[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 26 of about 26
1. Yuca K, Cankaya H, Bayram I, Ozbek H, Kiris M: Local irritant effects of topical oral sprays on oral mucosa in mice. Adv Ther; 2006 Jan-Feb;23(1):98-106
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] Local irritant effects of topical oral sprays on oral mucosa in mice.
  • Topical oral sprays are frequently used to prevent and manage oropharyngeal inflammation and lesions.
  • This study investigated the histopathologic changes noted in the oral mucosa of mice after topical application of 3 widely prescribed antibacterial products.
  • The 25 animals were divided into 5 groups and treated for 10 days with 2 sprays daily, as follows: group 1-chlorhexidine gluconate 0.12% + benzydamine hydrochloride 0.15%; group 2-benzydamine 0.27 mg/0.18 mL x 30 mL; group 3-chlorhexidine 0.2%; group 4-fusafungine 1%; and group 5 (cohort)-physiologic serum.
  • On day 10 after drug administration, biopsy specimens were taken from the oropharyngeal mucosa of the tongue, the cheek mucosa, and the tongue base; these were examined under a light microscope and were classified as normal or pathologic.
  • All topical oral sprays produced some degree of histopathologic change, such as hyperplasia, fibrosis, low-grade dysplasia, congestion, or edema.
  • The local irritant effects of topical oral sprays should be considered when treatment is selected for patients with oropharyngeal disorder.
  • [MeSH-major] Anti-Infective Agents, Local / adverse effects. Mouth Mucosa / drug effects
  • [MeSH-minor] Administration, Oral. Administration, Topical. Aerosols. Animals. Edema / chemically induced. Fibrosis. Hyperplasia. Male. Mice

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16644611.001).
  • [ISSN] 0741-238X
  • [Journal-full-title] Advances in therapy
  • [ISO-abbreviation] Adv Ther
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Aerosols; 0 / Anti-Infective Agents, Local
  •  go-up   go-down


2. Boyle JO, Gümüs ZH, Kacker A, Choksi VL, Bocker JM, Zhou XK, Yantiss RK, Hughes DB, Du B, Judson BL, Subbaramaiah K, Dannenberg AJ: Effects of cigarette smoke on the human oral mucosal transcriptome. Cancer Prev Res (Phila); 2010 Mar;3(3):266-78
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] Effects of cigarette smoke on the human oral mucosal transcriptome.
  • Use of tobacco is responsible for approximately 30% of all cancer-related deaths in the United States, including cancers of the upper aerodigestive tract.
  • In the current study, 40 current and 40 age- and gender-matched never smokers underwent buccal biopsies to evaluate the effects of smoking on the transcriptome.
  • Smoking altered the expression of numerous genes: 32 genes showed increased expression and 9 genes showed reduced expression in the oral mucosa of smokers versus never smokers.
  • Increased numbers of Langerhans cells were found in the oral mucosa of smokers.
  • Interestingly, smoking caused greater induction of aldo-keto reductases, enzymes linked to polycyclic aromatic hydrocarbon-induced genotoxicity, in the oral mucosa of women than men.
  • Striking similarities in expression changes were found in oral compared with the bronchial mucosa.
  • Collectively, these results provide new insights into the carcinogenic effects of tobacco smoke, support the potential use of oral epithelium as a surrogate tissue in future lung cancer chemoprevention trials, and illustrate the potential of computational biology to identify chemopreventive agents.

  • MedlinePlus Health Information. consumer health - Smoking.
  • 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
  • [Cites] Cancer Cell. 2003 Dec;4(6):431-6 [14706335.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):733-44 [14570033.001]
  • [Cites] Lung Cancer. 2004 Jun;44(3):287-93 [15140541.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10143-8 [15210990.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 2004;83:1-1438 [15285078.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5131-6 [15297416.001]
  • [Cites] Br J Dermatol. 1991 Jan;124(1):29-36 [1899617.001]
  • [Cites] J Oral Pathol Med. 1991 Feb;20(2):49-52 [2016696.001]
  • [Cites] Eur J Immunol. 1992 Sep;22(9):2469-72 [1325349.001]
  • [Cites] N Engl J Med. 1993 Jan 21;328(3):159-63 [8417381.001]
  • [Cites] Am J Epidemiol. 1993 Sep 1;138(5):281-93 [8395141.001]
  • [Cites] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329.001]
  • [Cites] Cancer Metastasis Rev. 1996 Mar;15(1):27-51 [8842478.001]
  • [Cites] J Clin Invest. 1997 Oct 15;100(8):2133-7 [9329980.001]
  • [Cites] Biochem Pharmacol. 1998 Feb 15;55(4):413-21 [9514075.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):2025-34 [10473082.001]
  • [Cites] J Biol Chem. 1951 Nov;193(1):265-75 [14907713.001]
  • [Cites] J Biol Chem. 1957 Oct;228(2):753-66 [13475357.001]
  • [Cites] N Engl J Med. 2005 Jul 14;353(2):123-32 [16014882.001]
  • [Cites] J Natl Cancer Inst. 2005 Sep 21;97(18):1319-21 [16174848.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2005 Oct;14(10):2287-93 [16214906.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] N Engl J Med. 2006 Jan 19;354(3):270-82 [16421368.001]
  • [Cites] J Natl Cancer Inst. 2006 Apr 5;98(7):441-50 [16595780.001]
  • [Cites] Clin Cancer Res. 2006 Apr 1;12(7 Pt 1):2166-71 [16609030.001]
  • [Cites] Mol Pharmacol. 2006 May;69(5):1662-72 [16478829.001]
  • [Cites] JAMA. 2006 Jul 12;296(2):180-4 [16835423.001]
  • [Cites] JAMA. 2006 Jul 12;296(2):218-9 [16835429.001]
  • [Cites] Science. 2006 Sep 29;313(5795):1929-35 [17008526.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2006 Nov;132(11):1231-6 [17116820.001]
  • [Cites] Nat Med. 2007 Mar;13(3):361-6 [17334370.001]
  • [Cites] BJU Int. 2007 Mar;99(3):564-9 [17166241.001]
  • [Cites] Arch Biochem Biophys. 2007 Aug 15;464(2):241-50 [17537398.001]
  • [Cites] Eur J Pharm Sci. 2008 Apr 23;33(4-5):380-9 [18328680.001]
  • [Cites] Nat Genet. 2008 May;40(5):616-22 [18385676.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 13;105(19):6846-51 [18474869.001]
  • [Cites] Toxicol Appl Pharmacol. 2008 Jul 15;230(2):252-60 [18433817.001]
  • [Cites] BMC Genomics. 2008;9:259 [18513428.001]
  • [Cites] Arch Toxicol. 2008 Sep;82(9):573-82 [18677463.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Jul;1(2):100-11 [19138943.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Nov;1(6):485-93 [19138996.001]
  • [Cites] J Biol Chem. 2009 Mar 20;284(12):7436-45 [19158084.001]
  • [Cites] Immunology. 2009 Jul;127(3):299-311 [19538249.001]
  • [Cites] Bioinformatics. 2004 Feb 12;20(3):323-31 [14960458.001]
  • [Cites] Chem Biol Interact. 2001 Jan 30;130-132(1-3):247-60 [11306049.001]
  • [Cites] Oncogene. 2002 Oct 21;21(48):7298-306 [12379874.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 15;31(4):e15 [12582260.001]
  • [Cites] Biochemistry. 2003 Feb 18;42(6):1410-20 [12578353.001]
  • [Cites] J Clin Invest. 2003 Jan;111(1):81-90 [12511591.001]
  • [Cites] Genome Biol. 2003;4(10):R70 [14519205.001]
  • [CommentIn] Cancer Prev Res (Phila). 2010 Mar;3(3):255-8 [20179303.001]
  • (PMID = 20179299.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA009685-08; United States / NCI NIH HHS / CA / T32 CA09685; United States / NCRR NIH HHS / RR / UL1 RR024996; United States / NCRR NIH HHS / RR / UL1 RR024996-01; United States / NCI NIH HHS / CA / P01 CA106451; United States / NCI NIH HHS / CA / R25 CA105012-04; United States / NCI NIH HHS / CA / R25 CA105012; United States / NCI NIH HHS / CA / T32 CA009685; United States / NCRR NIH HHS / RR / UL1-RR024996; United States / NCI NIH HHS / CA / T32 CA009685-08; United States / NCI NIH HHS / CA / CA106451-02; United States / NCI NIH HHS / CA / P01 CA106451-02
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / RNA, Messenger
  • [Other-IDs] NLM/ NIHMS154868; NLM/ PMC2833216
  •  go-up   go-down


3. Shabany K, Chiu PC, Raghian A, Chang KW, Solt DB: Rapid in vivo assay for topical oral cancer chemopreventive agents. Int J Oncol; 2002 Jul;21(1):159-64
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] Rapid in vivo assay for topical oral cancer chemopreventive agents.
  • The cancer chemopreventive effect of topically applied phenethyl isothiocyanate (PEIT) was examined in a hamster buccal pouch model, in which squamous cell carcinomas (SCC) are induced at high frequency, by topical application of N-methyl-N-benzylnitrosamine (MBN).
  • The buccal pouches of eleven hamsters were pretreated thrice-weekly for two weeks with corn oil (CO) containing 50 mM PEIT, followed by 22 weeks of twice-weekly application of CO containing MBN and PEIT, both at 50 mM.
  • Tumor analysis was performed 19 days after the last application of PEIT and MBN.
  • Although total tumor incidence was marginally decreased, PEIT inhibited significantly the tumor frequency and tumor burden by 79% and 74%, respectively.
  • Buccal pouches of four protected hamsters received 50 mM PEIT pretreatment on days 1 and 4, followed on days 6 and 9 by application of CO containing MBN and PEIT, both at 50 mM.
  • Four unprotected hamsters were similarly pretreated with CO, followed by MBN in CO. gamma-GT foci were enumerated in buccal pouch epithelial whole mounts prepared from pairs of protected and unprotected hamsters on days 10 through 13.
  • This model may be useful for rapid identification of chemopreventive agents, and combinations of agents, which inhibit initiation and promotion stages of oral carcinogenesis.
  • [MeSH-minor] Administration, Oral. Aldehyde Dehydrogenase / antagonists & inhibitors. Animals. Biological Assay / methods. Carcinogens / toxicity. Corn Oil. Cricetinae. Genes, p53 / drug effects. Genes, p53 / genetics. Male. Mesocricetus. Mouth Mucosa / drug effects. Mouth Mucosa / metabolism. gamma-Glutamyltransferase / metabolism

