Correction: Linking tumor mutations to drug responses via a quantitative chemical-genetic interaction map (Cancer Discovery, (2018) 5,2 (1-14), 10.1158/2159-8290.CD-14-0552);Linking tumor mutations to drug responses via a quantitative chemical–genetic interaction map

Cancer Discovery

Volumn 5, Issue 2, 2015, Pages 154-167

  Martins, Maria M ^a   Zhou, Alicia Y ^a   Corella, Alexandra ^a   Horiuchi, Dai ^a   Yau, Christina ^a   Rakshandehroo, Taha ^a   Gordan, John D ^a   Levin, Rebecca S ^a   Johnson, Jeff ^a   Jascur, John ^a   Shales, Mike ^a   Sorrentino, Antonio ^a   Cheah, Jaime ^b   Clemons, Paul A ^b   Shamji, Alykhan F ^b   Schreiber, Stuart L ^b,c   Krogan, Nevan J ^a   Shokat, Kevan M ^a,c   McCormick, Frank ^a   Goga, Andrei ^a   Bandyopadhyay, Sourav ^a   more..

^a UNIVERSITY OF CALIFORNIA   (United States)

^b BROAD INSTITUTE OF MIT AND HARVARD   (United States)

^c HOWARD HUGHES MEDICAL INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

6 [[2 [[4 (2, 4 DICHLOROPHENYL) 5 (4 METHYL 1H IMIDAZOL 2 YL) 2 PYRIMIDINYL] AMINO] ETHYL] AMINO] NICOTINONITRILE; DASATINIB; PHOSPHATIDYLINOSITOL 3 KINASE; PROTEIN KINASE B; PROTEIN KINASE LYN; SMALL INTERFERING RNA; UNCLASSIFIED DRUG; VOLASERTIB;

ARTICLE; CANCER CELL; CLINICAL TRIAL (TOPIC); CONTROLLED STUDY; DRUG DNA INTERACTION; DRUG EFFICACY; DRUG RESPONSE; GENE EXPRESSION; GENE MAPPING; GENE MUTATION; GENOTYPE; HIGH THROUGHPUT SCREENING; HUMAN; HUMAN CELL; IC50; IMMUNOBLOTTING; ONCOGENE MYC; TRIPLE NEGATIVE BREAST CANCER; TUMOR GENE; ANIMAL; BAGG ALBINO MOUSE; BREAST NEOPLASMS; DRUG RESISTANCE; DRUG SCREENING; FEMALE; GENETICS; GENOMICS; MOUSE; MUTATION; NUDE MOUSE; RANDOMIZATION; SIGNAL TRANSDUCTION; TUMOR CELL LINE;

ANIMALS; BREAST NEOPLASMS; CELL LINE, TUMOR; DRUG RESISTANCE, NEOPLASM; DRUG SCREENING ASSAYS, ANTITUMOR; FEMALE; GENOMICS; HIGH-THROUGHPUT SCREENING ASSAYS; HUMANS; MICE; MICE, INBRED BALB C; MICE, NUDE; MUTATION; RANDOM ALLOCATION; SIGNAL TRANSDUCTION; XENOGRAFT MODEL ANTITUMOR ASSAYS;

EID: 84922368099     PISSN: 21598274     EISSN: 21598290     Source Type: Journal    
DOI: 10.1158/2159-8290.CD-18-0714     Document Type: Erratum

References (66)

