[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 24 of about 24
1. Goto T, Tomizawa N, Kobayashi E, Fujimura A: A comparative pharmacology study between the intracolonic and oral routes of 5-FU administration in a colon cancer-bearing Yoshida sarcoma rat model. J Pharmacol Sci; 2004 Jun;95(2):163-73
Hazardous Substances Data Bank. FLUOROURACIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A comparative pharmacology study between the intracolonic and oral routes of 5-FU administration in a colon cancer-bearing Yoshida sarcoma rat model.
  • We prepared a colon cancer-bearing Yoshida sarcoma rat model to examine the dose-response relationship of antitumor activity of intracolonically or orally administered 5-fluorouracil (5-FU; 45, 30, 20, 13, and 8 mg/kg).
  • Regarding the time-course of body weight, even the 5-FU highest dose (45 mg/kg) intracolonic administration group showed no inhibited body weight increase compared to the control group.
  • [MeSH-major] Antimetabolites, Antineoplastic / administration & dosage. Antimetabolites, Antineoplastic / therapeutic use. Colonic Neoplasms / drug therapy. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use. Sarcoma, Yoshida / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Blood Cell Count. Body Weight / drug effects. Catheterization. Colon. Dose-Response Relationship, Drug. Hemoglobins / metabolism. Male. Neoplasm Transplantation. Rats

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15215640.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Hemoglobins; U3P01618RT / Fluorouracil
  •  go-up   go-down


2. Petre PM, Baciewicz FA Jr, Tigan S, Spears JR: Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of metastatic lung tumors in a rat model. J Thorac Cardiovasc Surg; 2003 Jan;125(1):85-95; discussion 95
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] Hyperbaric oxygen as a chemotherapy adjuvant in the treatment of metastatic lung tumors in a rat model.
  • OBJECTIVES: The objectives of the study were to test the hypothesis that hyperbaric levels of oxygen enhance the sensitivity of a sarcoma cell line to doxorubicin (Adriamycin) both in vitro and in vivo in a rat model of pulmonary metastases and to test the feasibility of arterialization of mixed venous blood by direct injection of aqueous oxygen into the pulmonary artery in a rat model.
  • METHODS: Rat sarcoma (MCA-2) cells were incubated in the presence of increasing concentrations of doxorubicin (0.1-2.0 micromol/L).
  • A dose-dependent toxicity relationship at 12 hours of treatment was examined with and without pretreatment with hyperbaric oxygen (3.7 atm absolute for 1.5-3.5 hours).
  • At that time the animals were divided into four groups: control (no treatment), doxorubicin at 2 mg/kg, hyperbaric oxygen (oxygen at 2 atm absolute for 30 minutes), and hyperbaric oxygen plus doxorubicin.
  • Seven days after treatment, the numbers of lung nodules were counted and the lung weights were determined.
  • CONCLUSIONS: Hyperbaric oxygen enhanced the chemotherapeutic effect of doxorubicin both in cell culture and in the rat model.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Doxorubicin / therapeutic use. Hyperbaric Oxygenation. Lung Neoplasms / therapy. Sarcoma, Experimental / therapy

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12538989.001).
  • [ISSN] 0022-5223
  • [Journal-full-title] The Journal of thoracic and cardiovascular surgery
  • [ISO-abbreviation] J. Thorac. Cardiovasc. Surg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 80168379AG / Doxorubicin
  •  go-up   go-down


3. Jancík S, Drábek J, Radzioch D, Hajdúch M: Clinical relevance of KRAS in human cancers. J Biomed Biotechnol; 2010;2010:150960
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The KRAS gene (Ki-ras2 Kirsten rat sarcoma viral oncogene homolog) is an oncogene that encodes a small GTPase transductor protein called KRAS.
  • Activating mutations in the KRAS gene impair the ability of the KRAS protein to switch between active and inactive states, leading to cell transformation and increased resistance to chemotherapy and biological therapies targeting epidermal growth factor receptors.
  • It also underlines the importance of activating mutations in the KRAS gene in relation to carcinogenesis and their importance as diagnostic biomarkers, providing clues regarding human cancer patients' prognosis and indicating potential therapeutic approaches.

  • 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] Biochemistry. 1998 Sep 29;37(39):13453-62 [9753431.001]
  • [Cites] Carcinogenesis. 1999 Aug;20(8):1507-10 [10426799.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Dec;54(6):497-504 [15258697.001]
  • [Cites] J Gastroenterol Hepatol. 2005 Jan;20(1):67-72 [15610449.001]
  • [Cites] Cell. 2005 Jan 14;120(1):15-20 [15652477.001]
  • [Cites] Nature. 2005 Feb 17;433(7027):769-73 [15685193.001]
  • [Cites] J Cell Sci. 2005 Mar 1;118(Pt 5):843-6 [15731001.001]
  • [Cites] Cell. 2005 Mar 11;120(5):635-47 [15766527.001]
  • [Cites] Ann Oncol. 2005 May;16 Suppl 4:iv50-55 [15923430.001]
  • [Cites] Expert Opin Pharmacother. 2005 Jun;6(6):985-93 [15952926.001]
  • [Cites] J Mol Diagn. 2005 Aug;7(3):413-21 [16049314.001]
  • [Cites] J Cell Biol. 2005 Aug 1;170(3):429-41 [16043511.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):5900-9 [16043828.001]
  • [Cites] Oncogene. 2005 Sep 1;24(38):5878-87 [15897875.001]
  • [Cites] Electrophoresis. 2005 Sep;26(17):3380-6 [16097023.001]
  • [Cites] Oncologist. 2005 Sep;10(8):565-78 [16177281.001]
  • [Cites] Biochim Biophys Acta. 2005 Nov 25;1756(2):81-2 [16269215.001]
  • [Cites] Methods. 2005 Oct;37(2):165-72 [16288888.001]
  • [Cites] Clin Cancer Res. 2006 Mar 1;12(5):1647-53 [16533793.001]
  • [Cites] Br J Cancer. 2006 Mar 27;94(6):896-903 [16552419.001]
  • [Cites] Nucleic Acids Res. 2006;34(9):2536-49 [16687659.001]
  • [Cites] Cancer Biol Ther. 2006 Oct;5(10):1392-9 [17106238.001]
  • [Cites] Cancer Biol Ther. 2006 Nov;5(11):1481-6 [17172815.001]
  • [Cites] Mol Cancer Res. 2007 Feb;5(2):195-201 [17314276.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):295-308 [17384584.001]
  • [Cites] Clin Cancer Res. 2007 May 15;13(10):2890-6 [17504988.001]
  • [Cites] J Epidemiol Community Health. 2007 Jul;61(7):641-9 [17568059.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1773(8):1177-95 [17428555.001]
  • [Cites] Curr Treat Options Oncol. 2007 Feb;8(1):28-37 [17634830.001]
  • [Cites] J Int Med Res. 2007 Jul-Aug;35(4):450-7 [17697521.001]
  • [Cites] Mol Interv. 2007 Aug;7(4):199-202, 180 [17827440.001]
  • [Cites] Nucleic Acids Res. 2007;35(19):e131 [17932053.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):374-9 [18202412.001]
  • [Cites] Hum Mutat. 2008 Mar;29(3):441-50 [18186519.001]
  • [Cites] Clin Cancer Res. 2008 Mar 1;14(5):1296-302 [18316547.001]
  • [Cites] Exp Mol Pathol. 2008 Apr;84(2):79-89 [18279851.001]
  • [Cites] Med J Aust. 2008 Sep 1;189(5):277-82 [18759727.001]
  • [Cites] J Mol Diagn. 2008 Nov;10(6):520-6 [18832461.001]
  • [Cites] Strahlenther Onkol. 2008 Nov;184(11):592-7 [19016018.001]
  • [Cites] Leukemia. 2008 Dec;22(12):2269-72 [18509354.001]
  • [Cites] J Thorac Oncol. 2009 Jan;4(1):12-21 [19096301.001]
  • [Cites] Gastroenterology. 2009 Feb;136(2):459-70 [19026650.001]
  • [Cites] Biochem Soc Trans. 2009 Apr;37(Pt 2):427-32 [19290875.001]
  • [Cites] Biochem Soc Trans. 2009 Apr;37(Pt 2):433-7 [19290876.001]
  • [Cites] Am Rev Respir Dis. 1990 Dec;142(6 Pt 2):S27-30 [2252272.001]
  • [Cites] Trends Genet. 1991 Mar;7(3):91-5 [2031288.001]
  • [Cites] Mol Cell Biol. 1992 May;12(5):2050-6 [1569940.001]
  • [Cites] Genes Chromosomes Cancer. 1992 Sep;5(2):109-18 [1381946.001]
  • [Cites] Environ Health Perspect. 1992 Nov;98:13-24 [1486840.001]
  • [Cites] Electrophoresis. 2006 May;27(10):1878-85 [16619298.001]
  • [Cites] Am J Hum Genet. 2006 Jul;79(1):129-35 [16773572.001]
  • [Cites] Clin Chem. 2006 Oct;52(10):1855-63 [16916990.001]
  • [Cites] Semin Oncol. 2006 Oct;33(5 Suppl 10):S26-34 [17145522.001]
  • [Cites] Biochem J. 2003 Dec 15;376(Pt 3):e9-10 [14656216.001]
  • [Cites] Cancer Cell. 2003 Dec;4(6):437-50 [14706336.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 [14973191.001]
  • [Cites] Electrophoresis. 2004 Apr;25(7-8):1016-21 [15095442.001]
  • [Cites] Am J Pathol. 1993 Aug;143(2):545-54 [8342602.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1626-34 [18316791.001]
  • [Cites] Pharmacotherapy. 2008 Jun;28(6):742-54 [18503402.001]
  • [Cites] Curr Med Chem. 2008;15(15):1478-92 [18537624.001]
  • [Cites] Biochem Pharmacol. 2008 Jul 15;76(2):198-207 [18561895.001]
  • [Cites] Cancer Metastasis Rev. 2008 Sep;27(3):403-14 [18461427.001]
  • [Cites] Br J Cancer. 2009 Mar 24;100(6):985-92 [19293811.001]
  • [Cites] Cancer. 1993 Jul 15;72(2):432-8 [8319174.001]
  • [Cites] Clin Chem Lab Med. 1999 Sep;37(9):877-81 [10596953.001]
  • [Cites] Nat Genet. 2000 Feb;24(2):144-52 [10655059.001]
  • [Cites] J Epidemiol Community Health. 1999 Nov;53(11):702-9 [10656099.001]
  • [Cites] Int J Oncol. 2000 Mar;16(3):501-11 [10675482.001]
  • [Cites] Nature. 2000 Feb 24;403(6772):901-6 [10706289.001]
  • [Cites] Nucleic Acids Res. 2000 Oct 1;28(19):3752-61 [11000267.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2000 Nov;9(11):1193-7 [11097226.001]
  • [Cites] Clin Chem. 2000 Dec;46(12):1929-38 [11106325.001]
  • [Cites] Cancer. 2001 Aug 1;92(3):488-99 [11505392.001]
  • [Cites] Nat Genet. 2001 Sep;29(1):25-33 [11528387.001]
  • [Cites] Science. 2001 Oct 26;294(5543):853-8 [11679670.001]
  • [Cites] Mutat Res. 2002 Jan 15;513(1-2):37-48 [11719088.001]
  • [Cites] Semin Oncol. 2001 Oct;28(5 Suppl 17):19-26 [11740803.001]
  • [Cites] Cancer. 2001 Sep 15;92(6):1525-30 [11745231.001]
  • [Cites] Nat Genet. 2002 Apr;30(4):363-4 [11896390.001]
  • [Cites] Cancer. 2002 Apr 1;94(7):2055-62 [11932909.001]
  • [Cites] J Virol. 2002 May;76(9):4275-86 [11932393.001]
  • [Cites] Acta Biochim Pol. 2001;48(4):829-50 [11995995.001]
  • [Cites] Anal Biochem. 2002 May 15;304(2):200-5 [12009696.001]
  • [Cites] Oncogene. 2002 Jun 20;21(27):4301-6 [12082617.001]
  • [Cites] Cancer Res. 2002 Jul 15;62(14):4142-50 [12124353.001]
  • [Cites] Mol Biotechnol. 2002 Oct;22(2):115-21 [12405259.001]
  • [Cites] Mol Cancer Ther. 2001 Nov;1(1):29-41 [12467236.001]
  • [Cites] Mol Cell Biol. 2003 Jan;23(2):543-54 [12509453.001]
  • [Cites] Oncogene. 2003 Feb 27;22(8):1243-6 [12606951.001]
  • [Cites] Cell. 2003 Apr 4;113(1):25-36 [12679032.001]
  • [Cites] J Am Chem Soc. 2003 Jun 11;125(23):6937-45 [12783546.001]
  • [Cites] J Biol Chem. 2003 Aug 22;278(34):31871-8 [12805379.001]
  • [Cites] Cancer Cell. 2003 Aug;4(2):111-20 [12957286.001]
  • [Cites] Mol Cancer Res. 2003 Oct;1(12):882-91 [14573789.001]
  • [Cites] Cancer Res. 2004 Jun 1;64(11):3753-6 [15172979.001]
  • [Cites] Br J Cancer. 2004 Jul 19;91(2):355-8 [15188009.001]
  • [Cites] Clin Chem. 2004 Sep;50(9):1688-91 [15331511.001]
  • [Cites] Lung Cancer. 2004 Nov;46(2):255-61 [15474674.001]
  • [Cites] Proc Natl Acad Sci U S A. 1982 Aug;79(16):4848-52 [6289320.001]
  • [Cites] Cell. 1983 Jan;32(1):201-8 [6825168.001]
  • [Cites] Nature. 1983 Mar 3;302(5903):79-81 [6298638.001]
  • [Cites] Nature. 1983 Aug 11-17;304(5926):501-6 [6308466.001]
  • [Cites] Mol Cell Biol. 1983 Dec;3(12):2298-301 [6197628.001]
  • [Cites] Nucleic Acids Res. 1983 Dec 10;11(23):8221-36 [6672765.001]
  • [Cites] Somat Cell Mol Genet. 1985 Mar;11(2):149-55 [3856955.001]
  • [Cites] Nature. 1987 May 28-Jun 3;327(6120):293-7 [3587348.001]
  • [Cites] Nature. 1987 May 28-Jun 3;327(6120):298-303 [2438556.001]
  • [Cites] Annu Rev Biochem. 1987;56:779-827 [3304147.001]
  • [Cites] N Engl J Med. 1988 Sep 1;319(9):525-32 [2841597.001]
  • [Cites] Nucleic Acids Res. 1989 Apr 11;17(7):2503-16 [2785681.001]
  • [Cites] Cell. 1989 Jun 30;57(7):1167-77 [2661017.001]
  • [Cites] Eur J Clin Invest. 1990 Jun;20(3):225-35 [2114981.001]
  • [Cites] Cell. 1993 Dec 3;75(5):843-54 [8252621.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6257-64 [7954475.001]
  • [Cites] Eur J Cancer. 1995 Jul-Aug;31A(7-8):1171-3 [7577015.001]
  • [Cites] Semin Oncol. 1995 Dec;22(6 Suppl 14):12-8 [8553077.001]
  • [Cites] Blood. 1996 Apr 15;87(8):3368-74 [8605354.001]
  • [Cites] Int J Cancer. 1997 Mar 17;70(6):661-7 [9096646.001]
  • [Cites] Gut. 1997 May;40(5):660-3 [9203947.001]
  • [Cites] Pancreas. 1997 Jul;15(1):16-24 [9211488.001]
  • [Cites] Science. 1997 Jul 18;277(5324):333-8 [9219684.001]
  • [Cites] J Biol Chem. 1997 Oct 3;272(40):25128-34 [9312123.001]
  • [Cites] J Biol Chem. 1997 Oct 31;272(44):27902-7 [9346938.001]
  • [Cites] J Biol Chem. 1997 Nov 28;272(48):30362-70 [9374526.001]
  • [Cites] Exp Cell Res. 1997 Nov 25;237(1):7-13 [9417860.001]
  • [Cites] J Pathol. 1998 Jun;185(2):130-8 [9713338.001]
  • (PMID = 20617134.001).
  • [ISSN] 1110-7251
  • [Journal-full-title] Journal of biomedicine & biotechnology
  • [ISO-abbreviation] J. Biomed. Biotechnol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 3.6.5.2 / ras Proteins
  • [Other-IDs] NLM/ PMC2896632
  •  go-up   go-down