  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. N-NITROSODIMETHYLAMINE .
  • Hazardous Substances Data Bank. Corn oil .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12063563.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R03 CA89788-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Isothiocyanates; 6U7TFK75KV / phenethyl isothiocyanate; 8001-30-7 / Corn Oil; 937-40-6 / nitrosobenzylmethylamine; EC 1.2.1.3 / Aldehyde Dehydrogenase; EC 2.3.2.2 / gamma-Glutamyltransferase; M43H21IO8R / Dimethylnitrosamine
  •  go-up   go-down


Advertisement
4. Bessette EE, Goodenough AK, Langouët S, Yasa I, Kozekov ID, Spivack SD, Turesky RJ: Screening for DNA adducts by data-dependent constant neutral loss-triple stage mass spectrometry with a linear quadrupole ion trap mass spectrometer. Anal Chem; 2009 Jan 15;81(2):809-19
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 loss of the deoxyribose (dR) from the protonated DNA adducts ([M + H - 116]+) in the MS/MS scan mode triggered the acquisition of MS3 product ion spectra of the aglycone adducts [BH2]+.
  • Buccal cell DNA from tobacco smokers was screened for DNA adducts of various classes of carcinogens in tobacco smoke including 4-ABP, 2-amino-9H-pyrido[2,3-b]indole (AalphaC), and benzo[a]pyrene (BaP); the cooked-meat carcinogens MeIQx, AalphaC, and 2-amino-1-methyl-6-phenylmidazo[4,5-b]pyridine (PhIP); and the lipid peroxidation products acrolein (AC) and trans-4-hydroxynonenal (HNE).

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 2-Amino-3,8-dimethylimidazo[4,5-f]quinoxaline .
  • Hazardous Substances Data Bank. 4-BIPHENYLAMINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Methods. 2007 Oct;4(10):798-806 [17901869.001]
  • [Cites] J Am Soc Mass Spectrom. 2007 Dec;18(12):2107-18 [17936011.001]
  • [Cites] Angew Chem Int Ed Engl. 2008;47(2):381-4 [18022988.001]
  • [Cites] Chem Res Toxicol. 2008 Jan;21(1):129-37 [18052111.001]
  • [Cites] Acc Chem Res. 2008 Jul;41(7):793-804 [18500830.001]
  • [Cites] Chem Res Toxicol. 2008 Jul;21(7):1477-83 [18549250.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):353-9 [10688855.001]
  • [Cites] Chem Res Toxicol. 2000 May;13(5):421-9 [10813660.001]
  • [Cites] Mol Med Today. 2000 Jul;6(7):271-6 [10859563.001]
  • [Cites] Carcinogenesis. 2001 Mar;22(3):481-8 [11238190.001]
  • [Cites] Org Lett. 2001 Nov 1;3(22):3603-5 [11678719.001]
  • [Cites] Carcinogenesis. 2002 Jan;23(1):115-22 [11756232.001]
  • [Cites] Anal Chem. 2001 Dec 1;73(23):5635-44 [11774901.001]
  • [Cites] Chem Biol Interact. 2002 Feb 20;139(2):199-213 [11823007.001]
  • [Cites] Chem Res Toxicol. 2002 Apr;15(4):551-61 [11952342.001]
  • [Cites] Chem Res Toxicol. 2002 May;15(5):607-13 [12018980.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Oct 5;778(1-2):323-43 [12376138.001]
  • [Cites] Chem Res Toxicol. 2002 Oct;15(10):1295-301 [12387628.001]
  • [Cites] J Chromatogr A. 2002 Oct 18;974(1-2):91-101 [12458929.001]
  • [Cites] Chem Res Toxicol. 2003 Oct;16(10):1251-63 [14565767.001]
  • [Cites] Nat Rev Cancer. 2003 Oct;3(10):733-44 [14570033.001]
  • [Cites] J Am Soc Mass Spectrom. 2003 Dec;14(12):1488-92 [14652195.001]
  • [Cites] Anal Chem. 2004 Feb 1;76(3):823-32 [14750881.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2004 Mar 25;802(1):155-66 [15036007.001]
  • [Cites] Cancer Sci. 2004 Apr;95(4):290-9 [15072585.001]
  • [Cites] Carcinogenesis. 2004 Aug;25(8):1525-33 [15059926.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6805-13 [15375000.001]
  • [Cites] Cancer Res. 1978 Jun;38(6):1479-96 [348302.001]
  • [Cites] Cancer Lett. 1980 Aug;10(2):141-9 [7006799.001]
  • [Cites] Cancer Lett. 1981 Mar;12(1-2):105-10 [7272995.001]
  • [Cites] Environ Health Perspect. 1985 Oct;62:19-30 [4085422.001]
  • [Cites] Carcinogenesis. 1989 Aug;10(8):1429-34 [2502322.001]
  • [Cites] Anal Chem. 1989 Sep 15;61(18):1023A-1024A, 1026A-1029A, 1031A-103 [2802152.001]
  • [Cites] Carcinogenesis. 1991 Oct;12(10):1945-7 [1934275.001]
  • [Cites] Carcinogenesis. 1992 Jul;13(7):1053-74 [1638670.001]
  • [Cites] Chem Res Toxicol. 1992 Jul-Aug;5(4):479-90 [1391614.001]
  • [Cites] Chem Res Toxicol. 1992 Sep-Oct;5(5):691-7 [1446011.001]
  • [Cites] Chem Res Toxicol. 1992 Nov-Dec;5(6):749-55 [1489923.001]
  • [Cites] Free Radic Res Commun. 1986;1(3):163-72 [2577733.001]
  • [Cites] Carcinogenesis. 1993 Nov;14(11):2383-8 [8242870.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1995 Mar;4(2):133-8 [7537994.001]
  • [Cites] Toxicol Lett. 1995 Dec;82-83:751-6 [8597138.001]
  • [Cites] Anticancer Res. 1997 Jul-Aug;17(4A):2827-30 [9252724.001]
  • [Cites] Cancer Res. 1998 Feb 15;58(4):581-4 [9485001.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 1998 Aug;7(8):719-24 [9718225.001]
  • [Cites] Chem Res Toxicol. 1999 Jan;12(1):68-77 [9894020.001]
  • [Cites] Toxicol Lett. 1998 Dec 28;102-103:435-9 [10022292.001]
  • [Cites] Mutat Res. 1999 Mar 8;424(1-2):71-81 [10064851.001]
  • [Cites] Chem Res Toxicol. 2005 Apr;18(4):692-9 [15833029.001]
  • [Cites] Chem Res Toxicol. 2005 Aug;18(8):1306-15 [16097804.001]
  • [Cites] Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):293-301 [15990134.001]
  • [Cites] Anal Chem. 2005 Sep 15;77(18):5982-9 [16159131.001]
  • [Cites] Rapid Commun Mass Spectrom. 2005;19(23):3482-92 [16261644.001]
  • [Cites] Carcinogenesis. 2006 Feb;27(2):178-96 [16272169.001]
  • [Cites] Proteomics. 2006 Mar;6(6):1735-40 [16475232.001]
  • [Cites] Rapid Commun Mass Spectrom. 2006;20(8):1369-80 [16557497.001]
  • [Cites] Chem Res Toxicol. 2006 May;19(5):674-82 [16696570.001]
  • [Cites] Chem Res Toxicol. 2006 May;19(5):710-8 [16696574.001]
  • [Cites] Antioxid Redox Signal. 2006 May-Jun;8(5-6):993-1001 [16771689.001]
  • [Cites] Biochim Biophys Acta. 2006 Dec;1764(12):1811-22 [17118725.001]
  • [Cites] Chem Res Toxicol. 2007 Feb;20(2):263-76 [17305409.001]
  • [Cites] Chem Res Toxicol. 2007 Mar;20(3):520-30 [17316027.001]
  • [Cites] Chem Res Toxicol. 2007 Apr;20(4):565-71 [17385896.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 17;104(29):12129-34 [17620607.001]
  • (PMID = 19086795.001).
  • [ISSN] 1520-6882
  • [Journal-full-title] Analytical chemistry
  • [ISO-abbreviation] Anal. Chem.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / P01 ES005355-18; United States / NIEHS NIH HHS / ES / R21 ES014438-02; United States / NIEHS NIH HHS / ES / R21 ES014438; United States / NIEHS NIH HHS / ES / R21ES-014438; United States / NIEHS NIH HHS / ES / P01ES-05355; United States / NCI NIH HHS / CA / R01 CA122320-02; United States / NIEHS NIH HHS / ES / ES014438-02; United States / NIEHS NIH HHS / ES / P01 ES005355; United States / NCI NIH HHS / CA / R01 CA122320; United States / NCI NIH HHS / CA / R01CA-122320; United States / NCI NIH HHS / CA / CA122320-02; United States / NIEHS NIH HHS / ES / ES005355-18
  • [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 / Aminobiphenyl Compounds; 0 / Carcinogens; 0 / DNA Adducts; 0 / Quinoxalines; 16054949HJ / 4-biphenylamine; 77500-04-0 / 2-amino-3,8-dimethylimidazo(4,5-f)quinoxaline
  • [Other-IDs] NLM/ NIHMS86732; NLM/ PMC2646368
  •  go-up   go-down