1. Yaffe MB. The scientific drunk and the lamppost: massive sequencing efforts in cancer discovery and treatment. Sci Signal 2013; 6: pe13.
2. Barretina J, Caponigro G, Stransky N, Venkatesan K, Margolin AA, Kim S, et al. The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity. Nature 2012; 483: 603-7.
3. Basu A, Bodycombe NE, Cheah JH, Price EV, Liu K, Schaefer G I, et al. An interactive resource to identify cancer genetic and lineage dependencies targeted by small molecules. Cell 2013; 154: 1151- 61.
4. Garnett MJ, Edelman EJ, Heidorn SJ, Greenman CD, Dastur A, Lau KW, et al. Systematic identification of genomic markers of drug sensitivity in cancer cells. Nature 2012; 483: 570-5.
5. Ashworth A, Lord CJ, Reis-Filho JS. Genetic interactions in cancer progression and treatment. Cell 2011; 145: 30-8.
6. Nijman SM, Friend SH. Cancer. Potential of the synthetic lethality principle. Science 2013; 342: 809-11.
7. Bandyopadhyay S, Mehta M, Kuo D, Sung MK, Chuang R, Jaehnig EJ, et al. Rewiring of genetic networks in response to DNA damage. Science 2010; 330: 1385-9.
8. Costanzo M, Baryshnikova A, Bellay J, Kim Y, Spear ED, Sevier CS, et al. The genetic landscape of a cell. Science 2010; 327: 425-31.
9. Corcoran RB, Cheng KA, Hata AN, Faber AC, Ebi H, Coffee EM, et al. Synthetic lethal interaction of combined BCL-XL and MEK inhibition promotes tumor regressions in KRAS mutant cancer models. Cancer Cell 2013; 23: 121-8.
10. Luo J, Emanuele MJ, Li D, Creighton CJ, Schlabach MR, Westbrook TF, et al. A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene. Cell 2009; 137: 835-48.
11. Scholl C, Frohling S, Dunn IF, Schinzel AC, Barbie DA, Kim SY, et al. Synthetic lethal interaction between oncogenic KRAS dependency and STK33 suppression in human cancer cells. Cell 2009; 137: 821-34.
12. Steckel M, Molina-Arcas M, Weigelt B, Marani M, Warne PH, Kuznetsov H, et al. Determination of synthetic lethal interactions in KRAS oncogene-dependent cancer cells reveals novel therapeutic targeting strategies. Cell Res 2012; 22: 1227-45.
13. Yang WS, Stockwell BR. Synthetic lethal screening identifies compounds activating iron-dependent, nonapoptotic cell death in oncogenic- RAS-harboring cancer cells. Chem Biol 2008; 15: 234-45.
14. Wang Y, Ngo VN, Marani M, Yang Y, Wright G, Staudt LM, et al. Critical role for transcriptional repressor Snail2 in transformation by oncogenic RAS in colorectal carcinoma cells. Oncogene 2010; 29: 4658-70.
15. Barbie DA, Tamayo P, Boehm JS, Kim SY, Moody SE, Dunn IF, et al. Systematic RNA interference reveals that oncogenic KRAS-driven cancers require TBK1. Nature 2009; 462: 108-12.
16. Beaver JA, Gustin JP, Yi KH, Rajpurohit A, Thomas M, Gilbert SF, et al. PIK3CA and AKT1 mutations have distinct effects on sensitivity to targeted pathway inhibitors in an isogenic luminal breast cancer model system. Clin Cancer Res 2013; 19: 5413-22.
17. Goga A, Yang D, Tward AD, Morgan DO, Bishop JM. Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC. Nat Med 2007; 13: 820-7.
18. Muellner MK, Uras IZ, Gapp BV, Kerzendorfer C, Smida M, Lechtermann H, et al. A chemical-genetic screen reveals a mechanism of resistance to PI3K inhibitors in cancer. Nat Chem Biol 2011; 7: 787-93.
19. Zecchin D, Boscaro V, Medico E, Barault L, Martini M, Arena S, et al. BRAF V600E is a determinant of sensitivity to proteasome inhibitors. Mol Cancer Ther 2013; 12: 2950-61.
20. Alles MC, Gardiner-Garden M, Nott DJ, Wang Y, Foekens JA, Sutherland RL, et al. Meta-analysis and gene set enrichment relative to er status reveal elevated activity of MYC and E2F in the "basal" breast cancer subgroup. PLoS One 2009; 4: e4710.
21. Chandriani S, Frengen E, Cowling VH, Pendergrass SA, Perou CM, Whitfield ML, et al. A core MYC gene expression signature is prominent in basal-like breast cancer but only partially overlaps the core serum response. PLoS ONE 2009; 4: e6693.
22. Gatza ML, Lucas JE, Barry WT, Kim JW, Wang Q, Crawford MD, et al. A pathway-based classification of human breast cancer. Proc Natl Acad Sci U S A 2010; 107: 6994-9.
23. Cancer Genome Atlas N. Comprehensive molecular portraits of human breast tumours. Nature 2012; 490: 61-70.