Advertisement
4. Tanaka T, Kaneda Y, Li TS, Matsuoka T, Zempo N, Esato K: Digitonin enhances the anti-tumor effect of cisplatin against methylcholanthrene-induced rat sarcoma cells in vitro. Anticancer Res; 2001 Jan-Feb;21(1A):313-5
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] Digitonin enhances the anti-tumor effect of cisplatin against methylcholanthrene-induced rat sarcoma cells in vitro.
  • BACKGROUND: This study was designed to evaluate cellular uptake and cytotoxicity of cisplatin in methylcholanthrene (MCA)-induced rat sarcoma cells when used in combination with a detergent, digitonin.
  • MATERIALS AND METHODS: In the cellular intake study, after MCA sarcoma cells (10(7)) were treated with cisplatin alone (50 micrograms/ml) and with cisplatin (50 micrograms/ml) in combination with digitonin at 20 microM and 50 microM, the cells were washed twice with PBS and the platinum levels were measured by flameless atomic spectrometry.
  • For the anti-tumor effect MCA sarcoma cells (10(3)) were seeded in cell culture dishes and loaded for 10 minutes with PBS, digitonin (5 microM), cisplatin (5 micrograms/ml) or a combination of cisplatin (5 micrograms/ml) and digitonin (5 microM).
  • The number of viable cells was significantly decreased with, the combined cisplatin (5 micrograms/ml)--digitonin (5 microM) treatment (p < 0.0001 CONCLUSION: Digitonin enhances the antitumor effect of cisplatin against methylcholanthrene-induced rat sarcoma in vitro.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Cisplatin / pharmacokinetics. Cisplatin / pharmacology. Digitonin / pharmacology. Sarcoma, Experimental / drug therapy
  • [MeSH-minor] Animals. Biological Transport, Active. Cell Membrane Permeability. Detergents / pharmacology. Drug Synergism. Methylcholanthrene. Rats. Tumor Cells, Cultured. Tumor Stem Cell Assay

  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. 3-Methylcholanthrene .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11299754.001).
  • [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 / Detergents; 56-49-5 / Methylcholanthrene; KOO5CM684H / Digitonin; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


5. Hu X, Cao BN, Hu G, He J, Yang DQ, Wan YS: Attenuation of cell migration and induction of cell death by aged garlic extract in rat sarcoma cells. Int J Mol Med; 2002 Jun;9(6):641-3
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Attenuation of cell migration and induction of cell death by aged garlic extract in rat sarcoma cells.
  • In this study we investigated whether the aged garlic extract inhibits growth and migration of rat sarcoma tumor cells.
  • The results showed that aged garlic extract inhibited the growth of rat sarcoma cancer cells in a dose-dependent manner, compared to the numbers of the cells grown in control group.
  • This is the first report to show that the aged garlic extract inhibits rat sarcoma cell migration, a critical feature of tumor cell metastasis.
  • The results suggest that garlic, as a natural plant, unlike other cancer treatment methods, may play a role in fighting cancer without significant side effects.
  • [MeSH-major] Garlic / metabolism. Sarcoma / drug therapy. Sarcoma / pathology
  • [MeSH-minor] Animals. Cell Death. Cell Movement. Cells, Cultured. Dose-Response Relationship, Drug. Rats. Time Factors. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12011982.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  •  go-up   go-down


6. Babincov M, Altanerov V, Altaner C, Bergemann C, Babinec P: In vitro analysis of cisplatin functionalized magnetic nanoparticles in combined cancer chemotherapy and electromagnetic hyperthermia. IEEE Trans Nanobioscience; 2008 Mar;7(1):15-9
Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] In vitro analysis of cisplatin functionalized magnetic nanoparticles in combined cancer chemotherapy and electromagnetic hyperthermia.
  • A novel platform has been developed for combined cancer chemotherapy and hyperthermia based on iron oxide magnetic nanoparticles functionalized with cis-diamminedichloroplatinum(II) (cisplatin).
  • The capabilities of this system for heating and controlled drug release were investigated, and the system was tested in vitro by the treatment of BP6 rat sarcoma cells, where we demonstrated a synergism between the effects of cisplatin-targetMAG nanoparticles and the application of electromagnetic field.
  • [MeSH-major] Cisplatin / administration & dosage. Drug Carriers / administration & dosage. Hyperthermia, Induced / methods. Magnetics / therapeutic use. Nanoparticles / administration & dosage. Sarcoma / pathology. Sarcoma / therapy
  • [MeSH-minor] Animals. Antineoplastic Agents / administration & dosage. Cell Line, Tumor. Combined Modality Therapy. Drug Therapy / methods. Rats. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18334449.001).
  • [ISSN] 1536-1241
  • [Journal-full-title] IEEE transactions on nanobioscience
  • [ISO-abbreviation] IEEE Trans Nanobioscience
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Carriers; Q20Q21Q62J / Cisplatin
  •  go-up   go-down


