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Cancer Program

Genomic Profiling of Smoldering Multiple Myeloma Identifies Patients at a High Risk of Disease Progression.
Bustoros M, Sklavenitis-Pistofidis R, Park J, et al. Genomic Profiling of Smoldering Multiple Myeloma Identifies Patients at a High Risk of Disease Progression. J Clin Oncol. 2020:JCO2000437. doi:10.1200/JCO.20.00437.
Loss of heterozygosity of essential genes represents a widespread class of potential cancer vulnerabilities.
Nichols CA, Gibson WJ, Brown MS, et al. Loss of heterozygosity of essential genes represents a widespread class of potential cancer vulnerabilities. Nat Commun. 2020;11(1):2517. doi:10.1038/s41467-020-16399-y.
Cas9 activates the p53 pathway and selects for p53-inactivating mutations.
Enache OM, Rendo V, Abdusamad M, et al. Cas9 activates the p53 pathway and selects for p53-inactivating mutations. Nat Genet. 2020. doi:10.1038/s41588-020-0623-4.
The genomic landscape of intrinsic and acquired resistance to cyclin-dependent kinase 4/6 inhibitors in patients with hormone receptor positive metastatic breast cancer.
Wander SA, Cohen O, Gong X, et al. The genomic landscape of intrinsic and acquired resistance to cyclin-dependent kinase 4/6 inhibitors in patients with hormone receptor positive metastatic breast cancer. Cancer Discov. 2020. doi:10.1158/2159-8290.CD-19-1390.
Comprehensive Analysis of Genetic Ancestry and Its Molecular Correlates in Cancer.
Carrot-Zhang J, Chambwe N, Damrauer JS, et al. Comprehensive Analysis of Genetic Ancestry and Its Molecular Correlates in Cancer. Cancer Cell. 2020;37(5):639-654.e6. doi:10.1016/j.ccell.2020.04.012.
Reversion and non-reversion mechanisms of resistance to PARP inhibitor or platinum chemotherapy in BRCA1/2-mutant metastatic breast cancer.
Waks AG, Cohen O, Kochupurakkal B, et al. Reversion and non-reversion mechanisms of resistance to PARP inhibitor or platinum chemotherapy in BRCA1/2-mutant metastatic breast cancer. Ann Oncol. 2020;31(5):590-598. doi:10.1016/j.annonc.2020.02.008.
Patterns of chromosome 18 loss of heterozygosity in multifocal ileal neuroendocrine tumors.
Zhang Z, Mäkinen N, Kasai Y, et al. Patterns of chromosome 18 loss of heterozygosity in multifocal ileal neuroendocrine tumors. Genes Chromosomes Cancer. 2020. doi:10.1002/gcc.22850.
Sensitive detection of minimal residual disease in patients treated for early-stage breast cancer.
Parsons HA, Rhoades J, Reed SC, et al. Sensitive detection of minimal residual disease in patients treated for early-stage breast cancer. Clin Cancer Res. 2020. doi:10.1158/1078-0432.CCR-19-3005.
Mechanistic insights into cancer cell killing through interaction of phosphodiesterase 3A and schlafen family member 12.
Wu X, Schnitzler GR, Gao GF, et al. Mechanistic insights into cancer cell killing through interaction of phosphodiesterase 3A and schlafen family member 12. J Biol Chem. 2020;295(11):3431-3446. doi:10.1074/jbc.RA119.011191.
Prevalence and mutational determinants of high tumor mutation burden in breast cancer.
Barroso-Sousa R, Jain E, Cohen O, et al. Prevalence and mutational determinants of high tumor mutation burden in breast cancer. Ann Oncol. 2020;31(3):387-394. doi:10.1016/j.annonc.2019.11.010.
Gain-of-Function Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer.
Zhang H, Schaefer A, Wang Y, et al. Gain-of-Function Mutations Promote Focal Adhesion Kinase Activation and Dependency in Diffuse Gastric Cancer. Cancer Discov. 2020;10(2):288-305. doi:10.1158/2159-8290.CD-19-0811.
Early TP53 alterations engage environmental exposures to promote gastric premalignancy in an integrative mouse model.
Sethi NS, Kikuchi O, Duronio GN, et al. Early TP53 alterations engage environmental exposures to promote gastric premalignancy in an integrative mouse model. Nat Genet. 2020;52(2):219-230. doi:10.1038/s41588-019-0574-9.