5. Armstrong WB, Kennedy AR, Wan XS, Atiba J, McLaren CE, Meyskens FL Jr: Single-dose administration of Bowman-Birk inhibitor concentrate in patients with oral leukoplakia. Cancer Epidemiol Biomarkers Prev; 2000 Jan;9(1):43-7
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] Single-dose administration of Bowman-Birk inhibitor concentrate in patients with oral leukoplakia.
  • The Bowman-Birk inhibitor (BBI) is a soybean-derived serine protease inhibitor and a potential cancer chemopreventive agent for humans.
  • In this Phase I clinical trial, BBI concentrate was administered as a single oral dose to 24 subjects with oral leukoplakia.
  • BBI was taken up rapidly, and a metabolic product of BBI was excreted in the urine within 24-48 h.
  • Protease activity was also measured in buccal cells to evaluate usefulness as a biomarker.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Leukoplakia, Oral / drug therapy. Trypsin Inhibitor, Bowman-Birk Soybean / therapeutic use. Trypsin Inhibitors / therapeutic use
  • [MeSH-minor] Administration, Oral. Aged. Biomarkers / analysis. Chemoprevention. Chymotrypsin / antagonists & inhibitors. Endopeptidases / analysis. Female. Follow-Up Studies. Humans. Male. Middle Aged. Mouth Mucosa / enzymology

  • Genetic Alliance. consumer health - Leukoplakia.
  • Genetic Alliance. consumer health - Oral leukoplakia.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CHYMOTRYPSIN .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10667462.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA46496; United States / NCI NIH HHS / CA / P30CA 62203
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Biomarkers; 0 / Trypsin Inhibitor, Bowman-Birk Soybean; 0 / Trypsin Inhibitors; EC 3.4.- / Endopeptidases; EC 3.4.21.1 / Chymotrypsin
  •  go-up   go-down


6. Borrie F, Musthyala R, Macintyre D: Ectopic geographic tongue--a case report. Dent Update; 2007 Mar;34(2):121-2
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 report describes a case of 'ectopic' geographic tongue where lesions, clinically and histologically similar to those normally confined to the tongue, presented on the floor of the mouth and cheek mucosa.
  • The patient, a type II diabetic, had a history of thrombocytopaenia and, more recently, autoimmune haemolytic anaemia.
  • CLINICAL RELEVANCE: Geographic tongue is a common oral medicine condition and the purpose of this paper is to highlight the fact that it can present ectopically on the oral mucosa.
  • [MeSH-minor] Diagnosis, Differential. Female. Humans. Middle Aged. Mouth Mucosa / pathology

  • Genetic Alliance. consumer health - Geographic Tongue.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17432777.001).
  • [ISSN] 0305-5000
  • [Journal-full-title] Dental update
  • [ISO-abbreviation] Dent Update
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] England
  •  go-up   go-down


7. Squier CA, Mantz MJ, Wertz PW: Effect of menthol on the penetration of tobacco carcinogens and nicotine across porcine oral mucosa ex vivo. Nicotine Tob Res; 2010 Jul;12(7):763-7
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] Effect of menthol on the penetration of tobacco carcinogens and nicotine across porcine oral mucosa ex vivo.
  • As oral mucosa is exposed to both smoke and smokeless tobacco in tobacco users, the objective of this study was to determine whether menthol influenced the penetration of the TC nitrosonornicotine (NNN) across porcine buccal (BM) and floor of mouth (FM) mucosa.
  • METHODS: Porcine BM and FM were collected at slaughter, mounted in perfusion chambers (n = 7/group), and exposed to tritiated NNN ((3)H-NNN; Amersham, activity 1 muCi/ml) and tritiated nicotine ((3)H-nicotine; Sigma) in 3% nicotine/phosphate-buffered saline (0.01 M, pH 7.4) containing 0.01% unlabeled NNN (National Cancer Institute Chemical Carcinogen Repository) +/- 0.08% menthol for 0.5, 1, 2, or 12 hr.
  • Oral mucosal permeability and stability of transforming growth factor beta-3 in vitro.
  • Pharmaceutical Research, 16, 1557-1563.
  • Practical implications are for a potentially increased oral exposure to carcinogens among users of menthol-flavored cigarettes and chewing tobacco.
  • [MeSH-major] Carcinogens / pharmacology. Central Nervous System Depressants / pharmacology. Menthol / pharmacology. Mouth Mucosa / metabolism. Nitrosamines / pharmacology. Tobacco / chemistry
  • [MeSH-minor] Animals. Cell Membrane Permeability / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Swine

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 4-(N-Nitrosomethylamino)-1-(3-pyridyl)-1-butanone .
  • Hazardous Substances Data Bank. MENTHOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20511349.001).
  • [ISSN] 1469-994X
  • [Journal-full-title] Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco
  • [ISO-abbreviation] Nicotine Tob. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Central Nervous System Depressants; 0 / Nitrosamines; 1490-04-6 / Menthol; 64091-91-4 / 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone
  •  go-up   go-down


8. Kupfer DM, White VL, Jenkins MC, Burian D: Examining smoking-induced differential gene expression changes in buccal mucosa. BMC Med Genomics; 2010;3:24
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] Examining smoking-induced differential gene expression changes in buccal mucosa.
  • BACKGROUND: Gene expression changes resulting from conditions such as disease, environmental stimuli, and drug use, can be monitored in the blood.
  • Buccal mucosa cells are easily collected and may be an alternative sample material for biomarker testing.
  • A limited number of studies, primarily in the smoker/oral cancer literature, address this tissue's efficacy as an RNA source for expression analysis.
  • The current study was undertaken to determine if total RNA isolated from buccal mucosa could be used as an alternative tissue source to assay relative gene expression.
  • The amplified cDNA was used in RT-qPCR and microarray analyses to evaluate gene expression in buccal cells.
  • Initially, RT-qPCR was used to assess relative transcript levels of four genes from whole blood and buccal cells collected from the same seven individuals, concurrently.
  • Second, buccal cell RNA was used for microarray-based differential gene expression studies by comparing gene expression between a group of female smokers and nonsmokers.
  • RESULTS: An amplification protocol allowed use of less buccal cell total RNA (50 ng) than had been reported previously with human microarrays.
  • Total RNA isolated from buccal cells was degraded but was of sufficient quality to be used with RT-qPCR to detect expression of specific genes.
  • We report here the finding of a small number of statistically significant differentially expressed genes between smokers and nonsmokers, using buccal cells as starting material.
  • CONCLUSIONS: Our results suggest that despite a high degree of degradation, RNA from buccal cells from cheek mucosa could be used to detect differential gene expression between smokers and nonsmokers.
  • However the RNA degradation, increase in sample variability and microarray failure rate show that buccal samples should be used with caution as source material in expression studies.
  • [MeSH-major] Gene Expression Profiling. Mouth Mucosa / metabolism. Smoking

  • MedlinePlus Health Information. consumer health - Smoking.
  • SciCrunch. ArrayExpress: Data: Microarray .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Carcinogenesis. 2001 Mar;22(3):481-8 [11238190.001]
  • [Cites] Genome Biol. 2009;10(11):R130 [19919682.001]
  • [Cites] Biotechniques. 2003 Feb;34(2):374-8 [12613259.001]
  • [Cites] Biostatistics. 2003 Apr;4(2):249-64 [12925520.001]
  • [Cites] OMICS. 2003 Fall;7(3):235-52 [14583114.001]
  • [Cites] Biotechniques. 2004 Mar;36(3):484-7 [15038164.001]
  • [Cites] FEBS Lett. 2004 Aug 27;573(1-3):83-92 [15327980.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6805-13 [15375000.001]
  • [Cites] Acta Paediatr Scand. 1985 Jan;74(1):102-6 [3984714.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D573-9 [15608264.001]
  • [Cites] Clin Chem Lab Med. 2005;43(2):157-62 [15843209.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] Methods Enzymol. 2006;411:134-93 [16939790.001]
  • [Cites] Genome Biol. 2007;8(2):R19 [17291332.001]
  • [Cites] BMC Genomics. 2008;9:259 [18513428.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • (PMID = 20576139.001).
  • [ISSN] 1755-8794
  • [Journal-full-title] BMC medical genomics
  • [ISO-abbreviation] BMC Med Genomics
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 63231-63-0 / RNA
  • [Other-IDs] NLM/ PMC3161387
  •  go-up   go-down