7. Health Quality Ontario: KRAS Testing for Anti-EGFR Therapy in Advanced Colorectal Cancer: An Evidence-Based and Economic Analysis. Ont Health Technol Assess Ser; 2010;10(25):1-49
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] KRAS Testing for Anti-EGFR Therapy in Advanced Colorectal Cancer: An Evidence-Based and Economic Analysis.
  • Within the PEPP, subgroup committees were developed for each disease area.
  • For each technology, an economic analysis was also completed by the Toronto Health Economics and Technology Assessment Collaborative (THETA) and is summarized within the reports.THE FOLLOWING REPORTS CAN BE PUBLICLY ACCESSED AT THE MAS WEBSITE AT: www.health.gov.on.ca/mas or at www.health.gov.on.ca/english/providers/program/mas/mas_about.htmlGENE EXPRESSION PROFILING FOR GUIDING ADJUVANT CHEMOTHERAPY DECISIONS IN WOMEN WITH EARLY BREAST CANCER: An Evidence-Based and Economic AnalysisEpidermal Growth Factor Receptor Mutation (EGFR) Testing for Prediction of Response to EGFR-Targeting Tyrosine Kinase Inhibitor (TKI) Drugs in Patients with Advanced Non-Small-Cell Lung Cancer: an Evidence-Based and Economic AnalysisK-RAS testing in Treatment Decisions for Advanced Colorectal Cancer: an Evidence-Based and Economic Analysis.
  • OBJECTIVE: The objective of this systematic review is to determine the predictive value of KRAS testing in the treatment of metastatic colorectal cancer (mCRC) with two anti-EGFR agents, cetuximab and panitumumab.
  • KRAS (Kristen-RAS, a member of the rat sarcoma virus (ras) gene family of oncogenes) is frequently mutated in epithelial cancers such as colorectal cancer, with mutations occurring in mutational hotspots (codons 12 and 13) of the KRAS protein.
  • Such a mutation is also hypothesized to be involved in resistance to targeted anti-EGFR (epidermal growth factor receptor with tyrosine kinase activity) treatments such as cetuximab and panitumumab, hence, the important in evaluating the evidence on the predictive value of KRAS testing in this context.
  • KRAS MUTATION TESTING IN ADVANCED COLORECTAL CANCER: Both cetuximab and panitumumab are indicated by Health Canada in the treatment of patients with metastatic colorectal cancer whose tumours are WT for the KRAS gene.
  • Cetuximab may be offered as monotherapy in patients intolerant to irinotecan-based chemotherapy or in patients who have failed both irinotecan and oxaliplatin-based regimens and who received a fluoropyrimidine.
  • It can also be administered in combination with irinotecan in patients refractory to other irinotecan-based chemotherapy regimens.
  • Panitumumab is only indicated as a single agent after failure of fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy regimens.
  • In Ontario, patients with advanced colorectal cancer who are refractory to chemotherapy may be offered the targeted anti-EGFR treatments cetuximab or panitumumab.
  • Eligibility for these treatments is based on the KRAS status of their tumour, derived from tissue collected from surgical or biopsy specimens.
  • It is believed that KRAS status is not affected by treatments, therefore, for patients for whom surgical tissue is available for KRAS testing, additional biopsies prior to treatment with these targeted agents is not necessary.
  • For patients that have not undergone surgery or for whom surgical tissue is not available, a biopsy of either the primary or metastatic site is required to determine their KRAS status.
  • RESEARCH QUESTION: To determine if there is predictive value of KRAS testing in guiding treatment decisions with anti-EGFR targeted therapies in advanced colorectal cancer patients refractory to chemotherapy.
  • In total, 14 observational studies were identified for inclusion in this EBA: 4 for cetuximab monotherapy, 7 for the cetuximab-irinotecan combination therapy, and 3 to be included in the review for panitumumab monotherapy INCLUSION CRITERIA: English-language articles, and English or French-language HTAs published from January 2005 to May 2010, inclusive.Randomized controlled trials (RCTs) or observational studies, including single arm treatment studies that include KRAS testing.Studies with data on main outcomes of interest, overall and progression-free survival.Studies of third line treatment with cetuximab or panitumumab in patients with advanced colorectal cancer refractory to chemotherapy.For the cetuximab-irinotecan evaluation, studies in which at least 70% of patients in the study received this combination therapy.
  • CETUXIMAB-IRINOTECAN COMBINATION THERAPY: There is low GRADE evidence that testing for KRAS may optimize survival benefits in patients without the KRAS mutation (KRAS wildtype, or KRAS WT) compared to those with the mutation.
  • However, cetuximab-irinotecan combination treatments based on KRAS status discount any effect of cetuximab in possibly reversing resistance to irinotecan in patients with the mutation, as observed effects were lower than for patients without the mutation.
  • Evaluation of relative cost-effectiveness, based on a decision-analytic cost-utility analysis, assessed testing for KRAS genetic mutations versus no testing in the context of treatment with cetuximab monotherapy, panitumumab monotherapy, cetuximab in combination with irinotecan, and best supportive care.
  • Of importance to note is that the cost-effectiveness analysis focused on the impact of testing for KRAS mutations compared to no testing in the context of different treatment options, and does not assess the cost-effectiveness of the drug treatments alone.
  • CONCLUSIONS: KRAS status is predictive of outcomes in cetuximab and panitumumab monotherapy, and in cetuximab-irinotecan combination therapy.
  • While KRAS testing is cost-effective for all strategies considered, it is not equally cost-effective for all treatment options.

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Br J Cancer. 2008 Jul 8;99(1):83-9 [18577988.001]
  • [Cites] J Clin Oncol. 2008 Sep 1;26(25):4217-9 [18757341.001]
  • [Cites] N Engl J Med. 2008 Oct 23;359(17):1757-65 [18946061.001]
  • [Cites] J Clin Oncol. 2009 Mar 1;27(7):1122-9 [19164213.001]
  • [Cites] Ann Oncol. 2009 May;20(5):879-84 [19179548.001]
  • [Cites] J Clin Oncol. 2009 Apr 20;27(12):2091-6 [19188670.001]
  • [Cites] Clin Cancer Res. 2009 May 1;15(9):3184-8 [19366826.001]
  • [Cites] Br J Cancer. 2009 Apr 21;100(8):1330-5 [19367287.001]
  • [Cites] J Clin Oncol. 2009 Jun 1;27(16):2622-9 [19398573.001]
  • [Cites] Br J Cancer. 2009 Aug 18;101(4):715-21 [19603018.001]
  • [Cites] Curr Oncol. 2010 Jul;17 Suppl 1:S31-40 [20680106.001]
  • [Cites] Clin Colorectal Cancer. 2008 May;7(3):184-90 [18621636.001]
  • [Cites] Clin Cancer Res. 2008 Dec 1;14(23):7884-95 [19047118.001]
  • [Cites] Jpn J Clin Oncol. 2009 May;39(5):321-6 [19287023.001]
  • [Cites] J Natl Cancer Inst. 2009 Sep 2;101(17):1182-92 [19666851.001]
  • [Cites] Int J Technol Assess Health Care. 1994 Fall;10(4):714-5 [7843894.001]
  • [Cites] BMJ. 2004 Jun 19;328(7454):1490 [15205295.001]
  • [Cites] N Engl J Med. 2004 Jul 22;351(4):337-45 [15269313.001]
  • [Cites] BMC Med Res Methodol. 2005;5:13 [15840177.001]
  • [Cites] J Clin Oncol. 2007 May 1;25(13):1658-64 [17470858.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3230-7 [17664471.001]
  • [Cites] Ann Oncol. 2008 Jan;19(1):92-8 [17785764.001]
  • [Cites] N Engl J Med. 2007 Nov 15;357(20):2040-8 [18003960.001]
  • [Cites] Br J Cancer. 2007 Dec 3;97(11):1469-74 [18040272.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10):1626-34 [18316791.001]
  • [Cites] BMC Cancer. 2008;8:169 [18544172.001]
  • (PMID = 23074403.001).
  • [ISSN] 1915-7398
  • [Journal-full-title] Ontario health technology assessment series
  • [ISO-abbreviation] Ont Health Technol Assess Ser
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC3377508
  •  go-up   go-down


8. Ciocca DR, Rozados VR, Cuello Carrión FD, Gervasoni SI, Matar P, Scharovsky OG: Hsp25 and Hsp70 in rodent tumors treated with doxorubicin and lovastatin. Cell Stress Chaperones; 2003;8(1):26-36
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.
  • Heat shock protein 27 (Hsp27) and Hsp70 have been involved in resistance to anticancer drugs in human breast cancer cells growing in vitro and in vivo.
  • In this study, we examined the expression of Hsp25 (the rodent homologue to human Hsp27) and Hsp70 in 3 different rodent tumors (a mouse breast carcinoma, a rat sarcoma, and a rat lymphoma maintained by subcutaneous passages) treated in vivo with doxorubicin (DOX) and lovastatin (LOV).
  • All tumors showed massive cell death under control untreated conditions, and this massive death increased after cytotoxic drug administration.
  • The tumor type that was more resistant to cell death was the sarcoma, and this was found in sarcomas growing both under control conditions and after cytotoxic drug administration.
  • After drug treatment, only sarcoma tumor cells showed a significant increase in Hsp70.
  • In sarcomas, Hsp25 and Hsp70 were found in viable tumor cells located around the blood vessels, and these areas showed the most resistant tumor cell phenotype after chemotherapy.
  • In conclusion, our study shows that each tumor type has unique features regarding the expression of Hsp25 and Hsp70 and that these proteins seem to be implicated in drug resistance mainly in sarcomas, making these model systems important to perform more mechanistic studies on the role of Hsps in resistance to certain cytotoxic drugs.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Fibrosarcoma / metabolism. HSP70 Heat-Shock Proteins / biosynthesis. Heat-Shock Proteins. Mammary Neoplasms, Animal / metabolism. Neoplasm Proteins / biosynthesis
  • [MeSH-minor] Animals. Apoptosis. Doxorubicin / administration & dosage. Drug Resistance, Neoplasm. Endothelium, Vascular / metabolism. Female. HSP27 Heat-Shock Proteins. Lovastatin / administration & dosage. Lymphoma, B-Cell / metabolism. Lymphoma, B-Cell / pathology. Mice. Mice, Inbred Strains. Rats. Rats, Inbred Strains

  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. LOVASTATIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Breast Cancer Res Treat. 1999 Jul;56(2):187-96 [10573111.001]
  • [Cites] Cancer Res. 1999 Sep 1;59(17):4208-12 [10485456.001]
  • [Cites] Cancer Biother Radiopharm. 1998 Oct;13(5):387-93 [10851430.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):7871-6 [10884417.001]
  • [Cites] J Biomed Sci. 2000 Jul-Aug;7(4):292-8 [10895051.001]
  • [Cites] Nat Rev Mol Cell Biol. 2001 Aug;2(8):589-98 [11483992.001]
  • [Cites] Cell Stress Chaperones. 2001 Jan;6(1):49-58 [11525243.001]
  • [Cites] BJU Int. 2001 Sep;88(4):425-31 [11564034.001]
  • [Cites] Prog Mol Subcell Biol. 2002;28:185-204 [11908059.001]
  • [Cites] Prog Mol Subcell Biol. 2002;28:205-18 [11908061.001]
  • [Cites] IARC Sci Publ. 1979;23:43-90 [233006.001]
  • [Cites] Cancer Res. 1989 Aug 1;49(15):4298-304 [2743317.001]
  • [Cites] Cancer. 1989 Sep 1;64(5):1067-73 [2474367.001]
  • [Cites] Cancer Res. 1992 Jul 1;52(13):3648-54 [1617638.001]
  • [Cites] J Natl Cancer Inst. 1993 Apr 7;85(7):570-4 [8455204.001]
  • [Cites] Eur J Cancer. 1996 Jun;32A(6):921-6 [8763333.001]
  • [Cites] Cancer Detect Prev. 1997;21(5):441-51 [9307847.001]
  • [Cites] Clin Cancer Res. 1998 May;4(5):1263-6 [9607585.001]
  • [Cites] Int J Cancer. 1998 Oct 23;79(5):468-75 [9761114.001]
  • [Cites] J Histochem Cytochem. 1999 Jun;47(6):837-9 [10330461.001]
  • [Cites] Clin Exp Metastasis. 1999 Feb;17(1):19-25 [10390143.001]
  • [Cites] Radiat Res. 2000 Feb;153(2):186-95 [10629618.001]
  • (PMID = 12820652.001).
  • [ISSN] 1355-8145
  • [Journal-full-title] Cell stress & chaperones
  • [ISO-abbreviation] Cell Stress Chaperones
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP27 Heat-Shock Proteins; 0 / HSP70 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / Hspb1 protein, mouse; 0 / Hspb1 protein, rat; 0 / Neoplasm Proteins; 80168379AG / Doxorubicin; 9LHU78OQFD / Lovastatin
  • [Other-IDs] NLM/ PMC514851
  •  go-up   go-down