Analyses of non-coding somatic drivers in 2,658 cancer whole genomes.
Rheinbay E, Nielsen MMuhlig, Abascal F, et al. Analyses of non-coding somatic drivers in 2,658 cancer whole genomes. Nature. 2020;578(7793):102-111. doi:10.1038/s41586-020-1965-x.
The Angiosarcoma Project: enabling genomic and clinical discoveries in a rare cancer through patient-partnered research.
Painter CA, Jain E, Tomson BN, et al. The Angiosarcoma Project: enabling genomic and clinical discoveries in a rare cancer through patient-partnered research. Nat Med. 2020;26(2):181-187. doi:10.1038/s41591-019-0749-z.
Resistance Mechanisms to SYK Inhibition in Acute Myeloid Leukemia.
Cremer A, Ellegast JM, Alexe G, et al. Resistance Mechanisms to SYK Inhibition in Acute Myeloid Leukemia. Cancer Discov. 2020;10(2):214-231. doi:10.1158/2159-8290.CD-19-0209.
Quantitative Proteomics of the Cancer Cell Line Encyclopedia.
Nusinow DP, Szpyt J, Ghandi M, et al. Quantitative Proteomics of the Cancer Cell Line Encyclopedia. Cell. 2020;180(2):387-402.e16. doi:10.1016/j.cell.2019.12.023.
STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells.
Kim JWook, Berrios C, Kim M, et al. STRIPAK directs PP2A activity toward MAP4K4 to promote oncogenic transformation of human cells. Elife. 2020;9. doi:10.7554/eLife.53003.
Genomic analyses of PMBL reveal new drivers and mechanisms of sensitivity to PD-1 blockade.
Chapuy B, Stewart C, Dunford AJ, et al. Genomic analyses of PMBL reveal new drivers and mechanisms of sensitivity to PD-1 blockade. Blood. 2019;134(26):2369-2382. doi:10.1182/blood.2019002067.
Agreement between two large pan-cancer CRISPR-Cas9 gene dependency data sets.
Dempster JM, Pacini C, Pantel S, et al. Agreement between two large pan-cancer CRISPR-Cas9 gene dependency data sets. Nat Commun. 2019;10(1):5817. doi:10.1038/s41467-019-13805-y.
Genomics and Targeted Therapies in Gastroesophageal Adenocarcinoma.
Nagaraja AK, Kikuchi O, Bass AJ. Genomics and Targeted Therapies in Gastroesophageal Adenocarcinoma. Cancer Discov. 2019;9(12):1656-1672. doi:10.1158/2159-8290.CD-19-0487.
Genomic and immune profiling of pre-invasive lung adenocarcinoma.
Chen H, Carrot-Zhang J, Zhao Y, et al. Genomic and immune profiling of pre-invasive lung adenocarcinoma. Nat Commun. 2019;10(1):5472. doi:10.1038/s41467-019-13460-3.
CREB5 Promotes Resistance to Androgen-Receptor Antagonists and Androgen Deprivation in Prostate Cancer.
Hwang JH, Seo J-H, Beshiri ML, et al. CREB5 Promotes Resistance to Androgen-Receptor Antagonists and Androgen Deprivation in Prostate Cancer. Cell Rep. 2019;29(8):2355-2370.e6. doi:10.1016/j.celrep.2019.10.068.
Optimization of PDE3A Modulators for SLFN12-Dependent Cancer Cell Killing.
Lewis TA, de Waal L, Wu X, et al. Optimization of PDE3A Modulators for SLFN12-Dependent Cancer Cell Killing. ACS Med Chem Lett. 2019;10(11):1537-1542. doi:10.1021/acsmedchemlett.9b00360.
A nuclease-polymerase chain reaction enables amplification of probes used for capture-based DNA target enrichment.
Leong KWai, Yu F, Adalsteinsson VA, et al. A nuclease-polymerase chain reaction enables amplification of probes used for capture-based DNA target enrichment. Nucleic Acids Res. 2019. doi:10.1093/nar/gkz870.
Metabolomic adaptations and correlates of survival to immune checkpoint blockade.
Li H, Bullock K, Gurjao C, et al. Metabolomic adaptations and correlates of survival to immune checkpoint blockade. Nat Commun. 2019;10(1):4346. doi:10.1038/s41467-019-12361-9.
Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies.
