In vitro differential sensitivity of melanomas to phenothiazines is based on the presence of codon 600 BRAF mutation

Molecular Cancer Therapeutics

Volumn 7, Issue 6, 2008, Pages 1337-1346

  Ikediobi, Ogechi N ^a,b,c   Reimers, Mark ^a   Durinck, Steffen ^d   Blower, Paul E ^e   Futreal, Andrew P ^b   Stratton, Michael R ^b   Weinstein, John N ^a  

^a NATIONAL CANCER INSTITUTE   (United States)

^b WELLCOME TRUST SANGER INSTITUTE   (United Kingdom)

^c UNIVERSITY OF CALIFORNIA   (United States)

^d LAWRENCE BERKELEY NATIONAL LABORATORY   (United States)

^e OHIO STATE UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

3 (4,5 DIMETHYL 2 THIAZOLYL) 2,5 DIPHENYLTETRAZOLIUM BROMIDE; ANTIEMETIC AGENT; NEUROLEPTIC AGENT; NSC 17474; NSC 46061; PHENOTHIAZINE DERIVATIVE; UNCLASSIFIED DRUG; ANTINEOPLASTIC AGENT; B RAF KINASE; BRAF PROTEIN, HUMAN; GLUTAMIC ACID; MUTANT PROTEIN; PHENOTHIAZINE; RAF PROTEIN; RAS PROTEIN; VALINE;

ANTINEOPLASTIC ACTIVITY; APC GENE; ARTICLE; BRAF GENE; CANCER CELL CULTURE; CDKN2A GENE; CODON; GENE; GENE MUTATION; GENE SEQUENCE; GENETIC ASSOCIATION; HUMAN; HUMAN CELL; IN VITRO STUDY; MADH4 GENE; MELANOMA; ONCOGENE; ONCOGENE K RAS; ONCOGENE N RAS; PHARMACOGENOMICS; PIK3CA GENE; PRIORITY JOURNAL; PTEN GENE; RB1 GENE; STK11 GENE; TP53 GENE; AMINO ACID SUBSTITUTION; CELL PROLIFERATION; DRUG EFFECT; DRUG SCREENING; GENETICS; METABOLISM; MUTATION; PATHOLOGY; REPRODUCIBILITY; TUMOR CELL LINE;

AMINO ACID SUBSTITUTION; ANTINEOPLASTIC AGENTS; CELL LINE, TUMOR; CELL PROLIFERATION; CODON; DRUG SCREENING ASSAYS, ANTITUMOR; GLUTAMIC ACID; HUMANS; MELANOMA; MUTANT PROTEINS; MUTATION; PHENOTHIAZINES; PROTO-ONCOGENE PROTEINS B-RAF; PROTO-ONCOGENE PROTEINS C-RAF; RAS PROTEINS; REPRODUCIBILITY OF RESULTS; VALINE;

EID: 49849101476     PISSN: 15357163     EISSN: None     Source Type: Journal    
DOI: 10.1158/1535-7163.MCT-07-2308     Document Type: Article

References (45)