9. Adjei AA, Croghan GA, Erlichman C, Marks RS, Reid JM, Sloan JA, Pitot HC, Alberts SR, Goldberg RM, Hanson LJ, Bruzek LM, Atherton P, Thibault A, Palmer PA, Kaufmann SH: A Phase I trial of the farnesyl protein transferase inhibitor R115777 in combination with gemcitabine and cisplatin in patients with advanced cancer. Clin Cancer Res; 2003 Jul;9(7):2520-6
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] A Phase I trial of the farnesyl protein transferase inhibitor R115777 in combination with gemcitabine and cisplatin in patients with advanced cancer.
  • Toxicities were graded by the National Cancer Institute Common Toxicity Criteria and recorded as maximum grade per patient for each treatment cycle.
  • At the maximum tolerated dose, accumulation of prelamin A in buccal mucosa cells of patients was evaluated as a marker of farnesyl transferase inhibition by R115777.
  • At the maximum tolerated dose, defined as R115777 300 mg twice daily p.o., 1000 mg/m(2) gemcitabine, and 75 mg/m(2) cisplatin, inhibition of prelamin A farnesylation in buccal mucosa cells of patients was demonstrated, confirming that R115777 inhibits protein farnesylation in vivo.
  • This combination warrants further evaluation in a number of tumor types.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cisplatin / administration & dosage. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Enzyme Inhibitors / therapeutic use. Neoplasms / drug therapy. Quinolones / administration & dosage
  • [MeSH-minor] Adult. Aged. Alkyl and Aryl Transferases / antagonists & inhibitors. Dose-Response Relationship, Drug. Electrolytes. Farnesyltranstransferase. Female. Humans. Immunohistochemistry. Male. Maximum Tolerated Dose. Middle Aged. Mouth Mucosa / metabolism. Time Factors

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12855626.001).
  • [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 / NCI NIH HHS / CA / U01 CA069912; United States / NCI NIH HHS / CA / CA69912; United States / NCRR NIH HHS / RR / RR00585
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; 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 / Electrolytes; 0 / Enzyme Inhibitors; 0 / Quinolones; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase; MAT637500A / tipifarnib; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


10. Martins RA, Gomes GA, Aguiar O Jr, Ribeiro DA: Biomonitoring of oral epithelial cells in petrol station attendants: comparison between buccal mucosa and lateral border of the tongue. Environ Int; 2009 Oct;35(7):1062-5
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] Biomonitoring of oral epithelial cells in petrol station attendants: comparison between buccal mucosa and lateral border of the tongue.
  • The aim of the present study was to comparatively evaluate DNA damage (micronucleus) and cellular death (pyknosis, karyolysis and karyorrhexis) in exfoliated oral mucosa cells from gas petrol attendants using two different anatomic buccal sites: cheek mucosa and lateral border of the tongue.
  • Individuals had epithelial cells from cheek and lateral border of the tongue mechanically exfoliated, placed in fixative and dropped in clean slides which were checked for the above nuclear phenotypes.
  • The results pointed out significant statistical differences (p<0.05) of micronucleated oral mucosa cells from gas petrol attendants for both oral sites evaluated.
  • [MeSH-major] Carcinogens, Environmental / toxicity. Gasoline / toxicity. Mouth Mucosa / drug effects. Occupational Exposure. Tongue / drug effects
  • [MeSH-minor] Adult. Cell Death. DNA Damage. Environmental Monitoring. Epithelial Cells / drug effects. Female. Humans. Male. Micronuclei, Chromosome-Defective. Micronucleus Tests. Middle Aged

  • MedlinePlus Health Information. consumer health - Occupational Health.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19559482.001).
  • [ISSN] 1873-6750
  • [Journal-full-title] Environment international
  • [ISO-abbreviation] Environ Int
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Carcinogens, Environmental; 0 / Gasoline
  •  go-up   go-down


11. Adjei AA, Mauer A, Bruzek L, Marks RS, Hillman S, Geyer S, Hanson LJ, Wright JJ, Erlichman C, Kaufmann SH, Vokes EE: Phase II study of the farnesyl transferase inhibitor R115777 in patients with advanced non-small-cell lung cancer. J Clin Oncol; 2003 May 1;21(9):1760-6
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] Phase II study of the farnesyl transferase inhibitor R115777 in patients with advanced non-small-cell lung cancer.
  • PURPOSE: This phase II study was undertaken to define the efficacy and pharmacodynamics of R115777, a farnesyl transferase inhibitor, in the first-line treatment of patients with advanced non-small-cell lung cancer.
  • PATIENTS AND METHODS: Forty-four patients with measurable stage IIIB (pleural effusion) or stage IV disease received 193 courses of treatment (median, 2.0; range, 1 to 22) with R115777 300 mg administered orally twice daily for 21 of every 28 days.
  • Buccal mucosa samples and peripheral blood mononuclear cells (PBMCs) were collected before and after 8 days of treatment to evaluate inhibition of farnesyl transferase in vivo.
  • CONCLUSION: Single-agent R115777 was well tolerated in patients with advanced NSCLC, but demonstrated minimal clinical activity.
  • On the basis of promising results of farnesyl transferase inhibitor combinations with standard chemotherapy agents, future studies of this agent in NSCLC should be in combination with systemic chemotherapy.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Quinolones / pharmacology
  • [MeSH-minor] Administration, Oral. Adult. Aged. Aged, 80 and over. Alkyl and Aryl Transferases / antagonists & inhibitors. Alkyl and Aryl Transferases / pharmacology. Anemia / chemically induced. Disease Progression. Farnesyltranstransferase. Female. Humans. Leukocytes, Mononuclear / enzymology. Male. Middle Aged. Mouth Mucosa / enzymology. Neutropenia / chemically induced. Survival

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • 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 = 12721252.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / CA69912; United States / NCI NIH HHS / CM / N01-CM-17102-02; United States / NCI NIH HHS / CA / P30-CA-14599-27
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; 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 / Quinolones; 192185-72-1 / tipifarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
  •  go-up   go-down


12. Onishi H, Sakata O, Masuda K, Machida Y: Novel mucoadhesive oral patch containing diazepam. Drug Dev Ind Pharm; 2005 Aug;31(7):607-13
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 mucoadhesive oral patch containing diazepam.
  • The oral patch of diazepam (DZ) was developed to achieve a rapid absorption of DZ for the emergency treatment of epileptic seizure or anxiety disorder.
  • The patch was composed of the outer mucoadhesive Carbopol 934 region, central drug region, and Tegaderm backing film.
  • DZ (3 mg) was dissolved in propylene glycol (PG) alone or PG containing oleic acid (OA) at 5.6% (w/w), and used as the drug region.
  • The patches with and without OA were attached to the mucosa of cheek in rats.
  • To the contrary, in the in vitro drug permeation using a cellulose membrane, the patch without OA showed a three times faster permeation rate than the patch with OA, suggesting that the direct action of OA to mucosa might be associated with absorption enhancement.
  • It was demonstrated that the patch with OA showed a good adhesion to oral mucosa and worked efficiently for rapid absorption of DZ.
  • [MeSH-major] Diazepam / administration & dosage. Drug Delivery Systems. Mouth Mucosa / metabolism. Oleic Acid / pharmacology
  • [MeSH-minor] Absorption / drug effects. Acrylates / chemistry. Adhesiveness. Animals. Anti-Anxiety Agents / administration & dosage. Anti-Anxiety Agents / blood. Anti-Anxiety Agents / pharmacokinetics. Anticonvulsants / administration & dosage. Anticonvulsants / blood. Anticonvulsants / pharmacokinetics. Cellulose. Cheek. In Vitro Techniques. Male. Membranes, Artificial. Propylene Glycol / chemistry. Rats. Rats, Wistar

  • Hazardous Substances Data Bank. OLEIC ACID .
  • Hazardous Substances Data Bank. DIAZEPAM .
  • Hazardous Substances Data Bank. Propylene glycol .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16207607.001).
  • [ISSN] 0363-9045
  • [Journal-full-title] Drug development and industrial pharmacy
  • [ISO-abbreviation] Drug Dev Ind Pharm
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylates; 0 / Anti-Anxiety Agents; 0 / Anticonvulsants; 0 / Membranes, Artificial; 0 / carbopol 934P; 2UMI9U37CP / Oleic Acid; 6DC9Q167V3 / Propylene Glycol; 9004-34-6 / Cellulose; Q3JTX2Q7TU / Diazepam
  •  go-up   go-down


13. Liu S, Liao C, Wang D: [The clinical application and evaluation of combined chemotherapy in comprehensive treatment for oral squamous cell carcinoma]. Hua Xi Kou Qiang Yi Xue Za Zhi; 2003 Apr 20;21(2):109-11
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 clinical application and evaluation of combined chemotherapy in comprehensive treatment for oral squamous cell carcinoma].
  • OBJECTIVE: To study and evaluate the clinical effects of combined preoperative chemotherapy and their relations with multi drug resistance (MDR).
  • METHODS: 102 cases with oral squamous cell carcinoma(OSCC) were included in the study (63 males and 39 females, aged 22 to 67 years).
  • Among the subjects there were 57 cases with cancer of tongue and 45 cases with cancer of buccal mucosa.
  • 27 cases in the group were classified as stage II, 55 as stage III and 20 cases as stage IV according to TNM standard.
  • The diagnosis of all cases were proved as OSCC by biopsy.