Guièze R, Liu VM, Rosebrock D, et al. Mitochondrial Reprogramming Underlies Resistance to BCL-2 Inhibition in Lymphoid Malignancies. Cancer Cell. 2019. doi:10.1016/j.ccell.2019.08.005.
Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer.
Stover EH, Baco MB, Cohen O, et al. Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer. Mol Cancer Res. 2019. doi:10.1158/1541-7786.MCR-18-1243.
Small-Molecule and CRISPR Screening Converge to Reveal Receptor Tyrosine Kinase Dependencies in Pediatric Rhabdoid Tumors.
Oberlick EM, Rees MG, Seashore-Ludlow B, et al. Small-Molecule and CRISPR Screening Converge to Reveal Receptor Tyrosine Kinase Dependencies in Pediatric Rhabdoid Tumors. Cell Rep. 2019;28(9):2331-2344.e8. doi:10.1016/j.celrep.2019.07.021.
Genomic Evolutionary Patterns of Leiomyosarcoma and Liposarcoma.
Amin-Mansour A, George S, Sioletic S, et al. Genomic Evolutionary Patterns of Leiomyosarcoma and Liposarcoma. Clin Cancer Res. 2019;25(16):5135-5142. doi:10.1158/1078-0432.CCR-19-0271.
High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma.
Wang S, Hwang EE, Guha R, et al. High-throughput Chemical Screening Identifies Focal Adhesion Kinase and Aurora Kinase B Inhibition as a Synergistic Treatment Combination in Ewing Sarcoma. Clin Cancer Res. 2019;25(14):4552-4566. doi:10.1158/1078-0432.CCR-17-0375.
Patterns of substrate affinity, competition, and degradation kinetics underlie biological activity of thalidomide analogs.
Sperling AS, Burgess M, Keshishian H, et al. Patterns of substrate affinity, competition, and degradation kinetics underlie biological activity of thalidomide analogs. Blood. 2019;134(2):160-170. doi:10.1182/blood.2019000789.
Publisher Correction: The long tail of oncogenic drivers in prostate cancer.
Armenia J, Wankowicz SAM, Liu D, et al. Publisher Correction: The long tail of oncogenic drivers in prostate cancer. Nat Genet. 2019;51(7):1194. doi:10.1038/s41588-019-0451-6.
Mitochondrial metabolism promotes adaptation to proteotoxic stress.
Tsvetkov P, Detappe A, Cai K, et al. Mitochondrial metabolism promotes adaptation to proteotoxic stress. Nat Chem Biol. 2019;15(7):681-689. doi:10.1038/s41589-019-0291-9.
Integrative molecular characterization of resistance to neoadjuvant chemoradiation in rectal cancer.
Kamran SC, Lennerz JK, Margolis CA, et al. Integrative molecular characterization of resistance to neoadjuvant chemoradiation in rectal cancer. Clin Cancer Res. 2019. doi:10.1158/1078-0432.CCR-19-0908.
A CRISPR Way to Identify Cancer Targets.
Hahn WC. A CRISPR Way to Identify Cancer Targets. N Engl J Med. 2019;380(25):2475-2477. doi:10.1056/NEJMcibr1905048.
Intrinsic Resistance to Immune Checkpoint Blockade in a Mismatch Repair-Deficient Colorectal Cancer.
Gurjao C, Liu D, Hofree M, et al. Intrinsic Resistance to Immune Checkpoint Blockade in a Mismatch Repair-Deficient Colorectal Cancer. Cancer Immunol Res. 2019. doi:10.1158/2326-6066.CIR-18-0683.
RNA sequence analysis reveals macroscopic somatic clonal expansion across normal tissues.
Yizhak K, Aguet F, Kim J, et al. RNA sequence analysis reveals macroscopic somatic clonal expansion across normal tissues. Science. 2019;364(6444). doi:10.1126/science.aaw0726.
Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma.
Bandopadhayay P, Piccioni F, O'Rourke R, et al. Neuronal differentiation and cell-cycle programs mediate response to BET-bromodomain inhibition in MYC-driven medulloblastoma. Nat Commun. 2019;10(1):2400. doi:10.1038/s41467-019-10307-9.
Growth dynamics in naturally progressing chronic lymphocytic leukaemia.
Gruber M, Bozic I, Leshchiner I, et al. Growth dynamics in naturally progressing chronic lymphocytic leukaemia. Nature. 2019;570(7762):474-479. doi:10.1038/s41586-019-1252-x.
Genome-Wide Interrogation of Human Cancers Identifies EGLN1 Dependency in Clear Cell Ovarian Cancers.