1. Paull KD, Shoemaker RH, Hodes L, et al. Display and analysis of patterns of differential activity of drugs against human tumor cell lines: development of mean graph and COMPARE algorithm. J Natl Cancer Inst 1989;81:1088-92.
2. Boyd MR, Paull KD. Some practical considerations and applications of the National Cancer Institute in vitro anticancer drug discovery screen. Drug Dev Res 1995;34:91-109.
3. Holbeck SL. Update on NCI in vitro drug screen utilities. Eur J Cancer 2004;40:785-93.
4. Shoemaker RH. The NCI60 human tumour cell line anticancer drug screen. Nat Rev Cancer 2006;6:813-23.
5. Weinstein JN. Spotlight on molecular profiling: 'integromic' analysis of the NCI-60 cancer cell lines. Mol Cancer Ther 2006;5:2601-5.
6. Myers TG, Anderson NL, Waltham M, et al. A protein expression database for the molecular pharmacology of cancer. Electrophoresis 1997;18:647-53.
7. O'Connor PM, Jackman J, Bae I, et al. Characterization of the p53 tumor suppressor pathway in cell lines of the National Cancer Institute anticancer drug screen and correlations with the growth-inhibitory potency of 123 anticancer agents. Cancer Res 1997;57:4285-300.
8. Ross DT, Scherf U, Eisen MB, et al. Systematic variation in gene expression patterns in human cancer cell lines. Nat Genet 2000;24:227-35.
9. Scherf U, Ross DT, Waltham M, et al. A gene expression database for the molecular pharmacology of cancer. Nat Genet 2000;24:236-44.
10. Staunton JE, Slonim DK, Coller HA, et al. Chemosensitivity prediction by transcriptional profiling. Proc Natl Acad Sci U S A 2001;98:10787-92.
11. Nishizuka S, Charboneau L, Young L, et al. Proteomic profiling of the NCI60 cancer cell lines using new high density 'reverse-phase' lysate microarrays. Proc Natl Acad Sci U S A 2003;100:14229-34.
12. Szakacs G, Annereau JP, Lababidi S, et al. Predicting drug sensitivity and resistance: profiling ABC transporter genes in cancer cells. Cancer Cell 2004;6:129-37.
13. Ikediobi ON, Davies H, Bignell G, et al. Mutation analysis of 24 known cancer genes in the NCI-60 cell line set. Mol Cancer Ther 2006;5:2606-12.
14. Bussey KJ, Chin K, Lababidi S, et al. Integrating data on DNA copy number with gene expression levels and drug sensitivities in the NCI-60 cell line panel. Mol Cancer Ther 2006;5:853-67.
15. Solit DB, Garraway LA, Pratilas CA, et al. BRAF mutation predicts sensitivity to MEK inhibition. Nature 2006;439:358-62.
16. Shankavaram U, Reinhold WC, Nishizuka S, et al. Transcript and protein expression profiles of the NCI-60 cancer cell panel: an integromic microarray study. Mol Cancer Ther 2007;6:820-3.
17. Blower PE, Verducci JS, Lin S, et al. MicroRNA expression profiles for the NCI-60 cancer cell panel. Mol Cancer Ther 2007;6:1483-91.
18. Amundson SA, Do KT, Vinikoor LC, et al. Integrating global gene expression and radiation survival parameters across the 60 cell lines of the NCI anti-cancer drug screen. Cancer Res 2008;68:415-24.
19. Weinstein JN, Kohn KW, Grever MR, et al. Neural computing in cancer drug development: predicting mechanism of action. Science 1992;258:447-51.
20. van Osdol WW, Myers TG, Paull KD, et al. Use of the Kohonen self-organizing map to study the mechanisms of action of chemotherapeutic agents. J Natl Cancer Inst 1994;86:1853-9.
21. Weinstein JN, Myers TG, O'Connor PM, et al. An information-intensive approach to the molecular pharmacology of cancer. Science 1997;275:343-9.
22. Shi LM, Fan Y, Myers TG, Paull KD, Weinstein JN. Mining the NCI anticancer drug discovery databases: genetic function approximation for the quantitative structure-activity relationship study of anticancer ellipticine analogs. J Chem Inf Comput Sci 1998;38:189-99.
23. Rabow AA, Shoemaker RH, Sausville EA, Covell DG. Mining the National Cancer Institute's tumor-screening database: identification of compounds with similar cellular activities. J Med Chem 2002;45:818-40.