9. Yokota T, Shibata N, Ura T, Takahari D, Shitara K, Muro K, Yatabe Y: Cycleave polymerase chain reaction method is practically applicable for V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)/V-raf murine sarcoma viral oncogene homolog B1 (BRAF) genotyping in colorectal cancer. Transl Res; 2010 Aug;156(2):98-105
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] Cycleave polymerase chain reaction method is practically applicable for V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS)/V-raf murine sarcoma viral oncogene homolog B1 (BRAF) genotyping in colorectal cancer.
  • Activating V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) and V-raf murine sarcoma viral oncogene homolog B1 (BRAF) gene mutations are important predictive markers for antiepidermal growth factor receptor chemotherapy in colorectal cancer (CRC).
  • However, a rapid and accurate assay for KRAS/BRAF mutation detection from routine pathological specimens is lacking in clinical practice.
  • [MeSH-major] Colorectal Neoplasms / genetics. Genes, ras / genetics. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins B-raf / genetics. Sarcoma, Experimental / genetics. ras Proteins / genetics

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Mosby, Inc. All rights reserved.
  • (PMID = 20627194.001).
  • [ISSN] 1878-1810
  • [Journal-full-title] Translational research : the journal of laboratory and clinical medicine
  • [ISO-abbreviation] Transl Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Braf protein, mouse; EC 2.7.11.1 / Braf protein, rat; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


10. van Ijken MG, van Etten B, de Wilt JH, van Tiel ST, ten Hagen TL, Eggermont AM: Tumor necrosis factor-alpha augments tumor effects in isolated hepatic perfusion with melphalan in a rat sarcoma model. J Immunother; 2000 Jul-Aug;23(4):449-55
Hazardous Substances Data Bank. MELPHALAN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Tumor necrosis factor-alpha augments tumor effects in isolated hepatic perfusion with melphalan in a rat sarcoma model.
  • Isolated hepatic perfusion (IHP) is an attractive approach to treating nonresectable liver tumors, because the effects of systemic chemotherapy are poor and its application is hampered by severe general toxicity.
  • In clinical and experimental settings, the efficacy of isolated limb perfusion (ILP) with tumor necrosis factor-alpha (TNF alpha) in combination with melphalan to treat melanoma in transit and soft-tissue sarcoma has been well established.
  • In an ILP model in rats, the authors previously observed synergistic anti-tumor effects of TNF and melphalan on BN 175 soft-tissue sarcoma extremity tumors.
  • The aim of the current study was to determine whether similar synergy in anti-tumor effects could be achieved by treating experimental BN 175 soft-tissue sarcoma liver tumors by IHP using these agents.
  • Thus, as in the rat ILP setting, the anti-tumor effect is augmented when TNF is added to IHP with melphalan to treat BN 175 soft-tissue sarcoma tumor-bearing rats.
  • [MeSH-major] Chemotherapy, Cancer, Regional Perfusion / methods. Liver Neoplasms / drug therapy. Liver Neoplasms / therapy. Melphalan / therapeutic use. Sarcoma, Experimental / drug therapy. Sarcoma, Experimental / therapy. Tumor Necrosis Factor-alpha / administration & dosage
  • [MeSH-minor] Adjuvants, Immunologic / administration & dosage. Animals. Antineoplastic Agents, Alkylating / therapeutic use. Combined Modality Therapy. Liver / blood supply. Male. Rats

  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Immunother. 2000 Jul-Aug;23(4):505-6 [10916761.001]
  • (PMID = 10916754.001).
  • [ISSN] 1524-9557
  • [Journal-full-title] Journal of immunotherapy (Hagerstown, Md. : 1997)
  • [ISO-abbreviation] J. Immunother.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents, Alkylating; 0 / Tumor Necrosis Factor-alpha; Q41OR9510P / Melphalan
  •  go-up   go-down


11. García-Foncillas J, Díaz-Rubio E: Progress in metastatic colorectal cancer: growing role of cetuximab to optimize clinical outcome. Clin Transl Oncol; 2010 Aug;12(8):533-42
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.
  • The prognosis of metastatic colorectal cancer remains poor despite advances made in recent years, particularly with new treatments directed towards molecular targets.
  • There is evidence of the role of cetuximab not only in irinotecan-refractory or heavily pretreated patients, but also of the efficacy and safety of the addition of this agent to FOLFIRI (irinotecan/5-fluorouracil/leucovorin) in first-line metastatic colorectal cancer, with an enhanced effect in 5-fluorouracil patients with Kirsten rat sarcoma (KRAS) wild-type tumours.
  • In these patients, a recent meta-analysis of the pooled Cetuximab Combined with Irinotecan in First-Line Therapy for Metastatic Colorectal Cancer (CRYSTAL) and Oxaliplatin and Cetuximab in First-Line Treatment of mCRC (OPUS) patient populations confirms that the addition of cetuximab to first-line chemotherapy achieves a statistically significant improvement in the best overall response, overall survival time, and progression-free survival (PSF) compared with chemotherapy alone.
  • Also, preliminary data indicate that cetuximab can be administered in a more convenient 2-week schedule in combination with standard chemotherapy.
  • Up to the present time, the results obtained with targeted therapy combinations are not as encouraging as initially expected.
  • Clinical and molecular predictive markers of response are under active evaluation in order to better select patients who could benefit from cetuximab treatment, with the aim of both optimising patient outcomes and avoiding unnecessary toxicities.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Colorectal Neoplasms / pathology. Liver Neoplasms / drug therapy. Liver Neoplasms / secondary
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Antimetabolites, Antineoplastic / administration & dosage. Antineoplastic Agents, Phytogenic / administration & dosage. Biomarkers, Tumor. Camptothecin / administration & dosage. Camptothecin / analogs & derivatives. Camptothecin / therapeutic use. Cetuximab. Fluorouracil / administration & dosage. Fluorouracil / therapeutic use. Humans. Leucovorin / administration & dosage. Leucovorin / therapeutic use. Organoplatinum Compounds / administration & dosage. Organoplatinum Compounds / therapeutic use. Proto-Oncogene Proteins / genetics. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins p21(ras). Receptor, Epidermal Growth Factor / antagonists & inhibitors. Vitamin B Complex / administration & dosage. ras Proteins / genetics. ras Proteins / metabolism