Price C, Gill S, Ho ZV, et al. Genome-Wide Interrogation of Human Cancers Identifies EGLN1 Dependency in Clear Cell Ovarian Cancers. Cancer Res. 2019;79(10):2564-2579. doi:10.1158/0008-5472.CAN-18-2674.
Next-generation characterization of the Cancer Cell Line Encyclopedia.
Ghandi M, Huang FW, Jané-Valbuena J, et al. Next-generation characterization of the Cancer Cell Line Encyclopedia. Nature. 2019. doi:10.1038/s41586-019-1186-3.
A Functional Landscape of Resistance to MEK1/2 and CDK4/6 Inhibition in NRAS-Mutant Melanoma.
Hayes TK, Luo F, Cohen O, et al. A Functional Landscape of Resistance to MEK1/2 and CDK4/6 Inhibition in NRAS-Mutant Melanoma. Cancer Res. 2019;79(9):2352-2366. doi:10.1158/0008-5472.CAN-18-2711.
The landscape of cancer cell line metabolism.
Li H, Ning S, Ghandi M, et al. The landscape of cancer cell line metabolism. Nat Med. 2019;25(5):850-860. doi:10.1038/s41591-019-0404-8.
A GPX4-dependent cancer cell state underlies the clear-cell morphology and confers sensitivity to ferroptosis.
Zou Y, Palte MJ, Deik AA, et al. A GPX4-dependent cancer cell state underlies the clear-cell morphology and confers sensitivity to ferroptosis. Nat Commun. 2019;10(1):1617. doi:10.1038/s41467-019-09277-9.
WRN helicase is a synthetic lethal target in microsatellite unstable cancers.
Chan EM, Shibue T, McFarland JM, et al. WRN helicase is a synthetic lethal target in microsatellite unstable cancers. Nature. 2019;568(7753):551-556. doi:10.1038/s41586-019-1102-x.
A (fire)cloud-based DNA methylation data preprocessing and quality control platform.
Kangeyan D, Dunford A, Iyer S, et al. A (fire)cloud-based DNA methylation data preprocessing and quality control platform. BMC Bioinformatics. 2019;20(1):160. doi:10.1186/s12859-019-2750-4.
From cell lines to living biosensors: new opportunities to prioritize cancer dependencies using ex vivo tumor cultures.
Tseng Y-Y, Boehm JS. From cell lines to living biosensors: new opportunities to prioritize cancer dependencies using ex vivo tumor cultures. Curr Opin Genet Dev. 2019;54:33-40. doi:10.1016/j.gde.2019.02.007.
Circulating Tumor DNA Provides a Sneak Peek into Treatment Responses in Non-Small Cell Lung Cancer.
Zou T, Meyerson M. Circulating Tumor DNA Provides a Sneak Peek into Treatment Responses in Non-Small Cell Lung Cancer. Cancer Res. 2019;79(6):1038-1040. doi:10.1158/0008-5472.CAN-19-0231.
Renal medullary carcinomas depend upon loss and are sensitive to proteasome inhibition.
Hong AL, Tseng Y-Y, Wala JA, et al. Renal medullary carcinomas depend upon loss and are sensitive to proteasome inhibition. Elife. 2019;8. doi:10.7554/eLife.44161.
Subsets of exhausted CD8 T cells differentially mediate tumor control and respond to checkpoint blockade.
Miller BC, Sen DR, Abosy RAl, et al. Subsets of exhausted CD8 T cells differentially mediate tumor control and respond to checkpoint blockade. Nat Immunol. 2019;20(3):326-336. doi:10.1038/s41590-019-0312-6.
MCL1 and DEDD Promote Urothelial Carcinoma Progression.
Hong AL, Guerriero JL, Doshi MB, et al. MCL1 and DEDD Promote Urothelial Carcinoma Progression. Mol Cancer Res. 2019. doi:10.1158/1541-7786.MCR-18-0963.
MDM2 and MDM4 are Therapeutic Vulnerabilities in Malignant Rhabdoid Tumors.
Howard TP, Arnoff TE, Song MR, et al. MDM2 and MDM4 are Therapeutic Vulnerabilities in Malignant Rhabdoid Tumors. Cancer Res. 2019. doi:10.1158/0008-5472.CAN-18-3066.
Acquired HER2 mutations in ER metastatic breast cancer confer resistance to estrogen receptor-directed therapies.
