Evidence map›Paper›PMID 25217519›Full record

ArticleCancer research2014

Therapeutic targeting of BRCA1-mutated breast cancers with agents that activate DNA repair.

Elizabeth Alli, David Solow-Cordero, Stephanie C Casey, James M Ford

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Benserazide, a dopadecarboxylase inhibitor, suppresses tumor growth by targeting hexokinase 2.Journal of experimental & clinical cancer research : CR · 2017
    Article
  10. Article
  11. Synergistic suppressive effect of PARP-1 inhibitor PJ34 and HDAC inhibitor SAHA on proliferation of liver cancer cells.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015
    Article
  12. BRCA1: a movement toward cancer prevention.Molecular & cellular oncology
    Article
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

4 authors at 2 institutions in 1 country.

Elizabeth AlliDepartment of Medicine/Oncology, Stanford University School of Medicine, Stanford, California.
David Solow-CorderoDepartment of Chemical and Systems Biology and Stanford High-Throughput Bioscience Center, Stanford University School of Medicine, Stanford, California.
Stephanie C CaseyDepartment of Medicine/Oncology, Stanford University School of Medicine, Stanford, California.
James M FordDepartment of Medicine/Oncology, Stanford University School of Medicine, Stanford, California. Department of Genetics, Stanford University School of Medicine, Stanford, California. jmf@stanford.edu.
Stanford Medicine · USHigh Throughput Biology (United States) · US

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Melinda L. Telli · 2007 to 2026
$71.4M
Upgraded High-Content and High-Throughput siRNA Screening SystemS10RR026338 · NCRR · STANFORD UNIVERSITY · PI SOLOW-CORDERO, DAVID EDWARD · 2010 to 2010
$498k
A High-Throughput Assay for DNA Repair Activity in the Presence of AberrantBRCA1R21NS061674 · NINDS · STANFORD UNIVERSITY · PI FORD, JAMES M. · 2010 to 2010
$160k
NCI NIH HHS P30 CA124435NCRR NIH HHS S10 RR026338NINDS NIH HHS 1R21NS061674-01A2NINDS NIH HHS R21 NS061674
6 · The paper itself

Abstract

Cancers due to germline mutations in the BRCA1 gene tend to lack targets for approved chemoprevention agents. This study aimed at a targeted chemoprevention strategy for BRCA1-associated malignancies. Mutant BRCA1 limits the base-excision DNA repair activity that addresses oxidative DNA damage, the accumulation of which heightens one's risk for cancer. Therefore, we conducted a high-throughput chemical screen to identify drug candidates that could attenuate the inhibitory effects of mutant BRCA1 on this repair activity, thereby describing a new class of DNA repair-activating chemopreventive agents. In the screen design, such drugs functioned by enhancing base-excision DNA repair of oxidative DNA damage in the presence of mutant BRCA1, with minimal cytotoxicity. We identified at least one new agent that decreased malignant properties associated with tumorigenesis, including anchorage-independent growth and tumor progression. This work offers a preclinical proof-of-concept for a wholly new approach to chemoprevention in carriers of BRCA1 mutations as a strategy to reduce the prevalence of BRCA1-associated malignancy.

Indexed as

Molecular Targeted TherapyBRCA1 ProteinBreast NeoplasmsDNA RepairFemaleGerm-Line MutationHumansMCF-7 CellsSmall Molecule LibrariesBRCA1 ProteinSmall Molecule Libraries

Identifiers

PMID25217519
PMCPMC4388430
OpenAlexW2102998540

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.