  • Genetic Alliance. consumer health - Colorectal Cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Colorectal Cancer.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • Hazardous Substances Data Bank. CETUXIMAB .
  • Hazardous Substances Data Bank. FLUOROURACIL .
  • Hazardous Substances Data Bank. LEUCOVORIN .
  • 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
  • [Cites] Clin Cancer Res. 2008 Jul 1;14 (13):4219-24 [18594003.001]
  • [Cites] Clin Ther. 2005 Jun;27(6):684-94 [16117976.001]
  • [Cites] Lancet Oncol. 2008 Oct;9(10):962-72 [18804418.001]
  • [Cites] Clin Colorectal Cancer. 2008 Sep;7(5):300-8 [18794061.001]
  • [Cites] J Clin Oncol. 2007 Sep 20;25(27):4224-30 [17548839.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):2013-9 [18421054.001]
  • [Cites] BMC Cancer. 2009 Apr 14;9:112 [19366444.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23 ):2335-42 [15175435.001]
  • [Cites] World J Gastroenterol. 2007 Jul 28;13(28):3806-15 [17657834.001]
  • [Cites] J Clin Oncol. 2006 Nov 1;24(31):4983-90 [17075116.001]
  • [Cites] Ann Oncol. 2008 Jan;19(1):142-9 [17785763.001]
  • [Cites] Br J Cancer. 2007 Apr 23;96(8):1166-9 [17375050.001]
  • [Cites] Oncologist. 2007 Jan;12(1):38-50 [17227899.001]
  • [Cites] Lancet Oncol. 2006 Oct;7(10 ):807-8 [17039634.001]
  • [Cites] J Clin Oncol. 2005 Nov 20;23(33):8512-9 [16260687.001]
  • [Cites] Dis Colon Rectum. 2000 Oct;43(10):1341-6; discussion 1347-8 [11052509.001]
  • [Cites] Clin Ther. 2008 Jan;30(1):14-30 [18343240.001]
  • [Cites] J Clin Oncol. 2008 Apr 1;26(10 ):1626-34 [18316791.001]
  • [Cites] Tumour Biol. 2000 Mar-Apr;21(2):105-15 [10686540.001]
  • [Cites] Oncology. 2009;77(2):124-33 [19622903.001]
  • [Cites] J Clin Oncol. 2007 Aug 1;25(22):3230-7 [17664471.001]
  • [Cites] Ann Surg Oncol. 2007 Feb;14(2):766-70 [17103261.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] J Clin Oncol. 2009 Apr 20;27(12 ):2091-6 [19188670.001]
  • [Cites] Ann Oncol. 1999 Jun;10(6):623-6 [10442182.001]
  • [Cites] Oncologist. 2008 Feb;13(2):113-9 [18305055.001]
  • [Cites] Diagn Cytopathol. 2006 Mar;34(3):191-5 [16470859.001]
  • [Cites] N Engl J Med. 2009 Feb 5;360(6):563-72 [19196673.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):3992-5 [16618717.001]
  • [Cites] Oncologist. 2006 Oct;11(9):981-7 [17030638.001]
  • [Cites] J Clin Oncol. 2008 Jul 20;26(21):3523-9 [18640933.001]
  • [Cites] J Clin Oncol. 2005 Jul 10;23(20):4553-60 [16002847.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):663-71 [19114683.001]
  • [Cites] Oncologist. 2009 May;14 (5):478-88 [19411318.001]
  • [Cites] Clin Colorectal Cancer. 2006 Mar;5(6):422-8 [16635281.001]
  • [Cites] J Clin Oncol. 2007 Sep 20;25(27):4217-23 [17548840.001]
  • [Cites] J Clin Oncol. 2009 Feb 10;27(5):812-26 [19103723.001]
  • [Cites] Ann Oncol. 2007 Jun;18 Suppl 6:vi8-10 [17591840.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3502-8 [15908660.001]
  • [Cites] J Am Coll Surg. 2004 Jun;198(6):884-91 [15194069.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):2006-12 [18421053.001]
  • [Cites] Expert Opin Biol Ther. 2006 Nov;6(11):1229-35 [17049019.001]
  • [Cites] J Clin Oncol. 2004 Apr 15;22(8):1420-9 [15007086.001]
  • [Cites] J Mol Diagn. 2010 Jan;12 (1):43-50 [20007845.001]
  • [Cites] J Clin Oncol. 2009 Mar 1;27(7):1122-9 [19164213.001]
  • [Cites] Virchows Arch. 2008 Nov;453(5):417-31 [18802721.001]
  • [Cites] J Mol Diagn. 2010 Jul;12 (4):425-32 [20431034.001]
  • [Cites] Ann Oncol. 2006 Sep;17 Suppl 10:x122-8 [17018712.001]
  • [Cites] J Nucl Med. 2009 May;50 Suppl 1:43S-54S [19403879.001]
  • [Cites] Ann Oncol. 2005 Mar;16(3):481-8 [15718248.001]
  • [Cites] Hepatobiliary Pancreat Dis Int. 2008 Dec;7(6):569-70 [19073400.001]
  • [Cites] N Engl J Med. 2008 Oct 23;359(17):1757-65 [18946061.001]
  • [Cites] Eur J Cancer. 2000 Apr;36(6):748-53 [10762747.001]
  • [Cites] J Clin Oncol. 2007 Oct 10;25(29):4557-61 [17876013.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2009 Jun;18(6):1688-94 [19505900.001]
  • [Cites] J Clin Oncol. 2008 Nov 20;26(33):5335-43 [18854570.001]
  • [Cites] Br J Cancer. 2006 Mar 27;94(6):792-7 [16508634.001]
  • [Cites] J Clin Oncol. 2004 Jan 15;22(2):229-37 [14657227.001]
  • [Cites] Surgery. 2008 Mar;143(3):384-93 [18291260.001]
  • [Cites] Int J Biol Markers. 1997 Jan-Mar;12(1):18-21 [9176713.001]
  • [Cites] J Clin Oncol. 2006 Oct 20;24(30):4914-21 [17050875.001]
  • [Cites] Br J Cancer. 2006 Mar 27;94(6):798-805 [16508637.001]
  • [Cites] J Clin Oncol. 2007 Apr 20;25(12):1539-44 [17442997.001]
  • [Cites] J Mol Diagn. 2010 Jan;12 (1):35-42 [20007841.001]
  • [Cites] Ann Oncol. 2009 Nov;20(11):1842-7 [19406901.001]
  • [Cites] Cancer Imaging. 2006 Oct 31;6:S71-81 [17114081.001]
  • [Cites] Ann Oncol. 2006 Mar;17 (3):450-6 [16303861.001]
  • [Cites] N Engl J Med. 2004 Jul 22;351(4):337-45 [15269313.001]
  • [Cites] N Engl J Med. 2000 Sep 28;343 (13):905-14 [11006366.001]
  • [Cites] Clin Colorectal Cancer. 2008 Nov;7(6):364-8 [19036688.001]
  • [Cites] World J Gastroenterol. 2007 Nov 28;13(44):5867-76 [17990352.001]
  • [Cites] HPB (Oxford). 2007;9(4):251-8 [18345300.001]
  • [Cites] Mod Pathol. 2009 Aug;22(8):1023-31 [19430420.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):4866-75 [15939922.001]
  • [Cites] Cancer Sci. 2010 May;101(5):1080-8 [20331636.001]
  • [Cites] Oncology (Williston Park). 2006 Sep;20(10):1161-76, 1179; discussion 1179-80, 1185-6 [17024869.001]
  • [Cites] J Clin Oncol. 2003 Jan 1;21(1):60-5 [12506171.001]
  • [Cites] Ann Surg Oncol. 1997 Dec;4(8):613-20 [9416407.001]
  • [Cites] Oncologist. 2009 Jan;14 (1):29-39 [19144681.001]
  • [Cites] Ann Oncol. 2008 Aug;19(8):1442-9 [18441330.001]
  • [Cites] J Clin Oncol. 2004 Jan 1;22(1):23-30 [14665611.001]
  • [Cites] Cancer Cell. 2005 Apr;7(4):301-11 [15837620.001]
  • [Cites] Ann Oncol. 2007 Feb;18(2):305-10 [17079693.001]
  • [Cites] Br J Cancer. 2006 Apr 10;94(7):982-99 [16538219.001]
  • [Cites] Ann Oncol. 2008 Mar;19(3):508-15 [17998284.001]
  • [Cites] Clin Colorectal Cancer. 2006 Jul;6(2):152-6 [16945172.001]
  • [Cites] Clin Biochem. 2009 Mar;42(4-5):353-7 [19101531.001]
  • [Cites] Lancet. 2000 Mar 25;355(9209):1041-7 [10744089.001]
  • [Cites] Oncology. 2009;77(2):113-9 [19628950.001]
  • [Cites] Biologics. 2007 Jun;1(2):77-91 [19707318.001]
  • [Cites] Ann Surg Oncol. 1996 Sep;3(5):453-63 [8876887.001]
  • [Cites] J Clin Oncol. 2008 May 10;26(14 ):2311-9 [18390971.001]
  • [Cites] Ann Surg. 2009 Mar;249(3):420-5 [19247029.001]
  • [Cites] Ann Surg Oncol. 2006 Jan;13(1):58-65 [16372158.001]
  • [Cites] J Clin Oncol. 2009 Apr 10;27(11):1822-8 [19273701.001]
  • [Cites] Int J Colorectal Dis. 2009 Jun;24(6):677-85 [19184059.001]
  • [Cites] Cancer. 2004 Nov 15;101(10 ):2170-6 [15470715.001]
  • [Cites] Ann Surg Oncol. 2008 Sep;15(9):2458-64 [18463927.001]
  • [Cites] Cancer Res. 2007 Mar 15;67(6):2643-8 [17363584.001]
  • [Cites] Br J Cancer. 2004 Mar 22;90(6):1190-7 [15026800.001]
  • [Cites] N Engl J Med. 2009 Apr 2;360(14):1408-17 [19339720.001]
  • [Cites] Ann Oncol. 2008 Oct;19(10 ):1720-6 [18550577.001]
  • [Cites] Eur J Radiol. 2006 May;58(2):229-35 [16457980.001]
  • [Cites] J Clin Oncol. 2008 Jan 20;26(3):374-9 [18202412.001]
  • [Cites] Eur J Gastroenterol Hepatol. 2009 Jan;21(1):92-100 [19011574.001]
  • [Cites] Am J Clin Pathol. 2008 Aug;130(2):247-53 [18628094.001]
  • [Cites] J Clin Oncol. 2000 Aug;18(16):2938-47 [10944126.001]
  • [Cites] J Clin Oncol. 2004 Apr 1;22(7):1201-8 [14993230.001]
  • [Cites] J Cancer Res Ther. 2009 Oct-Dec;5(4):272-6 [20160361.001]
  • [Cites] Dig Surg. 2008;25(6):413-20 [19212113.001]
  • (PMID = 20709651.001).
  • [ISSN] 1699-3055
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Organoplatinum Compounds; 0 / Proto-Oncogene Proteins; 04ZR38536J / oxaliplatin; 0H43101T0J / irinotecan; 12001-76-2 / Vitamin B Complex; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / Proto-Oncogene Proteins p21(ras); EC 3.6.5.2 / ras Proteins; PQX0D8J21J / Cetuximab; Q573I9DVLP / Leucovorin; U3P01618RT / Fluorouracil; XT3Z54Z28A / Camptothecin; Folfox protocol; IFL protocol
  •  go-up   go-down


12. Cappellacci L, Franchetti P, Vita P, Petrelli R, Grifantini M: Synthesis and antitumor activity of a heterodinucleotide of BVDU and gemcitabine. Nucleosides Nucleotides Nucleic Acids; 2008 May;27(5):460-8
Hazardous Substances Data Bank. BROMODEOXYURIDINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A heterodinucleotide comprising BVDU and Gemcitabine bound together by a 5',5'-pyrophospate bridge (BVDUp(2)dFdC) has been synthesized and evaluated as antitumor agent against AH13 rat sarcoma cells.
  • [MeSH-minor] Animals. Antiviral Agents / chemical synthesis. Antiviral Agents / chemistry. Antiviral Agents / pharmacology. Cell Line, Tumor. Drug Screening Assays, Antitumor. Rats. Sarcoma, Experimental / drug therapy

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18569785.001).
  • [ISSN] 1525-7770
  • [Journal-full-title] Nucleosides, nucleotides & nucleic acids
  • [ISO-abbreviation] Nucleosides Nucleotides Nucleic Acids
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antiviral Agents; 0W860991D6 / Deoxycytidine; 2M3055079H / brivudine; B76N6SBZ8R / gemcitabine; G34N38R2N1 / Bromodeoxyuridine
  •  go-up   go-down


13. Durrleman N, El Hamamsy I, Demaria R, Carrier M, Perrault LP, Albat B: [Is Dacron carcinogenic? Apropos of a case and review of the literature]. Arch Mal Coeur Vaiss; 2004 Mar;97(3):267-70

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Malignant lymphoma is a haematological form of sarcoma.
  • Survival after "pure" medical therapy (chemotherapy alone or associated with radiotherapy) is 6 to 8 months after diagnosis.
  • Dacron has been implicated in the pathogenesis of primary cardiac sarcoma.
  • Oppenheimer demonstrated experimental induction of sarcoma in the rat by subcutaneous implantation of polymers.
  • [MeSH-minor] Abdominal Neoplasms / drug therapy. Abdominal Neoplasms / secondary. Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Asthenia / etiology. Diagnostic Errors. Fatal Outcome. Female. Humans. Mitral Valve / surgery. Multiple Organ Failure / etiology. Myxoma / diagnosis. Sarcoma / chemically induced. Thrombosis / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15106752.001).
  • [ISSN] 0003-9683
  • [Journal-full-title] Archives des maladies du coeur et des vaisseaux
  • [ISO-abbreviation] Arch Mal Coeur Vaiss
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Polyethylene Terephthalates
  • [Number-of-references] 10
  •  go-up   go-down


14. Miller PD: Safety of parathyroid hormone for the treatment of osteoporosis. Curr Osteoporos Rep; 2008 Mar;6(1):12-6
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] Safety of parathyroid hormone for the treatment of osteoporosis.
  • Teriparatide (recombinant human 1-34 parathyroid hormone) has been registered for the treatment of postmenopausal osteoporosis and osteoporosis in men for more than 5 years, whereas 1-84 parathyroid hormone has just recently been registered in Europe for osteoporosis management.
  • The issues to be considered are the effects of the registered dose of teriparatide (20 microg/day) on the incidence of hypercalcemia, hypercalciuria, and hyperuricemia, and the US Food and Drug Administration's "black-box" warning regarding osteogenic sarcoma in the rat model.
  • [MeSH-major] Bone Density Conservation Agents / adverse effects. Osteoporosis / drug therapy. Parathyroid Hormone / adverse effects. Teriparatide / adverse effects
  • [MeSH-minor] Animals. Bone Neoplasms / chemically induced. Disease Models, Animal. Dose-Response Relationship, Drug. Humans. Osteosarcoma / chemically induced. Rats. Rats, Inbred F344