  • Genetic Alliance. consumer health - Carcinoma, Squamous Cell.
  • Genetic Alliance. consumer health - Oral squamous cell carcinoma.
  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • Hazardous Substances Data Bank. BLEOMYCIN .
  • 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 = 12838692.001).
  • [ISSN] 1000-1182
  • [Journal-full-title] Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology
  • [ISO-abbreviation] Hua Xi Kou Qiang Yi Xue Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 11056-06-7 / Bleomycin; 77108-50-0 / zhengguangmycin; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
  •  go-up   go-down


14. Karp JE, Kaufmann SH, Adjei AA, Lancet JE, Wright JJ, End DW: Current status of clinical trials of farnesyltransferase inhibitors. Curr Opin Oncol; 2001 Nov;13(6):470-6
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.
  • Farnesyltransferase inhibitors represent a new class of agents that target signal transduction pathways responsible for the proliferation and survival of diverse malignant cell types.
  • Although these agents were developed to prevent a processing step necessary for membrane attachment and maturation of Ras proteins, recent studies suggest that farnesyltransferase inhibitors block the farnesylation of additional cellular polypeptides, thereby exerting antitumor effects independent of the presence of activating ras gene mutations.
  • Clinical trials of two farnesyltransferase inhibitors--the tricyclic SCH66336 and the methylquinolone R115777--as single agents have demonstrated disease stabilization or objective responses in 10 to 15% of patients with refractory malignancies.
  • In patients with solid tumors, accessible normal tissues such as peripheral blood lymphocytes or, perhaps more germane to epithelial malignancies, buccal mucosa have provided surrogate tissues that allow confirmation that farnesyltransferase is inhibited in vivo at clinically achievable drug doses.
  • Preclinical studies of farnesyltransferase inhibitor resistance and clinical trials of farnesyltransferase inhibitors in combination with other agents currently are in progress.
  • [MeSH-minor] Clinical Trials as Topic. Farnesyltranstransferase. Humans. Leukemia / drug therapy. Leukemia / physiopathology. Neoplasms / drug therapy. Signal Transduction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11673687.001).
  • [ISSN] 1040-8746
  • [Journal-full-title] Current opinion in oncology
  • [ISO-abbreviation] Curr Opin Oncol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA669854
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Piperidines; 0 / Pyridines; 0 / Quinolones; 192185-72-1 / tipifarnib; 193275-84-2 / lonafarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
  • [Number-of-references] 53
  •  go-up   go-down


15. Zorzetto DL, Garcia PJ, Toledo Filho JL, Zorzetto NL: Ultrastructural study of the cheek oral mucosa of rats submitted to experimental chronic alcoholism. J Submicrosc Cytol Pathol; 2002 Jul;34(3):345-53
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] Ultrastructural study of the cheek oral mucosa of rats submitted to experimental chronic alcoholism.
  • Ultrastructural features of the cheek oral mucosa of rats (Rattus norvegicus) submitted to experimental chronic alcoholism were studied by transmission electron microscopy.
  • The animals of the two groups were weighed and sacrificed after 60, 120, and 180 days of treatment.
  • Samples of the oral mucosa from the cheek region were dissected and processed for ultrastructural analysis.
  • The most frequent alterations observed were an increased intercellular space, the presence of lipid droplets in the cytoplasm, and irregular nuclei with a pyknotic aspect.
  • [MeSH-major] Alcoholism / pathology. Mouth Mucosa / drug effects. Mouth Mucosa / ultrastructure
  • [MeSH-minor] Animals. Cell Nucleus / drug effects. Cell Nucleus / ultrastructure. Cheek / pathology. Cytoplasm / drug effects. Cytoplasm / ultrastructure. Desmosomes / drug effects. Desmosomes / ultrastructure. Disease Models, Animal. Lipids. Male. Microscopy, Electron. Rats

  • MedlinePlus Health Information. consumer health - Alcoholism and Alcohol Abuse.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12408369.001).
  • [ISSN] 1122-9497
  • [Journal-full-title] Journal of submicroscopic cytology and pathology
  • [ISO-abbreviation] J. Submicrosc. Cytol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Lipids
  •  go-up   go-down


16. Attia S, Kolesar J, Mahoney MR, Pitot HC, Laheru D, Heun J, Huang W, Eickhoff J, Erlichman C, Holen KD: A phase 2 consortium (P2C) trial of 3-aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP) for advanced adenocarcinoma of the pancreas. Invest New Drugs; 2008 Aug;26(4):369-79
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.
  • 3-Aminopyridine-2-carboxaldehyde thiosemicarbazone (3-AP, Triapine) is a novel small molecule inhibitor of ribonucleotide reductase (RR) with clinical signs of activity in pancreatic cancer.
  • Therefore, the Phase 2 Consortium (P2C) initiated a trial (two single stage studies with planned interim analysis) of 3-AP at 96 mg/m(2) intravenously days 1-4 and 15-18 of a 28-day cycle in both chemotherapy-naive and gemcitabine-refractory (GR) patients with advanced pancreatic cancer.
  • Correlative studies confirmed that 3-AP increased the percentage of S-phase buccal mucosal cells, the presence of multidrug resistance gene polymorphisms appeared to predict leukopenia, and baseline pancreatic tumor RR M2 expression was low relative to other tumors treated with 3-AP.
  • In conclusion, this regimen appears inactive against predominantly GR pancreatic cancer.
  • RR M2 protein may not have a critical role in the malignant potential of pancreatic cancer.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18278438.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973; United States / NCI NIH HHS / CM / N01 CM062205; United States / NCI NIH HHS / CM / N01 CM-62205; United States / PHS HHS / / 1ULIRR025011; United States / NCRR NIH HHS / RR / UL1 RR025011; United States / NCI NIH HHS / CA / T32 CA009614; United States / PHS HHS / / 24XS090
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Pyridines; 0 / Thiosemicarbazones; 0W860991D6 / Deoxycytidine; 143621-35-6 / 3-aminopyridine-2-carboxaldehyde thiosemicarbazone; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / ribonucleotide reductase M2; EC 1.17.4.1 / Ribonucleoside Diphosphate Reductase
  • [Other-IDs] NLM/ NIHMS692508; NLM/ PMC4461052
  •  go-up   go-down


17. Mahalingam R, Ravivarapu H, Redkar S, Li X, Jasti BR: Transbuccal delivery of 5-aza-2 -deoxycytidine: effects of drug concentration, buffer solution, and bile salts on permeation. AAPS PharmSciTech; 2007;8(3):E55
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] Transbuccal delivery of 5-aza-2 -deoxycytidine: effects of drug concentration, buffer solution, and bile salts on permeation.
  • Delivery of 5-aza-2 -deoxycytidine (decitabine) across porcine buccal mucosa was evaluated as an alternative to the complex intravenous infusion regimen currently used to administer the drug.
  • A reproducible high-performance liquid chromatography method was developed and optimized for the quantitative determination of this drug.
  • Decitabine showed a concentration-dependent passive diffusion process across porcine buccal mucosa.
  • [MeSH-major] Azacitidine / analogs & derivatives. Bile Acids and Salts / pharmacology. Mouth Mucosa / metabolism
  • [MeSH-minor] Animals. Buffers. Cheek. Chromatography, High Pressure Liquid. Osmolar Concentration. Permeability. Swine

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Clin Oncol. 2000 Mar;18(5):956-62 [10694544.001]
  • [Cites] Leuk Res. 2006 Mar;30(3):338-42 [16162357.001]
  • [Cites] Int J Pharm. 2000 Nov 4;208(1-2):35-9 [11064209.001]
  • [Cites] Eur J Pharm Biopharm. 2001 Mar;51(2):93-109 [11226816.001]
  • [Cites] Int J Pharm. 2002 Jan 1;231(1):57-66 [11719014.001]
  • [Cites] Mutat Res. 2002 Feb 15;514(1-2):95-103 [11815248.001]
  • [Cites] Int J Pharm. 2002 Jul 8;241(1):127-34 [12086728.001]
  • [Cites] Biochim Biophys Acta. 2002 Aug 19;1564(1):149-55 [12101007.001]
  • [Cites] Blood. 2002 Oct 15;100(8):2957-64 [12351408.001]
  • [Cites] Cell. 1980 May;20(1):85-93 [6156004.001]
  • [Cites] Leuk Res. 1981;5(6):453-62 [6173545.001]
  • [Cites] Mol Pharmacol. 1983 Jul;24(1):109-14 [6191192.001]
  • [Cites] Blood. 1984 Oct;64(4):922-9 [6206904.001]
  • [Cites] Pharmacol Ther. 1985;30(3):277-86 [2433702.001]
  • [Cites] Br J Cancer. 1991 Jul;64(1):144-8 [1713050.001]
  • [Cites] Crit Rev Ther Drug Carrier Syst. 1991;8(3):237-69 [1954652.001]
  • [Cites] J Pharm Sci. 1992 Jan;81(1):1-10 [1619560.001]
  • [Cites] Leukemia. 1993 May;7 Suppl 1:30-5 [7683354.001]
  • [Cites] Leukemia. 1993 May;7 Suppl 1:51-60 [7683358.001]
  • [Cites] J Pharm Sci. 1996 May;85(5):457-60 [8742934.001]
  • [Cites] Pharm Res. 1996 Aug;13(8):1233-7 [8865318.001]
  • [Cites] Leukemia. 1997 Mar;11 Suppl 1:S19-23 [9130687.001]
  • [Cites] Leukemia. 1997 Mar;11 Suppl 1:S35-6 [9130691.001]
  • [Cites] Int J Pharm. 1999 Aug 20;185(2):215-25 [10460917.001]
  • [Cites] J Chromatogr B Analyt Technol Biomed Life Sci. 2004 Dec 25;813(1-2):81-8 [15556519.001]
  • [Cites] Biochem Pharmacol. 2005 Jul 1;70(1):121-33 [15885659.001]
  • [Cites] Blood. 2000 Oct 1;96(7):2379-84 [11001887.001]
  • (PMID = 17915805.001).
  • [ISSN] 1530-9932
  • [Journal-full-title] AAPS PharmSciTech
  • [ISO-abbreviation] AAPS PharmSciTech
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bile Acids and Salts; 0 / Buffers; 776B62CQ27 / decitabine; M801H13NRU / Azacitidine
  • [Other-IDs] NLM/ PMC2750551
  •  go-up   go-down