Nayar U, Cohen O, Kapstad C, et al. Acquired HER2 mutations in ER metastatic breast cancer confer resistance to estrogen receptor-directed therapies. Nat Genet. 2019;51(2):207-216. doi:10.1038/s41588-018-0287-5.
A Murine Model of Chronic Lymphocytic Leukemia Based on B Cell-Restricted Expression of Sf3b1 Mutation and Atm Deletion.
Yin S, Gambe RG, Sun J, et al. A Murine Model of Chronic Lymphocytic Leukemia Based on B Cell-Restricted Expression of Sf3b1 Mutation and Atm Deletion. Cancer Cell. 2019. doi:10.1016/j.ccell.2018.12.013.
Identification and characterization of oncogenic SOS1 mutations in lung adenocarcinoma.
Cai D, Choi PS, Gelbard M, Meyerson M. Identification and characterization of oncogenic SOS1 mutations in lung adenocarcinoma. Mol Cancer Res. 2019. doi:10.1158/1541-7786.MCR-18-0316.
Loss of ADAR1 in tumours overcomes resistance to immune checkpoint blockade.
Ishizuka JJ, Manguso RT, Cheruiyot CK, et al. Loss of ADAR1 in tumours overcomes resistance to immune checkpoint blockade. Nature. 2019;565(7737):43-48. doi:10.1038/s41586-018-0768-9.
Neoantigen vaccine generates intratumoral T cell responses in phase Ib glioblastoma trial.
Keskin DB, Anandappa AJ, Sun J, et al. Neoantigen vaccine generates intratumoral T cell responses in phase Ib glioblastoma trial. Nature. 2019;565(7738):234-239. doi:10.1038/s41586-018-0792-9.
Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells.
Gannon HS, Zou T, Kiessling MK, et al. Identification of ADAR1 adenosine deaminase dependency in a subset of cancer cells. Nat Commun. 2018;9(1):5450. doi:10.1038/s41467-018-07824-4.
Genomic evolution of cancer models: perils and opportunities.
Ben-David U, Beroukhim R, Golub TR. Genomic evolution of cancer models: perils and opportunities. Nat Rev Cancer. 2018. doi:10.1038/s41568-018-0095-3.
Intron retention is a source of neoepitopes in cancer.
Smart AC, Margolis CA, Pimentel H, et al. Intron retention is a source of neoepitopes in cancer. Nat Biotechnol. 2018;36(11):1056-1058. doi:10.1038/nbt.4239.
Amplification Associates with Aggressive Phenotype but Not Markers of AKT-MTOR Signaling in Endometrial Carcinoma.
Holst F, Werner HMJ, Mjøs, iv S, et al. Amplification Associates with Aggressive Phenotype but Not Markers of AKT-MTOR Signaling in Endometrial Carcinoma. Clin Cancer Res. 2018. doi:10.1158/1078-0432.CCR-18-0452.
KDM5 Histone Demethylase Activity Links Cellular Transcriptomic Heterogeneity to Therapeutic Resistance.
Hinohara K, Wu H-J, Vigneau S, et al. KDM5 Histone Demethylase Activity Links Cellular Transcriptomic Heterogeneity to Therapeutic Resistance. Cancer Cell. 2018. doi:10.1016/j.ccell.2018.10.014.
A combination CDK4/6 and IGF1R inhibitor strategy for Ewing sarcoma.
Guenther LM, Dharia NV, Ross L, et al. A combination CDK4/6 and IGF1R inhibitor strategy for Ewing sarcoma. Clin Cancer Res. 2018. doi:10.1158/1078-0432.CCR-18-0372.
Defining the human C2H2 zinc finger degrome targeted by thalidomide analogs through CRBN.
Sievers QL, Petzold G, Bunker RD, et al. Defining the human C2H2 zinc finger degrome targeted by thalidomide analogs through CRBN. Science. 2018;362(6414). doi:10.1126/science.aat0572.
Tumor fraction in cell-free DNA as a biomarker in prostate cancer.
Choudhury AD, Werner L, Francini E, et al. Tumor fraction in cell-free DNA as a biomarker in prostate cancer. JCI Insight. 2018;3(21). doi:10.1172/jci.insight.122109.
Defining T Cell States Associated with Response to Checkpoint Immunotherapy in Melanoma.
Sade-Feldman M, Yizhak K, Bjorgaard SL, et al. Defining T Cell States Associated with Response to Checkpoint Immunotherapy in Melanoma. Cell. 2018;175(4):998-1013.e20. doi:10.1016/j.cell.2018.10.038.