  • Genetic Alliance. consumer health - Osteoporosis.
  • MedlinePlus Health Information. consumer health - Osteoporosis.
  • Hazardous Substances Data Bank. TERIPARATIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Osteoporos Int. 2006 Jan;17(1):85-90 [15981021.001]
  • [Cites] J Bone Miner Res. 2007 Feb;22(2):334 [17129179.001]
  • [Cites] N Engl J Med. 2007 Jul 19;357(3):266-81 [17634462.001]
  • [Cites] Toxicol Pathol. 2002 May-Jun;30(3):312-21 [12051548.001]
  • [Cites] J Rheumatol. 2005 Aug;32(8):1556-62 [16078334.001]
  • [Cites] Clin Orthop Relat Res. 2007 Jun;459:40-7 [17414166.001]
  • [Cites] Am J Med. 1982 Jan;72(1):25-32 [6277190.001]
  • [Cites] J Am Soc Nephrol. 1998 May;9(5):917-24 [9596092.001]
  • [Cites] J Clin Endocrinol Metab. 2005 Jul;90(7):3970-7 [15840739.001]
  • [Cites] J Bone Miner Res. 2003 Jan;18(1):9-17 [12510800.001]
  • [Cites] J Bone Miner Res. 2006 Nov;21(11):1785-90 [17002571.001]
  • [Cites] J Bone Miner Res. 2005 Jun;20(6):962-70 [15883636.001]
  • [Cites] Kidney Int Suppl. 1999 Dec;73:S14-9 [10633458.001]
  • [Cites] J Bone Miner Res. 2002 Oct;17(10):1741-3 [12369776.001]
  • [Cites] J Bone Miner Res. 2001 Oct;16(10):1846-53 [11585349.001]
  • [Cites] Endocr Rev. 2005 Aug;26(5):688-703 [15769903.001]
  • [Cites] Osteoporos Int. 1999;9(1):13-8 [10367024.001]
  • [Cites] J Bone Miner Res. 2003 Nov;18(11):1932-41 [14606504.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1991 Jul;21(2):361-7 [1648044.001]
  • [Cites] Osteoporos Int. 2006 Feb;17(2):273-80 [16142502.001]
  • [Cites] N Engl J Med. 2007 Aug 30;357(9):905-16 [17761594.001]
  • [Cites] Cancer. 2005 Aug 15;104(4):856-63 [15981282.001]
  • [Cites] Arch Intern Med. 2005 Aug 8-22;165(15):1762-8 [16087825.001]
  • [Cites] J Bone Miner Res. 2003 Mar;18(3):539-43 [12619939.001]
  • [Cites] J Bone Miner Res. 2006 Mar;21(3):354-65 [16491282.001]
  • [Cites] J Clin Endocrinol Metab. 2007 Sep;92(9):3535-41 [17609307.001]
  • [Cites] J Bone Miner Res. 2007 Aug;22(8):1173-80 [17451369.001]
  • [Cites] Endocr Pract. 2004 Mar-Apr;10(2):139-48 [15256332.001]
  • [Cites] N Engl J Med. 2001 May 10;344(19):1434-41 [11346808.001]
  • [Cites] J Steroid Biochem Mol Biol. 2005 Oct;97(1-2):13-9 [16026981.001]
  • [Cites] N Engl J Med. 2007 Nov 15;357(20):2028-39 [18003959.001]
  • [Cites] N Engl J Med. 1995 Jul 20;333(3):166-74 [7791820.001]
  • [Cites] Toxicol Pathol. 2004 Jul-Aug;32(4):426-38 [15204966.001]
  • [Cites] J Bone Joint Surg Br. 2007 Jun;89(6):808-13 [17613509.001]
  • [Cites] Curr Med Res Opin. 2005 Jul;21(7):1027-34 [16004669.001]
  • (PMID = 18430395.001).
  • [ISSN] 1544-2241
  • [Journal-full-title] Current osteoporosis reports
  • [ISO-abbreviation] Curr Osteoporos Rep
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bone Density Conservation Agents; 0 / Parathyroid Hormone; 10T9CSU89I / Teriparatide
  • [Number-of-references] 41
  •  go-up   go-down


15. Mordant P, Loriot Y, Leteur C, Calderaro J, Bourhis J, Wislez M, Soria JC, Deutsch E: Dependence on phosphoinositide 3-kinase and RAS-RAF pathways drive the activity of RAF265, a novel RAF/VEGFR2 inhibitor, and RAD001 (Everolimus) in combination. Mol Cancer Ther; 2010 Feb;9(2):358-68
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Activation of phosphatidylinositol-3-kinase (PI3K)-AKT and Kirsten rat sarcoma viral oncogene homologue (KRAS) can induce cellular immortalization, proliferation, and resistance to anticancer therapeutics such as epidermal growth factor receptor inhibitors or chemotherapy.
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Eukaryotic Initiation Factor-4E / metabolism. Everolimus. Genes, ras. Humans. Immunosuppressive Agents / pharmacology. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mutation. Protein-Serine-Threonine Kinases / metabolism. TOR Serine-Threonine Kinases

  • Hazardous Substances Data Bank. SIROLIMUS .
  • 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 .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20124452.001).
  • [ISSN] 1538-8514
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Eukaryotic Initiation Factor-4E; 0 / Immunosuppressive Agents; 0 / Intracellular Signaling Peptides and Proteins; 9HW64Q8G6G / Everolimus; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-raf; EC 3.6.5.2 / ras Proteins; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


16. Beganovic S: Clinical significance of the KRAS mutation. Bosn J Basic Med Sci; 2009 Oct;9 Suppl 1:17-20
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.
  • Physicians now have the opportunity to use specific biomarkers to personalize therapeutic options in various settings.
  • Recent research has demonstrated that presence of Kirsten rat sarcoma viral oncogene homolog (KRAS) mutation may directly influence medical decisions in patients with colon and lung cancer.
  • Use of KRAS oncogene as a selection marker for specific treatment is a good example of individualized medicine approach to cancer treatment.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19912113.001).
  • [ISSN] 1512-8601
  • [Journal-full-title] Bosnian journal of basic medical sciences
  • [ISO-abbreviation] Bosn J Basic Med Sci
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Bosnia and Herzegovina
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 2S9ZZM9Q9V / Bevacizumab; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


17. Legrier ME, Yang CP, Yan HG, Lopez-Barcons L, Keller SM, Pérez-Soler R, Horwitz SB, McDaid HM: Targeting protein translation in human non small cell lung cancer via combined MEK and mammalian target of rapamycin suppression. Cancer Res; 2007 Dec 1;67(23):11300-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Lung cancer is a genetically heterogeneous disease characterized by the acquisition of somatic mutations in numerous protein kinases, including components of the rat sarcoma viral oncogene homolog (RAS) and AKT signaling cascades.
  • These pathways intersect at various points, rendering this network highly redundant and suggesting that combined mitogen-activated protein/extracellular signal-regulated kinase (MEK) and mammalian target of rapamycin (mTOR) inhibition may be a promising drug combination that can overcome its intrinsic plasticity.
  • Furthermore, the combination of PD0325901 and rapamycin was significantly superior to either drug alone or PD0325901 at the maximum tolerated dose in nude mice bearing human lung tumor xenografts or heterotransplants.
  • These data (a) provide evidence that both pathways converge on factors that regulate translation initiation and (b) support therapeutic strategies in lung cancer that simultaneously suppress the RAS and AKT signaling network.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Peptide Chain Initiation, Translational / drug effects. Protein Kinases / chemistry
  • [MeSH-minor] Animals. Benzamides / pharmacology. Cell Death / drug effects. Cell Proliferation / drug effects. Diphenylamine / analogs & derivatives. Diphenylamine / pharmacology. Drug Synergism. Drug Therapy, Combination. Feedback, Physiological. Humans. Immunoblotting. Immunosuppressive Agents / pharmacology. Mice. Mice, Nude. PTEN Phosphohydrolase. Proto-Oncogene Proteins c-akt / metabolism. Signal Transduction. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

  • 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.
  • Hazardous Substances Data Bank. N,N-DIPHENYLAMINE .
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18056456.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA077263; United States / NCI NIH HHS / CA / CA083185
  • [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 / Benzamides; 0 / Immunosuppressive Agents; 0 / PD 0325901; 9N3CBB0BIQ / Diphenylamine; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.1.1 / mTOR protein, rat; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; W36ZG6FT64 / Sirolimus
  •  go-up   go-down


18. da Cunha Santos G, Dhani N, Tu D, Chin K, Ludkovski O, Kamel-Reid S, Squire J, Parulekar W, Moore MJ, Tsao MS: Molecular predictors of outcome in a phase 3 study of gemcitabine and erlotinib therapy in patients with advanced pancreatic cancer: National Cancer Institute of Canada Clinical Trials Group Study PA.3. Cancer; 2010 Dec 15;116(24):5599-607
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] Molecular predictors of outcome in a phase 3 study of gemcitabine and erlotinib therapy in patients with advanced pancreatic cancer: National Cancer Institute of Canada Clinical Trials Group Study PA.3.
  • Mutation status of the v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) and EGFR gene copy number (GCN) were evaluated as predictive markers in 26% of patients who had tumor samples available for analysis.
  • The hazard ratio of death between gemcitabine/erlotinib and gemcitabine/placebo was 0.66 (95% confidence interval [CI], 0.28-1.57) for patients with wild-type KRAS and 1.07 (95% CI, 0.68-1.66) for patients with mutant KRAS (P value for interaction = .38), and the hazard ratio was 0.6 (95% CI, 0.34-1.07) for FISH-negative patients and 0.90 (95% CI, 0.49-1.65) for FISH-positive patients (P value for interaction = .32).
  • CONCLUSIONS: In a molecular subset analysis of patients from NCIC CTG PA.3, EGFR GCN and KRAS mutation status were not identified as markers predictive of a survival benefit from the combination of erlotinib with gemcitabine for the first-line treatment of APC.
  • [MeSH-major] Biomarkers, Tumor / analysis. Deoxycytidine / analogs & derivatives. Pancreatic Neoplasms / drug therapy. Quinazolines / administration & dosage
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Canada. Disease-Free Survival. Erlotinib Hydrochloride. Gene Dosage. Humans. Mutation. Predictive Value of Tests. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics. Treatment Outcome. ras Proteins / analysis. ras Proteins / genetics

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • Genetic Alliance. consumer health - Pancreatic cancer 3.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 American Cancer Society.
  • (PMID = 20824720.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


19. Simó S, Pujadas L, Segura MF, La Torre A, Del Río JA, Ureña JM, Comella JX, Soriano E: Reelin induces the detachment of postnatal subventricular zone cells and the expression of the Egr-1 through Erk1/2 activation. Cereb Cortex; 2007 Feb;17(2):294-303
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.
  • Although rat sarcoma viral oncogene was weakly activated upon Reelin treatment, pharmacological inhibition of the PI3K pathway blocked Reelin-dependent ERK activation, which indicates cross talk between the ERK and PI3K pathways.
  • [MeSH-major] Cell Adhesion / physiology. Cell Adhesion Molecules, Neuronal / pharmacology. Cell Movement / physiology. Cerebral Ventricles / physiology. Early Growth Response Protein 1 / metabolism. Extracellular Matrix Proteins / pharmacology. Extracellular Signal-Regulated MAP Kinases / metabolism. Nerve Tissue Proteins / pharmacology. Neurons / physiology. Serine Endopeptidases / pharmacology
  • [MeSH-minor] Animals. Animals, Newborn. Cells, Cultured. Enzyme Activation. Gene Expression / drug effects. Gene Expression / physiology. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / physiology. Mice