18. Gabriel HE, Liu Z, Crott JW, Choi SW, Song BC, Mason JB, Johnson EJ: A comparison of carotenoids, retinoids, and tocopherols in the serum and buccal mucosa of chronic cigarette smokers versus nonsmokers. Cancer Epidemiol Biomarkers Prev; 2006 May;15(5):993-9
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] A comparison of carotenoids, retinoids, and tocopherols in the serum and buccal mucosa of chronic cigarette smokers versus nonsmokers.
  • BACKGROUND: Cigarette smoking, a major risk factor for oropharyngeal cancer, is reported to alter oral levels of carotenoids and tocopherols.
  • Such effects may be important because these nutrients, as well as retinoids, are putative chemoprotective agents.
  • OBJECTIVES: To determine whether chronic smoking is associated with altered concentrations of these nutrients in serum and buccal mucosa; to distinguish whether such effects are ascribable to diet; and to determine whether oral concentrations of these nutrients correlate with a putative biomarker of oral cancer risk.
  • METHODS: Serum and buccal mucosal cells (BMC) were analyzed for these nutrients and for BMC micronuclei in smokers (n = 35) and nonsmokers (n = 21).
  • RESULTS: General linear regression with adjustments for dietary intake showed that smokers possess lower serum concentrations of beta- and alpha-carotene, cryptoxanthin, lutein, and zeaxanthin (P </= 0.01) and a significantly higher serum gamma-tocopherol (P = 0.03).
  • BMC micronuclei did not correlate with the oral concentration of any micronutrient.
  • Nevertheless, the lack of concordance between oral concentrations of these nutrients and genetic damage in the BMCs of smokers does not support a protective role for these nutrients in oral carcinogenesis.
  • [MeSH-major] Biomarkers / metabolism. Carotenoids / metabolism. Mouth Mucosa / metabolism. Retinoids / metabolism. Smoking. Tocopherols / metabolism

  • MedlinePlus Health Information. consumer health - Smoking.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16702382.001).
  • [ISSN] 1055-9965
  • [Journal-full-title] Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology
  • [ISO-abbreviation] Cancer Epidemiol. Biomarkers Prev.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / K05 CA100048; United States / NCI NIH HHS / CA / U54 CA100971
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers; 0 / Retinoids; 1406-66-2 / Tocopherols; 36-88-4 / Carotenoids
  •  go-up   go-down


19. Ciolino LA, McCauley HA, Fraser DB, Wolnik KA: The relative buffering capacities of saliva and moist snuff: implications for nicotine absorption. J Anal Toxicol; 2001 Jan-Feb;25(1):15-25
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.
  • Commercial moist snuff products are used by placing a portion of tobacco inside the mouth between the inner cheek or lip and gum.
  • Nicotine is absorbed into the blood stream via transfer across various oral membranes including the buccal mucosa (cheek lining).
  • The resulting salivary pH when a given moist snuff product is placed in the mouth is an important factor for nicotine absorption because it will affect the proportion of free base nicotine that is readily available for absorption.
  • The resulting salivary pH for a given moist snuff product will be determined in part by the relative acid-base buffering capacities of the saliva and moist snuff, as well as the pHs of the saliva and moist snuff prior to coming in contact with one another.
  • In the current study, the acid-base buffering capacities (mu eq/g) of a series of commercial moist snuff products were determined and compared to the acid-base buffering capacity for unstimulated, whole human saliva.
  • The buffering capacities of the moist snuff products were determined to be 10-20 times higher than the buffering capacity of human saliva.
  • The resulting salivary pH ranges after contact between an artifical saliva and the various moist snuff products were also determined; the results were used to predict the proportion of free base nicotine that can be expected to occur in the mouth during the first few minutes of product use.
  • These studies provide a basis for examining and understanding the effects that moist snuff product pHs and buffering capacities may be expected to have on nicotine absorption.

  • MedlinePlus Health Information. consumer health - Smokeless Tobacco.
  • Hazardous Substances Data Bank. NICOTINE .
  • 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 = 11215994.001).
  • [ISSN] 0146-4760
  • [Journal-full-title] Journal of analytical toxicology
  • [ISO-abbreviation] J Anal Toxicol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Buffers; 6M3C89ZY6R / Nicotine
  •  go-up   go-down


20. Sridhar S, Schembri F, Zeskind J, Shah V, Gustafson AM, Steiling K, Liu G, Dumas YM, Zhang X, Brody JS, Lenburg ME, Spira A: Smoking-induced gene expression changes in the bronchial airway are reflected in nasal and buccal epithelium. BMC Genomics; 2008 May 30;9:259
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] Smoking-induced gene expression changes in the bronchial airway are reflected in nasal and buccal epithelium.
  • BACKGROUND: Cigarette smoking is a leading cause of preventable death and a significant cause of lung cancer and chronic obstructive pulmonary disease.
  • In this study, we explored relationships in whole-genome gene expression between extrathorcic (buccal and nasal) and intrathoracic (bronchial) epithelium in healthy current and never smokers.
  • Gene set enrichment analysis demonstrated that this set of genes was also highly enriched among the genes most altered by smoking in both nasal and buccal epithelial samples.
  • This relationship could potentially be utilized to develop a non-invasive biomarker for tobacco exposure as well as a non-invasive screening or diagnostic tool providing information about individual susceptibility to smoking-induced lung diseases.

  • MedlinePlus Health Information. consumer health - Smoking.
  • 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
  • [Cites] Acta Otolaryngol. 2005 Jun;125(6):618-24 [16076710.001]
  • [Cites] J Dent Res. 2004 Mar;83(3):199-203 [14981119.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9623-7 [16266979.001]
  • [Cites] Toxicol Lett. 2006 Aug 20;165(2):182-94 [16713138.001]
  • [Cites] Laryngoscope. 2006 Aug;116(8):1375-9 [16885739.001]
  • [Cites] Am J Respir Cell Mol Biol. 2006 Sep;35(3):327-36 [16614352.001]
  • [Cites] Am J Respir Cell Mol Biol. 2006 Dec;35(6):651-61 [16809635.001]
  • [Cites] Environ Health Perspect. 2006 Nov;114(11):1655-61 [17107849.001]
  • [Cites] Nat Med. 2007 Mar;13(3):361-6 [17334370.001]
  • [Cites] Ugeskr Laeger. 2008 Jan 28;170(5):328-30 [18252159.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2001 Aug;281(2):L509-16 [11435227.001]
  • [Cites] Gene. 2001 Dec 27;281(1-2):103-13 [11750132.001]
  • [Cites] J Biol Chem. 2002 May 17;277(20):17906-15 [11877439.001]
  • [Cites] Chest. 2002 May;121(5 Suppl):166S-182S [12010847.001]
  • [Cites] Toxicol Sci. 2003 Feb;71(2):229-36 [12563108.001]
  • [Cites] Ann Oncol. 1999;10 Suppl 5:S7-11 [10582132.001]
  • [Cites] Biotechniques. 2004 Mar;36(3):484-7 [15038164.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10143-8 [15210990.001]
  • [Cites] Clin Cancer Res. 2004 Aug 1;10(15):5131-6 [15297416.001]
  • [Cites] Cancer Res. 2004 Sep 15;64(18):6805-13 [15375000.001]
  • [Cites] Gut. 1982 Jan;23(1):58-62 [7056497.001]
  • [Cites] Acta Paediatr Scand. 1985 Jan;74(1):102-6 [3984714.001]
  • [Cites] Izv Akad Nauk SSSR Biol. 1989 Jan-Feb;(1):58-63 [2715495.001]
  • [Cites] Am J Physiol. 1994 Sep;267(3 Pt 1):L342-9 [7943261.001]
  • [Cites] J Allergy Clin Immunol. 1995 Jan;95(1 Pt 1):96-102 [7822670.001]
  • [Cites] Drug Metab Dispos. 1996 Aug;24(8):884-90 [8869824.001]
  • [Cites] Carcinogenesis. 1997 Feb;18(2):339-44 [9054626.001]
  • [Cites] Environ Health Perspect. 1997 Jun;105 Suppl 4:913-8 [9255580.001]
  • [Cites] J Natl Cancer Inst. 1997 Sep 17;89(18):1366-73 [9308707.001]
  • [Cites] J Clin Invest. 1997 Oct 15;100(8):2133-7 [9329980.001]
  • [Cites] Eur J Cancer. 1998 May;34(6):914-20 [9797707.001]
  • [Cites] Carcinogenesis. 1998 Oct;19(10):1867-71 [9806171.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Am J Respir Cell Mol Biol. 1999 Feb;20(2):209-18 [9922211.001]
  • [Cites] Am J Respir Cell Mol Biol. 1999 Apr;20(4):595-604 [10100990.001]
  • [Cites] Pharmacogenetics. 1999 Jun;9(3):295-306 [10471061.001]
  • [Cites] Clin Cancer Res. 1999 Aug;5(8):2025-34 [10473082.001]
  • [Cites] Carcinogenesis. 2004 Dec;25(12):2459-65 [15319297.001]
  • [Cites] J Allergy Clin Immunol. 2005 Feb;115(2):243-51 [15696077.001]
  • [Cites] Eur J Cancer. 2005 May;41(8):1223-36 [15911247.001]
  • [Cites] Am J Respir Crit Care Med. 2005 Jun 15;171(12):1343-9 [15750039.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):1054-8 [12615722.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3059-64 [12624187.001]
  • [Cites] Mod Pathol. 2004 Feb;17(2):150-7 [14657954.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • (PMID = 18513428.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA124640; United States / NIEHS NIH HHS / ES / U01 ES016035; United States / NCI NIH HHS / CA / R01CA124640; United States / NIEHS NIH HHS / ES / U01ES016035
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Smoke
  • [Other-IDs] NLM/ PMC2435556
  •  go-up   go-down