A Cancer Cell Program Promotes T Cell Exclusion and Resistance to Checkpoint Blockade.
Jerby-Arnon L, Shah P, Cuoco MS, et al. A Cancer Cell Program Promotes T Cell Exclusion and Resistance to Checkpoint Blockade. Cell. 2018;175(4):984-997.e24. doi:10.1016/j.cell.2018.09.006.
Mutational processes shape the landscape of TP53 mutations in human cancer.
Giacomelli AO, Yang X, Lintner RE, et al. Mutational processes shape the landscape of TP53 mutations in human cancer. Nat Genet. 2018;50(10):1381-1387. doi:10.1038/s41588-018-0204-y.
Genomic correlates of response to immune checkpoint blockade in microsatellite-stable solid tumors.
Miao D, Margolis CA, Vokes NI, et al. Genomic correlates of response to immune checkpoint blockade in microsatellite-stable solid tumors. Nat Genet. 2018;50(9):1271-1281. doi:10.1038/s41588-018-0200-2.
Selective gene dependencies in MYCN-amplified neuroblastoma include the core transcriptional regulatory circuitry.
Durbin AD, Zimmerman MW, Dharia NV, et al. Selective gene dependencies in MYCN-amplified neuroblastoma include the core transcriptional regulatory circuitry. Nat Genet. 2018. doi:10.1038/s41588-018-0191-z.
Widespread Chromosomal Losses and Mitochondrial DNA Alterations as Genetic Drivers in Hürthle Cell Carcinoma.
Gopal RK, Kübler K, Calvo SE, et al. Widespread Chromosomal Losses and Mitochondrial DNA Alterations as Genetic Drivers in Hürthle Cell Carcinoma. Cancer Cell. 2018;34(2):242-255.e5. doi:10.1016/j.ccell.2018.06.013.
Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition.
Wong GS, Zhou J, Bin Liu J, et al. Author Correction: Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition. Nat Med. 2018. doi:10.1038/s41591-018-0168-6.
Genome-scale CRISPR-Cas9 screen identifies druggable dependencies in wild-type Ewing sarcoma.
Stolte B, Iniguez ABalboni, Dharia NV, et al. Genome-scale CRISPR-Cas9 screen identifies druggable dependencies in wild-type Ewing sarcoma. J Exp Med. 2018;215(8):2137-2155. doi:10.1084/jem.20171066.
Autophosphorylation of the carboxyl-terminal domain is not required for oncogenic transformation by lung-cancer derived EGFR mutants.
Cho J, Kim S, Du J, Meyerson M. Autophosphorylation of the carboxyl-terminal domain is not required for oncogenic transformation by lung-cancer derived EGFR mutants. Int J Cancer. 2018;143(3):679-685. doi:10.1002/ijc.31332.
Genetic and transcriptional evolution alters cancer cell line drug response.
Ben-David U, Siranosian B, Ha G, et al. Genetic and transcriptional evolution alters cancer cell line drug response. Nature. 2018;560(7718):325-330. doi:10.1038/s41586-018-0409-3.
Crbn is sufficient to confer sensitivity to thalidomide and its derivatives in mice.
Fink EC, McConkey M, Adams DN, et al. Crbn is sufficient to confer sensitivity to thalidomide and its derivatives in mice. Blood. 2018. doi:10.1182/blood-2018-05-852798.
Genome-wide screen identifies cullin-RING ligase machinery required for lenalidomide-dependent CRL4 activity.
Sievers QL, Gasser JA, Cowley GS, Fischer ES, Ebert BL. Genome-wide screen identifies cullin-RING ligase machinery required for lenalidomide-dependent CRL4 activity. Blood. 2018. doi:10.1182/blood-2018-01-821769.
GATK PathSeq: A customizable computational tool for the discovery and identification of microbial sequences in libraries from eukaryotic hosts.
Walker MA, Pedamallu CSekhar, Ojesina AI, et al. GATK PathSeq: A customizable computational tool for the discovery and identification of microbial sequences in libraries from eukaryotic hosts. Bioinformatics. 2018. doi:10.1093/bioinformatics/bty501.
Genome-scale analysis identifies paralog lethality as a vulnerability of chromosome 1p loss in cancer.