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16514107.001).
  • [ISSN] 1047-3211
  • [Journal-full-title] Cerebral cortex (New York, N.Y. : 1991)
  • [ISO-abbreviation] Cereb. Cortex
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules, Neuronal; 0 / Early Growth Response Protein 1; 0 / Egr1 protein, mouse; 0 / Extracellular Matrix Proteins; 0 / Nerve Tissue Proteins; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / reelin protein
  •  go-up   go-down


20. Rozados VR, Sánchez AM, Gervasoni SI, Berra HH, Matar P, Graciela Scharovsky O: Metronomic therapy with cyclophosphamide induces rat lymphoma and sarcoma regression, and is devoid of toxicity. Ann Oncol; 2004 Oct;15(10):1543-50
Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Metronomic therapy with cyclophosphamide induces rat lymphoma and sarcoma regression, and is devoid of toxicity.
  • BACKGROUND: Our aim was to investigate the clinical efficacy and toxicity of metronomic administration of low-dose cyclophosphamide (Cy) in lymphoma and sarcoma rat tumour models.
  • METHODS: Adult inbred rats were challenged with lymphoma TACB and sarcoma E100 s.c. on day 0.
  • Animals were divided into two groups: group I, control, injected with saline three times a week; and group II, treated with Cy 10 mg/kg three times a week, from day 10 until the tumour was non-palpable, or 5 mg/kg three times a week from day 7.
  • RESULTS: The administration of low-dose Cy eradicated established rat lymphomas and sarcomas; there was neither metastatic growth nor recurrence at primary sites for 100% of the lymphomas and 83% of the sarcomas.
  • In addition, the treatment did not cause weight loss, and was devoid of haematological, cardiac, hepatic and renal toxicity.
  • CONCLUSIONS: Metronomic administration of Cy at low doses on a thrice weekly schedule to already grown rat lymphomas and sarcomas demonstrated itself to be a successful antitumour therapy that did not cause weight loss and was devoid of haematological, cardiac, hepatic and renal toxicity.

  • MedlinePlus Health Information. consumer health - Lymphoma.
  • MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Ann Oncol. 2005 Apr;16(4):673 [15716290.001]
  • (PMID = 15367416.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 8N3DW7272P / Cyclophosphamide
  •  go-up   go-down


21. Al-Jamal KT, Al-Jamal WT, Akerman S, Podesta JE, Yilmazer A, Turton JA, Bianco A, Vargesson N, Kanthou C, Florence AT, Tozer GM, Kostarelos K: Systemic antiangiogenic activity of cationic poly-L-lysine dendrimer delays tumor growth. Proc Natl Acad Sci U S A; 2010 Mar 02;107(9):3966-71
NCI caNanoLab Data Portal. supplemental materials - caNanoLab samples curated from the publication .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The PLL-dendrimer-inhibited tubule formation of SVEC4-10 murine endothelial cells and neovascularization in the chick embryo chick chorioallantoic membrane (CAM) assay.
  • Reduced vascularization of P22 rat sarcoma implanted in the dorsal window chamber of SCID mice was observed following tail vein administration (i.v.) of the PLL dendrimers.
  • Enhanced apoptosis/necrosis within tumors of PLL-dendrimer-treated animals only and reduction in the number of CD31 positive cells were observed in comparison to protamine treatment.
  • This study suggests that PLL-dendrimer molecules can exhibit a systemic antiangiogenic activity that may be used for therapy of solid tumors, and in combination with their capacity to carry other therapeutic or diagnostic agents may potentially offer capabilities for the design of theranostic systems.
  • [MeSH-major] Angiogenesis Inhibitors / pharmacology. Cell Division / drug effects. Dendrimers. Neoplasms, Experimental / pathology. Polylysine / pharmacology

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Anticancer Drugs. 1999 Sep;10(8):767-76 [10573209.001]
  • [Cites] Mol Pharm. 2009 Sep-Oct;6(5):1562-72 [19588994.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2001 Jun;21(6):943-8 [11397701.001]
  • [Cites] Bioorg Med Chem Lett. 2002 Mar 25;12(6):951-4 [11959001.001]
  • [Cites] Acad Radiol. 2002 Aug;9 Suppl 2:S511-3 [12188324.001]
  • [Cites] J Am Chem Soc. 2002 Nov 27;124(47):14137-46 [12440912.001]
  • [Cites] Cancer Res. 2002 Dec 1;62(23):6831-6 [12460895.001]
  • [Cites] Am J Physiol Heart Circ Physiol. 2003 Jan;284(1):H215-24 [12388259.001]
  • [Cites] Mol Cancer Ther. 2003 Apr;2(4):419-26 [12700286.001]
  • [Cites] Int J Cancer. 2003 Jun 20;105(3):419-29 [12704680.001]
  • [Cites] Methods Find Exp Clin Pharmacol. 2003 Apr;25(3):215-24 [12743627.001]
  • [Cites] Cancer Biol Ther. 2003 Jul-Aug;2(4 Suppl 1):S127-33 [14508090.001]
  • [Cites] Clin Cancer Res. 2004 Mar 15;10(6):2179-89 [15041739.001]
  • [Cites] N Engl J Med. 2004 Jun 3;350(23):2335-42 [15175435.001]
  • [Cites] Nat Biotechnol. 2004 Aug;22(8):977-84 [15258595.001]
  • [Cites] Exp Eye Res. 2004 Oct;79(4):525-35 [15381036.001]
  • [Cites] Ann Surg. 1972 Mar;175(3):409-16 [5077799.001]
  • [Cites] J Exp Med. 1980 Oct 1;152(4):931-44 [7420025.001]
  • [Cites] Nature. 1982 May 27;297(5864):307-12 [6176876.001]
  • [Cites] Science. 1987 Jan 23;235(4787):442-7 [2432664.001]
  • [Cites] J Invest Dermatol. 1989 Aug;93(2 Suppl):59S-61S [2754280.001]
  • [Cites] Cancer Res. 1992 Dec 1;52(23):6553-60 [1384965.001]
  • [Cites] Lab Invest. 1992 Oct;67(4):519-28 [1279270.001]
  • [Cites] N Engl J Med. 1995 Dec 28;333(26):1757-63 [7491141.001]
  • [Cites] Am J Pathol. 1996 Jul;149(1):59-71 [8686763.001]
  • [Cites] Angiogenesis. 2004;7(2):133-41 [15516834.001]
  • [Cites] Adv Drug Deliv Rev. 2005 Jan 2;57(1):135-52 [15518926.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5317-24 [15958579.001]
  • [Cites] Gene Ther. 2005 Nov;12(21):1544-50 [16034458.001]
  • [Cites] Adv Drug Deliv Rev. 2005 Dec 14;57(15):2177-202 [16310284.001]
  • [Cites] Mol Pharm. 2006 Sep-Oct;3(5):614-27 [17009860.001]
  • [Cites] J Drug Target. 2006 Jul;14(6):405-12 [17092840.001]
  • [Cites] J Control Release. 2006 Dec 1;116(3):330-6 [17118476.001]
  • [Cites] Biochem Soc Trans. 2007 Feb;35(Pt 1):61-7 [17233602.001]
  • [Cites] Nat Rev Drug Discov. 2007 Apr;6(4):273-86 [17396134.001]
  • [Cites] Clin Cancer Res. 2007 Jun 1;13(11):3395-402 [17545548.001]
  • [Cites] Mol Cancer Ther. 2008 Dec;7(12):3670-84 [19074844.001]
  • [Cites] Mol Pharm. 2009 Jul-Aug;6(4):1190-204 [19453158.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):505-15 [10688871.001]
  • (PMID = 20150514.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] eng
  • [Grant] United Kingdom / Cancer Research UK / / 9993
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Cations; 0 / Dendrimers; 25104-18-1 / Polylysine
  • [Other-IDs] NLM/ PMC2840079
  •  go-up   go-down


22. Tozer GM, Prise VE, Lewis G, Xie S, Wilson I, Hill SA: Nitric oxide synthase inhibition enhances the tumor vascular-damaging effects of combretastatin a-4 3-o-phosphate at clinically relevant doses. Clin Cancer Res; 2009 Jun 01;15(11):3781-90
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: The therapeutic potential of combining the prototype tumor vascular-disrupting agent combretastatin A-4 3-O-phosphate (CA-4-P) with systemic nitric oxide synthase (NOS) inhibition was investigated preclinically.
  • RESULTS: Inducible NOS selective inhibitors had no effect on blood flow in the P22 rat sarcoma.
  • In contrast, the non-isoform-specific NOS inhibitor N(omega)-nitro- l-arginine (l-NNA; 1 and 10 mg/kg i.v. or chronic 0.1 or 0.3 mg/mL in drinking water) decreased the P22 blood flow rate selectively down to 36% of control at 1 hour but did not induce tumor necrosis at 24 hours.
  • Bolus l-NNA given 3 hours after CA-4-P was the most effective cytotoxic schedule in the CaNT mouse mammary carcinoma, implicating a particular enhancement by l-NNA of the downstream consequences of CA-4-P treatment.
  • Repeated dosing of l-NNA with CA-4-P produced enhanced growth delay over either treatment alone in P22, CaNT, and spontaneous T138 mouse mammary tumors, which represented a true therapeutic enhancement.
  • CONCLUSIONS: The combination of NOS inhibition with CA-4-P is a promising approach for targeting tumor vasculature, with relevance for similar vascular-disrupting agents in development.
  • [MeSH-major] Blood Vessels / drug effects. Nitric Oxide Synthase / antagonists & inhibitors. Sarcoma, Experimental / drug therapy. Stilbenes / pharmacology
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Blood Flow Velocity / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Enzyme Inhibitors / administration & dosage. Enzyme Inhibitors / pharmacology. Male. Nitroarginine / administration & dosage. Nitroarginine / pharmacology. Rats. Rats, Inbred Strains. Time Factors. Tumor Burden / drug effects

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19470729.001).
  • [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 Kingdom / Cancer Research UK / / 9993; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Enzyme Inhibitors; 0 / Stilbenes; 2149-70-4 / Nitroarginine; EC 1.14.13.39 / Nitric Oxide Synthase; I5590ES2QZ / fosbretabulin
  •  go-up   go-down


