Evidence map›Paper›PMID 26069190›Full record

ArticleCancer discovery2015

ARID1A Deficiency Impairs the DNA Damage Checkpoint and Sensitizes Cells to PARP Inhibitors.

Jianfeng Shen, Yang Peng, Leizhen Wei, Wei Zhang, Lin Yang, Li Lan, Prabodh Kapoor, Zhenlin Ju, Qianxing Mo, Ie-Ming Shih and 6 more

Open access · greenAbstract read
In one paragraph

Article in Cancer discovery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 317 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
317citing papers in PubMed, 1 pooled it
13.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

317 citing papers in PubMed, 1 synthesis or guideline pooled it, 522 citations in OpenAlex.

  1. Pooled it
  2. SWI/SNF Complex-Deficient Undifferentiated Carcinoma of the Pancreas: Clinicopathologic and Genomic Analysis.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2024
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257 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 2 countries.

Jianfeng ShenDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Yang PengDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Leizhen WeiDepartment of Microbiology and Molecular Genetics, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. The University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Wei ZhangDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Lin YangDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Medical Oncology, Tongji Hospital, Tongji Medical College, The Huazhong University of Science and Technology, Wuhan, P.R. China.
Li LanDepartment of Microbiology and Molecular Genetics, The University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. The University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania.
Prabodh KapoorDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Zhenlin JuDepartment of Bioinformatics and Computational Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Qianxing MoDivision of Biostatistics, Dan L. Duncan Cancer Center, Baylor College of Medicine, Houston, Texas.
Ie-Ming ShihDepartment of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland.
Ivan P UrayDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Xiangwei WuDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Powel H BrownDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Xuetong ShenDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Gordon B MillsDepartment of Systems Biology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Guang PengDepartment of Clinical Cancer Prevention, The University of Texas MD Anderson Cancer Center, Houston, Texas. Department of Medical Oncology, Tongji Hospital, Tongji Medical College, The Huazhong University of Science and Technology, Wuhan, P.R. China. gpeng@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USUniversity of Pittsburgh · USChildren's Cancer Center · USJohns Hopkins University · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
UNIVERSITY OF TEXAS MD ANDERSON SPORE IN OVARIAN CANCERP50CA083639 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BAST, ROBERT C · 1999 to 2015
$33.0M
Targeting the PI3K Signaling Pathway in Endometrial CarcinomaP50CA098258 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI BODURKA, DIANE · 2003 to 2020
$32.0M
Mechanisms of radioresistance and strategies for radiosensitization in ovarian clear cell carcinomaR01CA181663 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Guang Peng · 2016 to 2026
$3.1M
Understanding and Targeting the DNA Repair Network in CancerR00CA149186 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PENG, GUANG · 2013 to 2015
$664k
Understanding and Targeting the DNA Repair Network in CancerK99CA149186 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PENG, GUANG · 2011 to 2012
$173k
NCI NIH HHS CA016672NCI NIH HHS K99 CA149186NCI NIH HHS P30 CA016672NCI NIH HHS P50 CA083639NCI NIH HHS P50 CA098258NCI NIH HHS P50 CA83639NCI NIH HHS R00 CA149186NCI NIH HHS R01 CA181663
6 · The paper itself

Abstract

unlabelledARID1A, SWI/SNF chromatin remodeling complex subunit, is a recently identified tumor suppressor that is mutated in a broad spectrum of human cancers. Thus, it is of fundamental clinical importance to understand its molecular functions and determine whether ARID1A deficiency can be exploited therapeutically. In this article, we report a key function of ARID1A in regulating the DNA damage checkpoint. ARID1A is recruited to DNA double-strand breaks (DSB) via its interaction with the upstream DNA damage checkpoint kinase ATR. At the molecular level, ARID1A facilitates efficient processing of DSB to single-strand ends and sustains DNA damage signaling. Importantly, ARID1A deficiency sensitizes cancer cells to PARP inhibitors in vitro and in vivo, providing a potential therapeutic strategy for patients with ARID1A-mutant tumors. SIGNIFICANCE: ARID1A has been identified as one of the most frequently mutated genes across human cancers. Our data suggest that clinical utility of PARP inhibitors might be extended beyond patients with BRCA mutations to a larger group of patients with ARID1A-mutant tumors, which may exhibit therapeutic vulnerability to PARP inhibitors.

Indexed as

DNA DamageAnimalsAtaxia Telangiectasia Mutated ProteinsBreast NeoplasmsCell Line, TumorDNA-Binding ProteinsDNA Breaks, Double-StrandedFemaleHCT116 CellsHumansLung NeoplasmsMaleMiceNuclear ProteinsPoly(ADP-ribose) Polymerase InhibitorsTranscription FactorsARID1A protein, humanAtaxia Telangiectasia Mutated ProteinsATR protein, humanDNA-Binding ProteinsNuclear ProteinsPoly(ADP-ribose) Polymerase InhibitorsTranscription Factors

Identifiers

PMID26069190
PMCPMC4497871
OpenAlexW2123454509

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.