Viswanathan SR, Nogueira MF, Buss CG, et al. Genome-scale analysis identifies paralog lethality as a vulnerability of chromosome 1p loss in cancer. Nat Genet. 2018;50(7):937-943. doi:10.1038/s41588-018-0155-3.
GeNets: a unified web platform for network-based genomic analyses.
Li T, Kim A, Rosenbluh J, et al. GeNets: a unified web platform for network-based genomic analyses. Nat Methods. 2018;15(7):543-546. doi:10.1038/s41592-018-0039-6.
PPM1D truncating mutations confer resistance to chemotherapy and sensitivity to PPM1D inhibition in hematopoietic cells.
Kahn JD, Miller PG, Silver AJ, et al. PPM1D truncating mutations confer resistance to chemotherapy and sensitivity to PPM1D inhibition in hematopoietic cells. Blood. 2018. doi:10.1182/blood-2018-05-850339.
DeTiN: overcoming tumor-in-normal contamination.
Taylor-Weiner A, Stewart C, Giordano T, et al. DeTiN: overcoming tumor-in-normal contamination. Nat Methods. 2018. doi:10.1038/s41592-018-0036-9.
Structural Alterations Driving Castration-Resistant Prostate Cancer Revealed by Linked-Read Genome Sequencing.
Viswanathan SR, Ha G, Hoff AM, et al. Structural Alterations Driving Castration-Resistant Prostate Cancer Revealed by Linked-Read Genome Sequencing. Cell. 2018. doi:10.1016/j.cell.2018.05.036.
A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer.
Takeda DY, Spisák S, Seo J-H, et al. A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer. Cell. 2018. doi:10.1016/j.cell.2018.05.037.
Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition.
Wong GS, Zhou J, Bin Liu J, et al. Targeting wild-type KRAS-amplified gastroesophageal cancer through combined MEK and SHP2 inhibition. Nat Med. 2018. doi:10.1038/s41591-018-0022-x.
Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models.
Ng SY, Yoshida N, Christie AL, et al. Targetable vulnerabilities in T- and NK-cell lymphomas identified through preclinical models. Nat Commun. 2018;9(1):2024. doi:10.1038/s41467-018-04356-9.
A Convergence-Based Framework for Cancer Drug Resistance.
Konieczkowski DJ, Johannessen CM, Garraway LA. A Convergence-Based Framework for Cancer Drug Resistance. Cancer Cell. 2018;33(5):801-815. doi:10.1016/j.ccell.2018.03.025.
Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes.
Chapuy B, Stewart C, Dunford AJ, et al. Molecular subtypes of diffuse large B cell lymphoma are associated with distinct pathogenic mechanisms and outcomes. Nat Med. 2018;24(5):679-690. doi:10.1038/s41591-018-0016-8.
Distinct mutational signatures characterize concurrent loss of polymerase proofreading and mismatch repair.
Haradhvala NJ, Kim J, Maruvka YE, et al. Distinct mutational signatures characterize concurrent loss of polymerase proofreading and mismatch repair. Nat Commun. 2018;9(1):1746. doi:10.1038/s41467-018-04002-4.
Whole-exome sequencing of cell-free DNA and circulating tumor cells in multiple myeloma.
Manier S, Park J, Capelletti M, et al. Whole-exome sequencing of cell-free DNA and circulating tumor cells in multiple myeloma. Nat Commun. 2018;9(1):1691. doi:10.1038/s41467-018-04001-5.
Developmental and oncogenic programs in H3K27M gliomas dissected by single-cell RNA-seq.
Filbin MG, Tirosh I, Hovestadt V, et al. Developmental and oncogenic programs in H3K27M gliomas dissected by single-cell RNA-seq. Science. 2018;360(6386):331-335. doi:10.1126/science.aao4750.
Cancer-Germline Antigen Expression Discriminates Clinical Outcome to CTLA-4 Blockade.
Shukla SA, Bachireddy P, Schilling B, et al. Cancer-Germline Antigen Expression Discriminates Clinical Outcome to CTLA-4 Blockade. Cell. 2018;173(3):624-633.e8. doi:10.1016/j.cell.2018.03.026.
Genomic and Functional Approaches to Understanding Cancer Aneuploidy.
Taylor AM, Shih J, Ha G, et al. Genomic and Functional Approaches to Understanding Cancer Aneuploidy. Cancer Cell. 2018;33(4):676-689.e3. doi:10.1016/j.ccell.2018.03.007.
The long tail of oncogenic drivers in prostate cancer.
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