24. Lee JK, Bussey KJ, Gwadry FG, et al. Comparing cDNA and oligonucleotide array data: concordance of gene expression across platforms for the NCI-60 cancer cells. Genome Biol 2003;4:R82.
25. Reinhold WC, Kouros-Mehr H, Kohn KW, et al. Apoptotic susceptibility of cancer cells selected for camptothecin resistance: gene expression profiling, functional analysis, and molecular interaction mapping. Cancer Res 2003;63:1000-11.
26. Lee JK, Havaleshko DM, Cho HJ, et al. A new strategy for predicting the chemosensitivity of human cancers and its application to drug discovery. Proc Natl Acad Sci U S A 2007;104:13086-91.
27. Capdeville R, Buchdunger E, Zimmermann J, Matter A. Glivec (STI571, imatinib), a rationally developed, targeted anticancer drug. Nat Rev Drug Discov 2002;1:493-502.
28. Lynch TJ, Bell DW, Sordella R, et al. Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib. N Engl J Med 2004;350:2129-39.
29. Paez JG, Janne PA, Lee JC, et al. EGFR mutations in lung cancer: correlation with clinical response to gefitinib therapy. Science 2004;304:1497-500.
30. Pao W, Miller V, Zakowski M, et al. EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib. Proc Natl Acad Sci U S A 2004;101:13306-11.
31. Nagata Y, Lan KH, Zhou X, et al. PTEN activation contributes to tumor inhibition by trastuzumab, and loss of PTEN predicts trastuzumab resistance in patients. Cancer Cell 2004;6:117-27.
32. Futreal PA, Coin L, Marshall M, et al. A census of human cancer genes. Nat Rev Cancer 2004;4:177-83.
33. She QB, Solit D, Basso A, Moasser MM. Resistance to gefitinib in PTEN-null HER-overexpressing tumor cells can be overcome through restoration of PTEN function or pharmacologic modulation of constitutive phosphatidylinositol 3′-kinase/Akt pathway signaling. Clin Cancer Res 2003;9:4340-6.
34. Albitar L, Carter MB, Davies S, Leslie KK. Consequences of the loss of p53, RB1, and PTEN: relationship to gefitinib resistance in endometrial cancer. Gynecol Oncol 2007;106:94-104.
35. Festuccia C, Muzi P, Millimaggi D, et al. Molecular aspects of gefitinib antiproliferative and pro-apoptotic effects in PTEN-positive and PTEN-negative prostate cancer cell lines. Endocr Relat Cancer 2005;12:983-98.
36. Montiel-Duarte C, Cordeu L, Agirre X, et al. Resistance to Imatinib Mesylate-induced apoptosis in acute lymphoblastic leukemia is associated with PTEN down-regulation due to promoter hypermethylation. Leuk Res 2008;32:709-16.
37. Wan PT, Garnett MJ, Roe SM, et al. Mechanism of activation of the RAF-ERK signaling pathway by oncogenic mutations of B-RAF. Cell 2004;116:855-67.
38. Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature 2002;417:949-54.
39. Garnett MJ, Marais R. Guilty as charged: B-RAF is a human oncogene. Cancer Cell 2004;6:313-9.
40. Yuen ST, Davies H, Chan TL, et al. Similarity of the phenotypic patterns associated with BRAF and KRAS mutations in colorectal neoplasia. Cancer Res 2002;62:6451-5.
41. Zhu HG, Tayeh I, Israel L, Castagna M. Different susceptibility of lung cell lines to inhibitors of tumor promotion and inducers of differentiation. J Biol Regul Homeost Agents 1991;5:52-8.
42. Eriksson A, Yachnin J, Lewensohn R, Nilsson A. DNA-dependent protein kinase is inhibited by trifluoperazine. Biochem Biophys Res Commun 2001;283:726-31.
43. Hait WN, Aftab DT. Rational design and pre-clinical pharmacology of drugs for reversing multidrug resistance. Biochem Pharmacol 1992;43:103-7.
44. Barancik M, Polekova L, Mrazova T, Breier A, Stankovicova T, Slezak J. Reversal effects of several Ca(2+)-entry blockers, neuroleptics and local anaesthetics on P-glycoprotein-mediated vincristine resistance of L1210/ VCR mouse leukaemic cell line. Drugs Exp Clin Res 1994;20:13-8.
45. Kau TR, Schroeder F, Ramaswamy S, et al. A chemical genetic screen identifies inhibitors of regulated nuclear export of a forkhead transcription factor in PTEN-deficient tumor cells. Cancer Cell 2003;4:463-76.