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Cancer Program

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.
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.
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.
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.
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. 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.
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. doi:10.1038/nbt.4239.
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.
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.
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.
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. doi:10.1038/s41592-018-0039-6.
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.
Armenia J, Wankowicz SAM, Liu D, et al. The long tail of oncogenic drivers in prostate cancer. Nat Genet. 2018. doi:10.1038/s41588-018-0078-z.
Convergent Therapeutic Strategies to Overcome the Heterogeneity of Acquired Resistance in Colorectal Cancer.
Hazar-Rethinam M, Kleyman M, G Han C, et al. Convergent Therapeutic Strategies to Overcome the Heterogeneity of Acquired Resistance in Colorectal Cancer. Cancer Discov. 2018;8(4):417-427. doi:10.1158/2159-8290.CD-17-1227.
SvABA: genome-wide detection of structural variants and indels by local assembly.
Wala JA, Bandopadhayay P, Greenwald NF, et al. SvABA: genome-wide detection of structural variants and indels by local assembly. Genome Res. 2018;28(4):581-591. doi:10.1101/gr.221028.117.
Landscapes of childhood tumours.
Bandopadhayay P, Meyerson M. Landscapes of childhood tumours. Nature. 2018;555(7696):316-317. doi:10.1038/d41586-018-01648-4.
Pooled in vivo screens for cancer immunotherapy target discovery.
Lane-Reticker SK, Manguso RT, W Haining N. Pooled in vivo screens for cancer immunotherapy target discovery. Immunotherapy. 2018;10(3):167-170. doi:10.2217/imt-2017-0164.
Inherited DNA-Repair Defects in Colorectal Cancer.
AlDubayan SH, Giannakis M, Moore ND, et al. Inherited DNA-Repair Defects in Colorectal Cancer. Am J Hum Genet. 2018;102(3):401-414. doi:10.1016/j.ajhg.2018.01.018.
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. doi:10.1002/ijc.31332.
EWS/FLI Confers Tumor Cell Synthetic Lethality to CDK12 Inhibition in Ewing Sarcoma.
Iniguez ABalboni, Stolte B, Wang EJue, et al. EWS/FLI Confers Tumor Cell Synthetic Lethality to CDK12 Inhibition in Ewing Sarcoma. Cancer Cell. 2018. doi:10.1016/j.ccell.2017.12.009.
Genomic correlates of response to immune checkpoint therapies in clear cell renal cell carcinoma.
Miao D, Margolis CA, Gao W, et al. Genomic correlates of response to immune checkpoint therapies in clear cell renal cell carcinoma. Science. 2018. doi:10.1126/science.aan5951.
Association of Cell-Free DNA Tumor Fraction and Somatic Copy Number Alterations With Survival in Metastatic Triple-Negative Breast Cancer.
Stover DG, Parsons HA, Ha G, et al. Association of Cell-Free DNA Tumor Fraction and Somatic Copy Number Alterations With Survival in Metastatic Triple-Negative Breast Cancer. J Clin Oncol. 2018:JCO2017760033. doi:10.1200/JCO.2017.76.0033.
NetSig: network-based discovery from cancer genomes.
Horn H, Lawrence MS, Chouinard CR, et al. NetSig: network-based discovery from cancer genomes. Nat Methods. 2018;15(1):61-66. doi:10.1038/nmeth.4514.