: We identified one highly sensitive cell line (PC9), eight cell lines displaying intermediate-sensitivity, and 14 resistant cell lines.
  • Eight out of the nine cell lines showing sensitivity had Akt phosphorylation without ligand stimulation, while only three out of the 14 resistant lines displayed this characteristic (P = 0.0059).
  • Akt phosphorylation was partially inhibited by gefitinib in all sensitive cell lines.
  • In addition, expression analyses of the EGFR family, EGFR gene mutation, and FISH (fluorescence in situ hybridization) analyses showed that the phosphorylated state of EGFR and Akt might be a useful clinical marker of Akt activation without ligand stimulation, in addition to EGFR gene mutation and amplification, particularly in adenocarcinomas.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Proto-Oncogene Proteins c-akt / metabolism. Quinazolines / pharmacology
  • [MeSH-minor] Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Proliferation / drug effects. DNA Mutational Analysis. Drug Resistance, Neoplasm. Enzyme Activation. Gene Expression Regulation, Neoplastic. Genes, ras. Humans. In Situ Hybridization, Fluorescence. Ligands. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3 / metabolism. PTEN Phosphohydrolase / metabolism. Phosphorylation. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Receptor, ErbB-2 / metabolism. Receptor, ErbB-3 / metabolism. p38 Mitogen-Activated Protein Kinases / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4885-92 [11156248.001]
  • [Cites] J Natl Cancer Inst. 2004 Aug 4;96(15):1133-41 [15292385.001]
  • [Cites] J Clin Oncol. 2002 May 1;20(9):2240-50 [11980995.001]
  • [Cites] Cancer Res. 2002 Oct 15;62(20):5749-54 [12384534.001]
  • [Cites] N Engl J Med. 2004 May 20;350(21):2129-39 [15118073.001]
  • [Cites] Science. 2004 Jun 4;304(5676):1497-500 [15118125.001]
  • [Cites] Oncol Rep. 2004 Nov;12(5):1053-7 [15492792.001]
  • [Cites] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682.001]
  • [Cites] Cancer Res. 1993 May 15;53(10 Suppl):2379-85 [7683573.001]
  • [Cites] Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182.001]
  • [Cites] Int J Cancer. 1996 Nov 27;68(5):605-11 [8938142.001]
  • [Cites] Oncogene. 1998 Feb 19;16(7):951-6 [9484787.001]
  • [Cites] J Biol Chem. 1999 Mar 26;274(13):8865-74 [10085130.001]
  • [Cites] Lung Cancer. 1999 Aug;25(2):87-93 [10470842.001]
  • [Cites] Cancer Res. 2005 Jan 1;65(1):226-35 [15665299.001]
  • [Cites] Lung Cancer. 2005 Apr;48(1):141-4 [15777982.001]
  • [Cites] J Clin Oncol. 2005 Apr 10;23(11):2493-501 [15710947.001]
  • [Cites] Br J Cancer. 2005 May 9;92(9):1711-9 [15870831.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):6838-45 [15998906.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):944-50 [16424029.001]
  • [Cites] Clin Cancer Res. 2006 Apr 15;12(8):2538-44 [16638863.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2751-8 [11289158.001]
  • (PMID = 17150102.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Ligands; 0 / Quinazolines; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.10.1 / Receptor, ErbB-3; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; S65743JHBS / gefitinib
  • [Other-IDs] NLM/ PMC1698934
  •  go-up   go-down


25. Shan G, Zhong H, Zhang F: [Expression and prognostic significance of multidrug resistance associated protein (MRP) gene in non-small cell lung cancer by in situ hybridization]. Zhonghua Zhong Liu Za Zhi; 2000 Jan;22(1):27-9
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Expression and prognostic significance of multidrug resistance associated protein (MRP) gene in non-small cell lung cancer by in situ hybridization].
  • OBJECTIVE: To study the effect of MRP gene overexpression on prognosis of patients with non-small cell lung cancer (NSCLC).
  • METHODS: Paraffin-embedded tissues from 47 cases of NSCLC who had undergone radical tumor resection were examined for expression of MRP gene mRNA by in situ hybridization using labelled digoxigenin probes combined with immunohistochemistry.
  • RESULTS: All of the 47 lung cancer specimens were found to have overexpression of MRP mRNA.
  • It was significantly correlated with patients' survival period, response to chemotherapy, recurrence and mestastases after surgery, but was not correlated with histology, tumor size, node status, TNM stage, degree of differentiation, age and sex.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma, Non-Small-Cell Lung / genetics. Gene Expression Regulation. Lung Neoplasms / genetics. Multidrug Resistance-Associated Proteins / genetics
  • [MeSH-minor] Adult. Aged. Female. Humans. In Situ Hybridization. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Survival Rate. Up-Regulation

