ArticleMolecular cancer research : MCR2019
Pooled Genomic Screens Identify Anti-apoptotic Genes as Targetable Mediators of Chemotherapy Resistance in Ovarian Cancer.
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Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37citing papers in PubMed
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37 citing papers in PubMed, 48 citations in OpenAlex.
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- ABT‑737 increases cisplatin sensitivity through the ROS‑ASK1‑JNK MAPK signaling axis in human ovarian cancer cisplatin‑resistant A2780/DDP cells.Oncology reports · 2024Article
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- The emerging role of JAK inhibitors in ovarian cancer: new kids on the block?Annals of medicine and surgery (2012) · 2024Article
- The Identification of New c-FLIP Inhibitors for Restoring Apoptosis in TRAIL-Resistant Cancer Cells.Current issues in molecular biology · 2024Article
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Authors and funding
29 authors at 5 institutions in 3 countries.
Elizabeth H StoverDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.ORCID https://orcid.org/0000-0002-6578-3216
Maria B BacoCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Ofir CohenDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Yvonne Y LiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Elizabeth L ChristiePeter MacCallum Cancer Centre, Melbourne, Victoria, Australia.ORCID https://orcid.org/0000-0002-9959-7024
Mukta BagulCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Amy GoodaleGenetic Perturbation Platform, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Yenarae LeeGenetic Perturbation Platform, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Sasha PantelGenetic Perturbation Platform, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Matthew G ReesCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.ORCID https://orcid.org/0000-0002-2987-7581
Guo WeiCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Adam G PresserJohn B. Little Center for Radiation Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Maya K GelbardDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Weiqun ZhangCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Ioannis K ZervantonakisDepartment of Cell Biology, Harvard Medical School, Boston, Massachusetts.ORCID https://orcid.org/0000-0003-2386-9553
Patrick D BholaDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Jeremy RyanDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.ORCID https://orcid.org/0000-0002-3327-1283
Jennifer L GuerrieroDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.ORCID https://orcid.org/0000-0002-2104-5457
Joan MonteroDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Felice J LiangCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Andrew D CherniackDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.ORCID https://orcid.org/0000-0003-0470-0111
Federica PiccioniGenetic Perturbation Platform, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Ursula A MatulonisDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
David D L BowtellPeter MacCallum Cancer Centre, Melbourne, Victoria, Australia.
Kristopher A SarosiekJohn B. Little Center for Radiation Sciences, Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts.
Anthony LetaiDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
Levi A GarrawayEli Lilly and Company, Indianapolis, Indiana.
Cory M JohannessenCancer Program, Broad Institute of Harvard and MIT, Cambridge, Massachusetts.ORCID https://orcid.org/0000-0002-2618-1036
Matthew MeyersonDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts. matthew_meyerson@dfci.harvard.edu.
Broad Institute · USDana-Farber Cancer Institute · USHarvard University · USPeter MacCallum Cancer Centre · AUEli Lilly (United States) · US
Funding
NKX2-1 Enhancer Amplification and Lineage Addiction in Lung AdenocarcinomaR35CA197568 · NCI · DANA-FARBER CANCER INST · PI Matthew L. Meyerson · 2015 to 2026
$12.4MHarvard Clinical and Translational Science CenterKL2TR001100 · NCATS · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2013 to 2017
$8.5MProject 2U54CA224068 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI CORCORAN, RYAN BRUCE, FLAHERTY, KEITH T · 2017 to 2021
$6.3MCharacterizing TP53 and PPM1D mutations as resistance drivers to radiation therapy in Diffuse Intrinsic Pontine GliomasR01CA219943 · NCI · BROAD INSTITUTE, INC. · PI BEROUKHIM, RAMEEN, LIGON, KEITH LLOYD · 2017 to 2021
$2.5MThe roles of anti-apoptotic proteins BCL-XL and MCL1 in mediating survival of high-grade serous ovarian cancer following drug-induced DNA damageK08CA237871 · NCI · DANA-FARBER CANCER INST · PI STOVER, ELIZABETH HARMON · 2019 to 2023
$921kAnalysis of tumor-stroma signaling that mediates HER2-therapy resistance in breast cancerR00CA222554 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZERVANTONAKIS, IOANNIS · 2019 to 2021
$741kAnalysis of tumor-stroma signaling that mediates HER2-therapy resistance in breast cancerK99CA222554 · NCI · HARVARD MEDICAL SCHOOL · PI ZERVANTONAKIS, IOANNIS · 2017 to 2018
$253kHarnessing anti-tumor macrophages for cancer therapyF32CA180733 · NCI · DANA-FARBER CANCER INST · PI GUERRIERO, JENNIFER L. · 2013 to 2015
$165kNCATS NIH HHS KL2 TR001100NCI NIH HHS F32 CA180733NCI NIH HHS K08 CA237871NCI NIH HHS K99 CA222554NCI NIH HHS R00 CA222554NCI NIH HHS R01 CA219943NCI NIH HHS R35 CA197568NCI NIH HHS U54 CA224068
Abstract
High-grade serous ovarian cancer (HGSOC) is often sensitive to initial treatment with platinum and taxane combination chemotherapy, but most patients relapse with chemotherapy-resistant disease. To systematically identify genes modulating chemotherapy response, we performed pooled functional genomic screens in HGSOC cell lines treated with cisplatin, paclitaxel, or cisplatin plus paclitaxel. Genes in the intrinsic pathway of apoptosis were among the top candidate resistance genes in both gain-of-function and loss-of-function screens. In an open reading frame overexpression screen, followed by a mini-pool secondary screen, anti-apoptotic genes including
Indexed as
Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisApoptosis Regulatory Proteinsbcl-X ProteinCell Line, TumorCisplatinFemaleGenomicsHumansMyeloid Cell Leukemia Sequence 1 ProteinOvarian NeoplasmsPaclitaxelAntineoplastic AgentsApoptosis Regulatory ProteinsBCL2L1 protein, humanbcl-X ProteinCisplatinMCL1 protein, humanMyeloid Cell Leukemia Sequence 1 ProteinPaclitaxel
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