23. Puhlmann M, Brown CK, Gnant M, Huang J, Libutti SK, Alexander HR, Bartlett DL: Vaccinia as a vector for tumor-directed gene therapy: biodistribution of a thymidine kinase-deleted mutant. Cancer Gene Ther; 2000 Jan;7(1):66-73
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] Vaccinia as a vector for tumor-directed gene therapy: biodistribution of a thymidine kinase-deleted mutant.
  • Tumor-directed gene therapy, such as "suicide gene" therapy, requires high levels of gene expression in a high percentage of tumor cells in vivo to be effective.
  • This report introduces the attenuated (thymidine kinase (TK)-negative) replication-competent vaccinia virus (VV) as a potential vector for tumor-directed gene therapy by studying the biodistribution of VV in animal tumor models.
  • Three other in vivo tumor models were examined for tumor-specific gene expression after intravenous delivery of VV (human melanoma in nude mice, adenocarcinoma liver metastasis in immunocompetent mice, and subcutaneous sarcoma in the rat).
  • [MeSH-major] Genetic Therapy. Genetic Vectors / genetics. Neoplasms, Experimental / therapy. Thymidine Kinase / genetics. Vaccinia virus / genetics
  • [MeSH-minor] Animals. Biomarkers, Tumor. Disease Models, Animal. Ficusin / pharmacology. Gene Expression / drug effects. Gene Expression / radiation effects. HT29 Cells. Humans. Luciferases / biosynthesis. Mice. Mice, Inbred C57BL. Mice, Nude. Mutation. Photosensitizing Agents / pharmacology. Rats. Rats, Inbred F344. Transfection / drug effects. Transfection / radiation effects. Tumor Cells, Cultured. Ultraviolet Rays. Virus Replication

  • MedlinePlus Health Information. consumer health - Genes and Gene Therapy.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. PSORALEN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 10678358.001).
  • [ISSN] 0929-1903
  • [Journal-full-title] Cancer gene therapy
  • [ISO-abbreviation] Cancer Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Photosensitizing Agents; EC 1.13.12.- / Luciferases; EC 2.7.1.21 / Thymidine Kinase; KTZ7ZCN2EX / Ficusin
  •  go-up   go-down


24. Sos ML, Michel K, Zander T, Weiss J, Frommolt P, Peifer M, Li D, Ullrich R, Koker M, Fischer F, Shimamura T, Rauh D, Mermel C, Fischer S, Stückrath I, Heynck S, Beroukhim R, Lin W, Winckler W, Shah K, LaFramboise T, Moriarty WF, Hanna M, Tolosi L, Rahnenführer J, Verhaak R, Chiang D, Getz G, Hellmich M, Wolf J, Girard L, Peyton M, Weir BA, Chen TH, Greulich H, Barretina J, Shapiro GI, Garraway LA, Gazdar AF, Minna JD, Meyerson M, Wong KK, Thomas RK: Predicting drug susceptibility of non-small cell lung cancers based on genetic lesions. J Clin Invest; 2009 Jun;119(6):1727-40
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] Predicting drug susceptibility of non-small cell lung cancers based on genetic lesions.
  • Somatic genetic alterations in cancers have been linked with response to targeted therapeutics by creation of specific dependency on activated oncogenic signaling pathways.
  • However, no tools currently exist to systematically connect such genetic lesions to therapeutic vulnerability.
  • We have therefore developed a genomics approach to identify lesions associated with therapeutically relevant oncogene dependency.
  • Using cell-based compound screening coupled with diverse computational approaches to integrate orthogonal genomic and biochemical data sets, we identified molecular and genomic predictors of therapeutic response to clinically relevant compounds.
  • Using this approach, we showed that v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations confer enhanced Hsp90 dependency and validated this finding in mice with KRAS-driven lung adenocarcinoma, as these mice exhibited dramatic tumor regression when treated with an Hsp90 inhibitor.
  • In addition, we found that cells with copy number enhancement of v-abl Abelson murine leukemia viral oncogene homolog 2 (ABL2) and ephrin receptor kinase and v-src sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (avian) (SRC) kinase family genes were exquisitely sensitive to treatment with the SRC/ABL inhibitor dasatinib, both in vitro and when it xenografted into mice.
  • Thus, genomically annotated cell-line collections may help translate cancer genomics information into clinical practice by defining critical pathway dependencies amenable to therapeutic inhibition.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Evaluation, Preclinical. Gene Expression Profiling. Humans. Magnetic Resonance Imaging. Mice. Models, Molecular. Mutation / genetics. Phenotype. Protein Structure, Tertiary. Receptor, Epidermal Growth Factor / chemistry. Receptor, Epidermal Growth Factor / genetics. Receptor, Epidermal Growth Factor / metabolism. Substrate Specificity

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • 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
  • [Cites] Cancer Res. 2006 Jul 1;66(13):6487-91 [16818618.001]
  • [Cites] Clin Lung Cancer. 2006 Jul;8(1):30-8 [16870043.001]
  • [Cites] Nat Rev Cancer. 2006 Oct;6(10):813-23 [16990858.001]
  • [Cites] J Biol Chem. 2006 Nov 3;281(44):33577-87 [16928683.001]
  • [Cites] BMC Genomics. 2006;7:289 [17096850.001]
  • [Cites] Cancer Cell. 2006 Dec;10(6):515-27 [17157791.001]
  • [Cites] N Engl J Med. 2006 Dec 28;355(26):2733-43 [17192538.001]
  • [Cites] PLoS Med. 2006 Dec;3(12):e467 [17194181.001]
  • [Cites] J Clin Invest. 2007 Feb;117(2):346-52 [17256054.001]
  • [Cites] J Clin Oncol. 2007 Feb 10;25(5):587-95 [17290067.001]
  • [Cites] Nat Rev Cancer. 2007 Mar;7(3):169-81 [17318210.001]
  • [Cites] Nat Genet. 2007 Mar;39(3):347-51 [17293865.001]
  • [Cites] Oncogene. 2007 Mar 1;26(10):1499-506 [16936777.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):217-27 [17349580.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):621-3 [15870427.001]
  • [Cites] J Natl Cancer Inst. 2005 May 4;97(9):643-55 [15870435.001]
  • [Cites] PLoS Med. 2005 Jan;2(1):e17 [15696205.001]
  • [Cites] PLoS Med. 2005 Mar;2(3):e73 [15737014.001]
  • [Cites] N Engl J Med. 2005 Jul 14;353(2):133-44 [16014883.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6401-8 [16024644.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11011-6 [16046538.001]
  • [Cites] J Clin Oncol. 2005 Sep 1;23(25):5900-9 [16043828.001]
  • [Cites] Genes Chromosomes Cancer. 2005 Nov;44(3):320-8 [16075462.001]
  • [Cites] J Clin Oncol. 2005 Oct 1;23(28):6838-45 [15998906.001]
  • [Cites] Cancer Cell. 2005 Nov;8(5):381-92 [16286246.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 3;103(1):57-62 [16371460.001]
  • [Cites] Br J Haematol. 2006 Feb;132(3):303-16 [16409295.001]
  • [Cites] Nature. 2006 Jan 19;439(7074):358-62 [16273091.001]
  • [Cites] BMC Bioinformatics. 2008;9:475 [19014471.001]
  • [Cites] Trends Cell Biol. 2000 Apr;10(4):147-54 [10740269.001]
  • [Cites] N Engl J Med. 2001 Mar 15;344(11):783-92 [11248153.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1031-7 [11287972.001]
  • [Cites] N Engl J Med. 2001 Apr 5;344(14):1038-42 [11287973.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
  • [Cites] Genes Dev. 2001 Dec 15;15(24):3243-8 [11751630.001]
  • [Cites] Nat Med. 2002 Aug;8(8):816-24 [12118244.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39858-66 [12176997.001]
  • [Cites] J Biol Chem. 2002 Nov 29;277(48):46265-72 [12196540.001]
  • [Cites] Cell. 2003 Aug 8;114(3):323-34 [12914697.001]
  • [Cites] J Clin Oncol. 2003 Dec 1;21(23):4342-9 [14645423.001]
  • [Cites] BMC Cancer. 2003 Nov 27;3:31 [14641932.001]
  • [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] Br J Cancer. 2004 Jul 19;91(2):355-8 [15188009.001]
  • [Cites] Science. 2004 Jul 16;305(5682):399-401 [15256671.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 7;101(36):13306-11 [15329413.001]
  • [Cites] Methods Mol Biol. 2005;290:25-34 [15361653.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7241-4 [15492241.001]
  • [Cites] Nature. 2006 Jan 19;439(7074):353-7 [16273092.001]
  • [Cites] Cancer Res. 2006 Feb 1;66(3):1500-8 [16452206.001]
  • [Cites] Mol Cancer Ther. 2007 Mar;6(3):820-32 [17339364.001]
  • [Cites] Cancer Res. 2007 Apr 15;67(8):3594-600 [17440070.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):4933-9 [17510423.001]
  • [Cites] Nat Rev Genet. 2007 Aug;8(8):601-9 [17607306.001]
  • [Cites] Cancer Biol Ther. 2007 May;6(5):661-7 [17495523.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Oct 16;104(42):16663-8 [17925434.001]
  • [Cites] PLoS One. 2007;2(11):e1226 [18030354.001]
  • [Cites] Nature. 2007 Dec 6;450(7171):893-8 [17982442.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19936-41 [18077425.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):20007-12 [18077431.001]
  • [Cites] Nat Biotechnol. 2008 Jan;26(1):127-32 [18183025.001]
  • [Cites] Cancer Res. 2008 Feb 1;68(3):664-73 [18245465.001]
  • [Cites] J Thorac Oncol. 2008 Feb;3(2):170-3 [18303439.001]
  • [Cites] J Clin Oncol. 2008 Apr 20;26(12):2046-51 [18421059.001]
  • [Cites] Oncogene. 2008 Jun 5;27(25):3635-40 [18212743.001]
  • [Cites] Nat Biotechnol. 2009 Jan;27(1):77-83 [19098899.001]
  • [Cites] J Cell Biochem Suppl. 1996;24:1-11 [8806089.001]
  • [Cites] J Cell Biochem Suppl. 1996;24:32-91 [8806092.001]
  • [Cites] Oncogene. 1998 Nov 19;17(20):2669-75 [9840931.001]
  • [Cites] Science. 1999 Oct 15;286(5439):531-7 [10521349.001]
  • [Cites] Cancer Res. 2004 Dec 15;64(24):9101-4 [15604279.001]
  • [Cites] N Engl J Med. 2005 Feb 24;352(8):786-92 [15728811.001]
  • [Cites] Cancer Res. 2006 Apr 15;66(8):4215-22 [16618744.001]
  • [Cites] Nat Genet. 2006 May;38(5):500-1 [16642009.001]
  • [Cites] Clin Cancer Res. 2006 May 15;12(10):3078-84 [16707605.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5542-8 [16740687.001]
  • [Cites] Cancer Res. 2006 Jun 1;66(11):5790-7 [16740718.001]
  • [Cites] N Engl J Med. 2006 Jun 8;354(23):2419-30 [16760442.001]
  • (PMID = 19451690.001).
  • [ISSN] 1558-8238
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA122794; United States / NCI NIH HHS / CA / P50CA70907; United States / NIGMS NIH HHS / GM / T32 GM007753; United States / NIA NIH HHS / AG / R01 AG2400401; United States / NCI NIH HHS / CA / P50 CA090578; United States / NCI NIH HHS / CA / P50 CA070907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  • [Other-IDs] NLM/ PMC2689116
  •  go-up   go-down






Advertisement