21. Adjei AA, Erlichman C, Davis JN, Cutler DL, Sloan JA, Marks RS, Hanson LJ, Svingen PA, Atherton P, Bishop WR, Kirschmeier P, Kaufmann SH: A Phase I trial of the farnesyl transferase inhibitor SCH66336: evidence for biological and clinical activity. Cancer Res; 2000 Apr 1;60(7):1871-7
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] A Phase I trial of the farnesyl transferase inhibitor SCH66336: evidence for biological and clinical activity.
  • Farnesyl protein transferase (FT), an enzyme that catalyzes the first step in the posttranslational modification of ras and a number of other polypeptides, has emerged as an important target for the development of anticancer agents.
  • We report a Phase I trial to assess the maximum tolerated dose, toxicities, and biological effectiveness of SCH66336 in inhibiting FT in vivo.
  • Inhibition of prelamin A farnesylation in buccal mucosa cells of patients treated with SCH66336 was demonstrated, confirming that SCH66336 inhibits protein farnesylation in vivo.
  • One partial response was observed in a patient with previously treated metastatic non-small cell lung cancer, who remained on study for 14 months.
  • This study not only establishes the dose for future testing on this schedule (350 mg b.i.d.) but also provides the first evidence of successful inhibition of FT in the clinical setting and the first hint of clinical activity for this class of agents.
  • [MeSH-major] Alkyl and Aryl Transferases / antagonists & inhibitors. Antineoplastic Agents / adverse effects. Neoplasms / drug therapy. Piperidines / adverse effects. Pyridines / adverse effects
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Dose-Response Relationship, Drug. Enzyme Inhibitors / adverse effects. Farnesyltranstransferase. Female. Humans. Lamin Type A. Lamins. Male. Middle Aged. Mouth Mucosa / pathology. Nuclear Proteins / analysis. Protein Precursors / analysis

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • 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 = 10766174.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA77112; United States / NCRR NIH HHS / RR / RR00585
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Lamin Type A; 0 / Lamins; 0 / Nuclear Proteins; 0 / Piperidines; 0 / Protein Precursors; 0 / Pyridines; 0 / prelamin A; 193275-84-2 / lonafarnib; EC 2.5.- / Alkyl and Aryl Transferases; EC 2.5.1.29 / Farnesyltranstransferase
  •  go-up   go-down


22. Clarke J, Butler R, Howarth G, Read L, Regester G: Exposure of oral mucosa to bioactive milk factors reduces severity of chemotherapy-induced mucositis in the hamster. Oral Oncol; 2002 Jul;38(5):478-85
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] Exposure of oral mucosa to bioactive milk factors reduces severity of chemotherapy-induced mucositis in the hamster.
  • A biologically active extract containing bovine whey proteins, whey growth factor extract-A (WGFE-A) was administered topically to the oral mucosa of hamsters and its ability to prevent and treat chemotherapy-induced oral mucositis investigated.
  • Oral mucositis was induced in Syrian golden hamsters through a combination treatment of the antimetabolite chemotherapy drug 5-fluorouracil (5-FU), and mild abrasion of the cheek pouch.
  • WGFE-A administered to the oral mucosa via hydrogel and liquid treatments, pre and concurrent to 5-FU therapy, resulted in significantly reduced mucosal ulceration.
  • In a separate study, cell cycle staining indicated that cheek pouch mucosal epithelial cells pre-exposed to WGFE-A in-vivo showed a reduced rate of proliferation, measured as a 21% reduction in the bromodeoxyuridine (BrdU) cell labelling index (P<0.04).
  • Several WGFE-A constituents are likely to confer protective effects on the cheek mucosa, including anti-proliferative, anti-apoptotic and anti-microbial factors.
  • WGFE-A provides a potentially valuable source of topically delivered proteins for clinical application in preventing severe oral mucositis caused by chemotherapy.
  • [MeSH-major] Antimetabolites, Antineoplastic / adverse effects. Fluorouracil / adverse effects. Milk Proteins / therapeutic use. Stomatitis / prevention & control
  • [MeSH-minor] Animals. Cell Division / drug effects. Cheek. Cricetinae. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Mesocricetus. Mouth Mucosa / cytology. Mouth Mucosa / drug effects. Whey Proteins

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12110343.001).
  • [ISSN] 1368-8375
  • [Journal-full-title] Oral oncology
  • [ISO-abbreviation] Oral Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Milk Proteins; 0 / Whey Proteins; U3P01618RT / Fluorouracil
  •  go-up   go-down


23. Solt DB, Chang Kw, Helenowski I, Rademaker AW: Phenethyl isothiocyanate inhibits nitrosamine carcinogenesis in a model for study of oral cancer chemoprevention. Cancer Lett; 2003 Dec 30;202(2):147-52
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] Phenethyl isothiocyanate inhibits nitrosamine carcinogenesis in a model for study of oral cancer chemoprevention.
  • The anticarcinogenic effect of phenethyl isothiocyanate (PEITC) was examined in hamster buccal pouch mucosa exposed to N-nitrosomethylbenzylamine (NMBA).
  • UDS mediated by in vitro exposure to NMBA (at 10 and 50 mM) was examined in mucosal samples derived following topical exposure of pouch mucosa to PEITC at concentrations of 0.5, 5, or 50 mM.
  • PEITC also reduced tumor formation by 94%.
  • gamma-GT, in particular, may be a useful indicator for identification of effective oral cancer chemopreventive agents and combinations of agents.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Isothiocyanates / pharmacology. Mouth Mucosa / drug effects. Mouth Neoplasms / prevention & control
  • [MeSH-minor] Animals. Biomarkers, Tumor. Cricetinae. DNA Replication / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Male. Mesocricetus. Nitrosamines / toxicity. gamma-Glutamyltransferase / metabolism

  • MedlinePlus Health Information. consumer health - Oral 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 = 14643444.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1 R03 CA89788-01A1
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor; 0 / Isothiocyanates; 0 / Nitrosamines; 6U7TFK75KV / phenethyl isothiocyanate; EC 2.3.2.2 / gamma-Glutamyltransferase
  •  go-up   go-down


24. Kreimann EL, Itoiz ME, Dagrosa A, Garavaglia R, Farías S, Batistoni D, Schwint AE: The hamster cheek pouch as a model of oral cancer for boron neutron capture therapy studies: selective delivery of boron by boronophenylalanine. Cancer Res; 2001 Dec 15;61(24):8775-81
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] The hamster cheek pouch as a model of oral cancer for boron neutron capture therapy studies: selective delivery of boron by boronophenylalanine.
  • Herein we propose and validate the hamster cheek pouch model of oral cancer for boron neutron capture therapy (BNCT) studies.
  • This model serves to explore new applications of the technique, study the biology and radiobiology of BNCT, and assess the uptake of boron compounds and response of tumor, precancerous tissue, and clinically relevant normal tissues.
  • The success of BNCT is dependent on the absolute amount of boron in the tumor, and the tumor:blood and tumor:normal tissue boron concentration ratios.
  • Tumors were induced in the hamsters with a carcinogenesis protocol that uses dimethyl-1,2-benzanthracene and mimics spontaneous tumor development in human oral mucosa.
  • The animals were then used for biodistribution and pharmacokinetic studies of boronophenylalanine (BPA).
  • Blood, tumor, precancerous pouch tissue surrounding tumor, normal pouch tissue, tongue, skin, cheek mucosa, palate mucosa, liver, and spleen, were sampled at 0-12 h after administration of 300 mg BPA/kg.
  • The data reveal selective uptake of BPA by tumor tissue and, to a lesser degree, by precancerous tissue.
  • Mean tumor boron concentration was 36.9 +/- 17.5 ppm at 3.5 h and the mean boron ratios were 2.4:1 for tumor:normal pouch tissue and 3.2:1 for tumor:blood.
  • Higher doses of BPA (600 and 1200 mg BPA/kg) increased tumor uptake.
  • Potentially therapeutic absolute boron concentrations, and tumor:normal tissue and tumor:blood ratios can be achieved in the hamster oral cancer model using BPA as the delivery agent.
  • [MeSH-major] Boron Compounds / administration & dosage. Boron Neutron Capture Therapy / methods. Mouth Neoplasms / metabolism. Mouth Neoplasms / radiotherapy. Phenylalanine / administration & dosage. Phenylalanine / analogs & derivatives. Radiation-Sensitizing Agents / administration & dosage
  • [MeSH-minor] 9,10-Dimethyl-1,2-benzanthracene. Animals. Boron / blood. Boron / pharmacokinetics. Carcinogens. Cheek. Cricetinae. Disease Models, Animal. Dose-Response Relationship, Drug. Injections, Intraperitoneal. Injections, Intravenous. Injections, Subcutaneous. Mesocricetus. Tissue Distribution

  • MedlinePlus Health Information. consumer health - Oral Cancer.
  • Hazardous Substances Data Bank. BORON COMPOUNDS .
  • Hazardous Substances Data Bank. 7,12-DIMETHYLBENZ(A)ANTHRACENE .
  • Hazardous Substances Data Bank. (L)-Phenylalanine .
  • Hazardous Substances Data Bank. BORON, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11751398.001).
  • [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 / Boron Compounds; 0 / Carcinogens; 0 / Radiation-Sensitizing Agents; 47E5O17Y3R / Phenylalanine; 57-97-6 / 9,10-Dimethyl-1,2-benzanthracene; N9E3X5056Q / Boron; UID84303EL / 4-boronophenylalanine
  •  go-up   go-down