24. Stewart TA, Pattengale PK, Leder P. Spontaneous mammary adenocarcinomas in transgenic mice that carry and express MTV/myc fusion genes. Cell 1984; 38: 627-37.
25. Sinn E, Muller W, Pattengale P, Tepler I, Wallace R, Leder P. Coexpression of MMTV/v-Ha-ras and MMTV/c-myc genes in transgenic mice: synergistic action of oncogenes in vivo. Cell 1987; 49: 465-75.
26. Podsypanina K, Politi K, Beverly LJ, Varmus HE. Oncogene cooperation in tumor maintenance and tumor recurrence in mouse mammary tumors induced by Myc and mutant Kras. Proc Natl Acad Sci U S A 2008; 105: 5242-7.
27. D'Cruz CM, Gunther EJ, Boxer RB, Hartman JL, Sintasath L, Moody SE, et al. c-MYC induces mammary tumorigenesis by means of a preferred pathway involving spontaneous Kras2 mutations. Nat Med 2001; 7: 235-9.
28. Soucek L, Helmer-Citterich M, Sacco A, Jucker R, Cesareni G, Nasi S. Design and properties of a Myc derivative that efficiently homodimerizes. Oncogene 1998; 17: 2463-72.
29. Soucek L, Jucker R, Panacchia L, Ricordy R, Tato F, Nasi S. Omomyc, a potential Myc dominant negative, enhances Myc-induced apoptosis. Cancer Res 2002; 62: 3507-10.
30. Jain M, Arvanitis C, Chu K, Dewey W, Leonhardt E, Trinh M, et al. Sustained loss of a neoplastic phenotype by brief inactivation of MYC. Science 2002; 297: 102-4.
31. Delmore JE, Issa GC, Lemieux ME, Rahl PB, Shi J, Jacobs HM, et al. BET bromodomain inhibition as a therapeutic strategy to target c-Myc. Cell 2011; 146: 904-17.
32. Lockwood WW, Zejnullahu K, Bradner JE, Varmus H. Sensitivity of human lung adenocarcinoma cell lines to targeted inhibition of BET epigenetic signaling proteins. Proc Natl Acad Sci U S A 2012; 109: 19408-13.
33. Horiuchi D, Kusdra L, Huskey NE, Chandriani S, Lenburg ME, Gonzalez-Angulo AM, et al. MYC pathway activation in triple-negative breast cancer is synthetic lethal with CDK inhibition. J Exp Med 2012; 209: 679-96.
34. Kessler JD, Kahle KT, Sun T, Meerbrey KL, Schlabach MR, Schmitt EM, et al. A SUMOylation-dependent transcriptional subprogram is required for Myc-driven tumorigenesis. Science 2012; 335: 348-53.
35. Toyoshima M, Howie HL, Imakura M, Walsh RM, Annis JE, Chang AN, et al. Functional genomics identifies therapeutic targets for MYC-driven cancer. Proc Natl Acad Sci U S A 2012; 109: 9545-50.
36. Yang D, Liu H, Goga A, Kim S, Yuneva M, Bishop JM. Therapeutic potential of a synthetic lethal interaction between the MYC protooncogene and inhibition of aurora-B kinase. Proc Natl Acad Sci U S A 2010; 107: 13836-41.
37. Cermelli S, Jang IS, Bernard B, Grandori C. Synthetic lethal screens as a means to understand and treat MYC-driven cancers. Cold Spring Harb Perspect Med 2014; 4:a014209.
38. Debnath J, Mills KR, Collins NL, Reginato MJ, Muthuswamy SK, Brugge JS. The role of apoptosis in creating and maintaining luminal space within normal and oncogene-expressing mammary acini. Cell 2002; 111: 29-40.
39. Collins SR, Roguev A, Krogan NJ. Quantitative genetic interaction mapping using the E-MAP approach. Methods Enzymol 2010; 470: 205-31.
40. Misale S, Yaeger R, Hobor S, Scala E, Janakiraman M, Liska D, et al. Emergence of KRAS mutations and acquired resistance to anti-EGFR therapy in colorectal cancer. Nature 2012; 486: 532-6.
41. Engelman JA, Zejnullahu K, Mitsudomi T, Song Y, Hyland C, Park JO, et al. MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling. Science 2007; 316: 1039-43.
42. Vazquez-Martin A, Cufi S, Oliveras-Ferraros C, Torres-Garcia VZ, Corominas-Faja B, Cuyas E, et al. IGF-1R/epithelial-to-mesenchymal transition (EMT) crosstalk suppresses the erlotinib-sensitizing effect of EGFR exon 19 deletion mutations. Sci Rep 2013; 3: 2560.
43. Ohashi K, Sequist LV, Arcila ME, Moran T, Chmielecki J, Lin YL, et al. Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1. Proc Natl Acad Sci U S A 2012; 109: E2127-33.
44. Wee S, Jagani Z, Xiang KX, Loo A, Dorsch M, Yao YM, et al. PI3K pathway activation mediates resistance to MEK inhibitors in KRAS mutant cancers. Cancer Res 2009; 69: 4286-93.