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11776590.001).
  • [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] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Multidrug Resistance-Associated Proteins
  •  go-up   go-down


26. Suzukawa M, Nakazora T, Kawasaki Y, Tominaga T, Shinohara K: Massive ascites associated with all-trans retinoic acid treatment in therapy-related acute promyelocytic leukemia. Intern Med; 2010;49(5):457-60
Hazardous Substances Data Bank. EPIRUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Massive ascites associated with all-trans retinoic acid treatment in therapy-related acute promyelocytic leukemia.
  • A 77-year-old man who developed pancytopenia was administered granulocyte colony-stimulating factor (G-CSF) by another doctor, and referred to us for the evaluation of pancytopenia.
  • He had hepatocellular carcinoma and was treated with transcatheter arterial chemoembolization (TACE) containg epirubicin (total dose: 300 mg over the last two years).
  • Cytogenetic analysis demonstrated del(7), t(15;17)(q22;q12), and a fluorescence in-situ hybridization (FISH) study demonstrated chimeric fusion genes of PML-RAR-alpha.
  • He was diagnosed with therapy-related acute promyelocytic leukemia (APL), and treated with all trans-retinoic acid (ATRA).
  • He showed the progressive accumulation of ascites with liver damage, without pulmonary symptoms of ATRA differentiation syndrome.
  • After 60 days of ATRA treatment, complete hematological and cytogenetic responses were achieved.
  • [MeSH-major] Ascites / chemically induced. Ascites / diagnosis. Chemoembolization, Therapeutic / adverse effects. Leukemia, Promyelocytic, Acute / drug therapy. Leukemia, Promyelocytic, Acute / etiology. Tretinoin / adverse effects. Tretinoin / therapeutic use
  • [MeSH-minor] Aged. Antibiotics, Antineoplastic / administration & dosage. Antineoplastic Agents / adverse effects. Antineoplastic Agents / therapeutic use. Carcinoma, Hepatocellular / therapy. Epirubicin / administration & dosage. Humans. Liver Neoplasms / therapy. Male

  • Genetic Alliance. consumer health - Acute Promyelocytic Leukemia.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20190483.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents; 3Z8479ZZ5X / Epirubicin; 5688UTC01R / Tretinoin
  •  go-up   go-down


27. Quirino R, Ornellas AA, Wisnescky A: [Treatment of patients with recurrent superficial bladder cancer with lyophilized Moureau-Rio de Janeiro BCG strain. Brazillian National Cancer Institute experience]. Prog Urol; 2005 Sep;15(4):667-73
MedlinePlus Health Information. consumer health - Bladder Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Treatment of patients with recurrent superficial bladder cancer with lyophilized Moureau-Rio de Janeiro BCG strain. Brazillian National Cancer Institute experience].
  • [Transliterated title] Traitement des patients présentant une tumeur superficielle de vessie par la souche de BCG Moureau-Rio de Janeiro. Expérience de l'Institut National Brésilien du Cancer.
  • PURPOSE: We present our experience with lyophilized Moureau-Rio de Janeiro BCG strain for treatment of patients with recurrent superficial bladder cancer.
  • The treatment included 6 inductions and 10 maintenance cycles of BCG instillations.
  • The patients received an initial dose with 40 mg and subsequent doses with 80 mg of lyophilized Moureau-Rio de Janeiro BCG strain.
  • RESULTS: Overall recurrence and progression rates after treatment were 45.6% and 13%, respectively.
  • Three of them had to be treated with antituberculous therapy.
  • These patients presented pulmonary disease, granulomatous prostatitis and epididymo-orchitis respectively.
  • CONCLUSIONS: Moureau-Rio de Janeiro BCG strain was overall well tolerated in intravesical instillations, similar to other strains used in literature.
  • Recurrence rates were decreased with adjuvant BCG therapy.
  • Tumor size, grade and presence of associated carcinoma in situ provided predictive information regarding the behavior of recurrent superficial tumors.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. BCG Vaccine / therapeutic use. Carcinoma, Transitional Cell / drug therapy. Neoplasm Recurrence, Local / drug therapy. Urinary Bladder Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Bladder cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16459683.001).
  • [ISSN] 1166-7087
  • [Journal-full-title] Progrès en urologie : journal de l'Association française d'urologie et de la Société française d'urologie
  • [ISO-abbreviation] Prog. Urol.
  • [Language] fre
  • [Publication-type] Clinical Trial; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / BCG Vaccine
  •  go-up   go-down






Advertisement