25. Caldeira EJ, Carvalho CA, Padovani CR, Camilli JA, Garcia PJ, Cagnon VH: Morphological alterations in the epithelium of the oral mucosa of rats (Rattus norvegicus) submitted to long-term systemic nicotine treatment. Arch Oral Biol; 2007 Jan;52(1):83-9
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] Morphological alterations in the epithelium of the oral mucosa of rats (Rattus norvegicus) submitted to long-term systemic nicotine treatment.
  • The local action of tobacco on the oral mucosa can cause precancerous and cancerous lesions.
  • Thus, the aim of the present study was to characterize the cellular changes of the cheek mucosa of rats submitted to long-term systemic nicotine treatment.
  • Twenty male rats were divided into two experimental groups: a nicotine group and a control group, each consisting of 10 animals.
  • All animals received a solid diet and water ad libitum.
  • After 90 days of treatment, all animals were weighed and sacrificed.
  • Samples of cheek mucosa were collected for light and transmission electron microscopy.
  • The results revealed oral epithelium containing atypical cells that were characterized by atrophy, cell membrane disorganization and tissue damage.
  • It was concluded that systemic administration of nicotine damaged the cellular integrity of the oral mucosa, impairing tissue function and predisposing the tissue to the action of different pathogenic agents and also to that of other carcinogenic substances present in tobacco.
  • [MeSH-major] Mouth Mucosa / drug effects. Nicotine / administration & dosage
  • [MeSH-minor] Animals. Drug Administration Schedule. Epithelial Cells / drug effects. Epithelial Cells / pathology. Epithelium / drug effects. Epithelium / pathology. Male. Microscopy, Electron / methods. Organelles / drug effects. Organelles / pathology. Rats. Rats, Wistar

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NICOTINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17097602.001).
  • [ISSN] 0003-9969
  • [Journal-full-title] Archives of oral biology
  • [ISO-abbreviation] Arch. Oral Biol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 6M3C89ZY6R / Nicotine
  •  go-up   go-down


26. Yamamoto T, Nakane T, Osaki T: The mechanism of mononuclear cell infiltration in oral lichen planus: the role of cytokines released from keratinocytes. J Clin Immunol; 2000 Jul;20(4):294-305
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 mechanism of mononuclear cell infiltration in oral lichen planus: the role of cytokines released from keratinocytes.
  • To clarify the pathogenesis of oral lichen planus (OLP), we investigated the roles of keratinocytes (KC) in mononuclear cell infiltration.
  • When peripheral blood mononuclear cells (PBMC) obtained from healthy donors were cultured in the presence of culture supernatants of KC separated from the noninflamed gingivae (Nor-KC) and cheek mucosae of patients with OLP (OLP-KC), the number of migrated PBMC across monolayered human umbilical vein endothelial cells (HUVEC) were increased to about 1.3-fold and 1.5-fold of the control level, respectively, with increases of the expression of CD11a, CD11b, CD18, and CD49d on PBMC and intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and endothelial-leukocyte adhesion molecule-1 on HUVEC.
  • In agreement with these results, the culture supernatants of OLP-KC up-regulated tyrosine phosphorylation of 62-kDa, 70-kDa, and 102-kDa proteins, phosphatidylinositol-3 kinase, and protein kinase C activities and activated Rho protein level more so than did those of Nor-KC.
  • [MeSH-major] Chemotactic Factors / secretion. Chemotaxis, Leukocyte. Cytokines / secretion. Keratinocytes / secretion. Leukocytes, Mononuclear / physiology. Lichen Planus, Oral / immunology. Neutrophil Infiltration
  • [MeSH-minor] Actin Cytoskeleton / drug effects. Actin Cytoskeleton / ultrastructure. Actins / drug effects. Actins / ultrastructure. Antibodies, Monoclonal / pharmacology. Antigens, CD18 / immunology. Antigens, CD18 / physiology. Cell Adhesion Molecules / biosynthesis. Cell Adhesion Molecules / genetics. Cells, Cultured / drug effects. Culture Media, Conditioned / pharmacology. Culture Media, Serum-Free. Cytoskeleton / ultrastructure. Endothelium, Vascular / cytology. Enzyme Activation / drug effects. Enzyme Inhibitors / pharmacology. Gene Expression Regulation / drug effects. Guanosine Triphosphate / physiology. Humans. Intercellular Adhesion Molecule-1 / immunology. Intercellular Adhesion Molecule-1 / physiology. Lymphocyte Function-Associated Antigen-1 / immunology. Lymphocyte Function-Associated Antigen-1 / physiology. Mouth Mucosa / immunology. Mouth Mucosa / pathology. Phosphorylation / drug effects. Protein Kinase Inhibitors. Protein Kinases / physiology. Protein Processing, Post-Translational / drug effects. Signal Transduction. Umbilical Veins. rho GTP-Binding Proteins / physiology

  • Genetic Alliance. consumer health - Oral lichen planus.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Crit Rev Immunol. 1995;15(3-4):285-316 [8834453.001]
  • [Cites] J Exp Med. 1992 Apr 1;175(4):1045-53 [1372641.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1995 Dec;80(6):698-704 [8680978.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):10148-52 [7937853.001]
  • [Cites] Crit Rev Oral Biol Med. 1998;9(1):86-122 [9488249.001]
  • [Cites] J Oral Pathol Med. 1995 Jan;24(1):1-8 [7722915.001]
  • [Cites] Oral Dis. 1996 Sep;2(3):188-92 [9081757.001]
  • [Cites] J Oral Pathol Med. 1990 Oct;19(9):389-96 [2269934.001]
  • [Cites] J Oral Pathol Med. 1997 Sep;26(8):362-6 [9379425.001]
  • [Cites] J Immunol. 1997 Feb 1;158(3):1061-7 [9013943.001]
  • [Cites] J Cell Biol. 1995 Nov;131(3):791-805 [7593197.001]
  • [Cites] Biochim Biophys Acta. 1991 Apr 16;1072(1):81-102 [2018780.001]
  • [Cites] J Biochem. 1994 Jun;115(6):1029-34 [7982876.001]
  • [Cites] J Immunol. 1992 Apr 15;148(8):2423-8 [1348518.001]
  • [Cites] J Oral Pathol Med. 1990 Nov;19(10):459-63 [1981078.001]
  • [Cites] Blood. 1995 Apr 1;85(7):1858-64 [7535591.001]
  • [Cites] J Biol Chem. 1995 Jan 6;270(1):269-73 [7814385.001]
  • [Cites] Pathol Res Pract. 1989 Aug;185(2):218-24 [2678033.001]
  • [Cites] Science. 1995 Apr 14;268(5208):233-9 [7716514.001]
  • [Cites] Science. 1996 Apr 5;272(5258):60-6 [8600538.001]
  • [Cites] J Oral Pathol Med. 1993 May;22(5):193-202 [8315598.001]
  • [Cites] J Cell Biol. 1998 Jan 12;140(1):211-21 [9425168.001]
  • [Cites] EMBO J. 1998 Aug 3;17(15):4391-403 [9687507.001]
  • [Cites] J Oral Pathol Med. 1994 Aug;23(7):309-15 [7965886.001]
  • [Cites] J Invest Dermatol. 1996 Apr;106(4):661-6 [8618001.001]
  • [Cites] Oral Dis. 1996 Jun;2(2):125-8 [8957924.001]
  • [Cites] J Invest Dermatol. 1995 May;104(5):784-8 [7738356.001]
  • [Cites] J Biol Chem. 1998 May 22;273(21):13223-9 [9582366.001]
  • [Cites] Immunology. 1987 Mar;60(3):439-44 [3494669.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1997 Mar;83(3):358-66 [9084200.001]
  • [Cites] Cell. 1996 Feb 9;84(3):345-57 [8608588.001]
  • [Cites] J Invest Dermatol. 1986 Jul;87(1):33-8 [2941489.001]
  • [Cites] Biochem Biophys Res Commun. 1989 Nov 30;165(1):349-54 [2686646.001]
  • [Cites] Mol Cell Biol. 1998 Aug;18(8):4744-51 [9671484.001]
  • [Cites] Eur J Immunol. 1998 Jan;28(1):104-13 [9485190.001]
  • [Cites] Oral Surg Oral Med Oral Pathol Oral Radiol Endod. 1996 Jun;81(6):682-90 [8784900.001]
  • [Cites] Pathol Res Pract. 1992 Dec;188(8):1033-41 [1300599.001]
  • [Cites] J Immunol. 1998 Feb 15;160(4):1901-9 [9469452.001]
  • [Cites] Mol Cell Biol. 1998 Jul;18(7):3936-46 [9632778.001]
  • [Cites] Science. 1992 Oct 23;258(5082):607-14 [1411571.001]
  • [Cites] Nature. 1990 Aug 2;346(6283):425-34 [1974032.001]
  • [Cites] Arch Dermatol Res. 1992;284 Suppl 1:S22-6 [1285652.001]
  • [Cites] Nature. 1994 Dec 22-29;372(6508):786-91 [7997267.001]
  • [Cites] Exp Dermatol. 1992 Jul;1(1):12-9 [1344656.001]
  • [Cites] Pathol Res Pract. 1990 Oct;186(5):625-32 [1705022.001]
  • [Cites] Immunol Today. 1997 May;18(5):231-40 [9153955.001]
  • (PMID = 10939717.001).
  • [ISSN] 0271-9142
  • [Journal-full-title] Journal of clinical immunology
  • [ISO-abbreviation] J. Clin. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Actins; 0 / Antibodies, Monoclonal; 0 / Antigens, CD18; 0 / Cell Adhesion Molecules; 0 / Chemotactic Factors; 0 / Culture Media, Conditioned; 0 / Culture Media, Serum-Free; 0 / Cytokines; 0 / Enzyme Inhibitors; 0 / Lymphocyte Function-Associated Antigen-1; 0 / Protein Kinase Inhibitors; 126547-89-5 / Intercellular Adhesion Molecule-1; 86-01-1 / Guanosine Triphosphate; EC 2.7.- / Protein Kinases; EC 3.6.5.2 / rho GTP-Binding Proteins
  •  go-up   go-down






Advertisement