45. Lin CJ, Nasr Z, Premsrirut PK, Porco JA Jr, Hippo Y, Lowe SW, et al. Targeting synthetic lethal interactions between Myc and the eIF4F complex impedes tumorigenesis. Cell Rep 2012; 1: 325-33.
46. Liu L, Ulbrich J, Muller J, Wustefeld T, Aeberhard L, Kress TR, et al. Deregulated MYC expression induces dependence upon AMPKrelated kinase 5. Nature 2012; 483: 608-12.
47. Liu P, Cheng H, Santiago S, Raeder M, Zhang F, Isabella A, et al. Oncogenic PIK3CA-driven mammary tumors frequently recur via PI3K pathway-dependent and PI3K pathway-independent mechanisms. Nat Med 2011; 17: 1116-20.
48. Heiser LM, Sadanandam A, Kuo WL, Benz SC, Goldstein TC, Ng S, et al. Subtype and pathway specific responses to anticancer compounds in breast cancer. Proc Natl Acad Sci U S A 2012; 109: 2724-9.
49. Gregory MA, Qi Y, Hann SR. Phosphorylation by glycogen synthase kinase-3 controls c-myc proteolysis and subnuclear localization. J Biol Chem 2003; 278: 51606-12.
50. Evan GI, Wyllie AH, Gilbert CS, Littlewood TD, Land H, Brooks M, et al. Induction of apoptosis in fibroblasts by c-myc protein. Cell 1992; 69: 119-28.
51. Hooper C, Killick R, Lovestone S. The GSK3 hypothesis of Alzheimer's disease. J Neurochem 2008; 104: 1433-9.
52. Kadota M, Yang HH, Gomez B, Sato M, Clifford RJ, Meerzaman D, et al. Delineating genetic alterations for tumor progression in the MCF10A series of breast cancer cell lines. PLoS ONE 2010; 5: e9201.
53. Yaswen P, Stampfer MR. Molecular changes accompanying senescence and immortalization of cultured human mammary epithelial cells. Int J Biochem Cell Biol 2002; 34: 1382-94.
54. Daemen A, Griffith OL, Heiser LM, Wang NJ, Enache OM, Sanborn Z, et al. Modeling precision treatment of breast cancer. Genome Biol 2013; 14: R110.
55. Davis MI, Hunt JP, Herrgard S, Ciceri P, Wodicka LM, Pallares G, et al. Comprehensive analysis of kinase inhibitor selectivity. Nat Biotechnol 2011; 29: 1046-51.
56. Bantscheff M, Eberhard D, Abraham Y, Bastuck S, Boesche M, Hobson S, et al. Quantitative chemical proteomics reveals mechanisms of action of clinical ABL kinase inhibitors. Nat Biotechnol 2007; 25: 1035-44.
57. Ingley E. Functions of the Lyn tyrosine kinase in health and disease. Cell Commun Signal 2012; 10: 21.
58. Azam M, Seeliger MA, Gray NS, Kuriyan J, Daley GQ. Activation of tyrosine kinases by mutation of the gatekeeper threonine. Nat Struct Mol Biol 2008; 15: 1109-18.
59. Finn RS, Dering J, Ginther C, Wilson CA, Glaspy P, Tchekmedyian N, et al. Dasatinib, an orally active small molecule inhibitor of both the src and abl kinases, selectively inhibits growth of basal-type/"triplenegative" breast cancer cell lines growing in vitro. Breast Cancer Res Treat 2007; 105: 319-26.
60. Bowman T, Broome MA, Sinibaldi D, Wharton W, Pledger WJ, Sedivy JM, et al. Stat3-mediated Myc expression is required for Src transformation and PDGF-induced mitogenesis. Proc Natl Acad Sci U S A 2001; 98: 7319-24.
61. Seitz V, Butzhammer P, Hirsch B, Hecht J, Gutgemann I, Ehlers A, et al. Deep sequencing of MYC DNA-binding sites in Burkitt lymphoma. PLoS ONE 2011; 6: e26837.
62. Croucher DR, Hochgrafe F, Zhang L, Liu L, Lyons RJ, Rickwood D, et al. Involvement of Lyn and the atypical kinase SgK269/PEAK1 in a basal breast cancer signaling pathway. Cancer Res 2013; 73: 1969-80.
63. Hochgrafe F, Zhang L, O'Toole SA, Browne BC, Pinese M, Porta Cubas A, et al. Tyrosine phosphorylation profiling reveals the signaling network characteristics of Basal breast cancer cells. Cancer Res 2010; 70: 9391-401.
64. Horiuchi D, Huskey NE, Kusdra L, Wohlbold L, Merrick KA, Zhang C, et al. Chemical-genetic analysis of cyclin dependent kinase 2 function reveals an important role in cellular transformation by multiple oncogenic pathways. Proc Natl Acad Sci U S A 2012; 109: E1019-27.
65. Finn RS, Bengala C, Ibrahim N, Roche H, Sparano J, Strauss LC, et al. Dasatinib as a single agent in triple-negative breast cancer: results of an open-label phase 2 study. Clin Cancer Res 2011; 17: 6905-13.
66. Moulder S, Yan K, Huang F, Hess KR, Liedtke C, Lin F, et al. Development of candidate genomic markers to select breast cancer patients for dasatinib therapy. Mol Cancer Ther 2010; 9: 1120-7.