Evidence map›Paper›PMID 22843421›Full record

ReviewCancer discovery2012

Mechanisms of BRCA1 tumor suppression.

Daniel P Silver, David M Livingston

Open access · greenAbstract readReview
In one paragraph

Review in Cancer discovery, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

92 citing papers in PubMed, 157 citations in OpenAlex.

  1. TumorClinical cancer research : an official journal of the American Association for Cancer Research · 2017
    Trial
  2. Trial
  3. Trial
  4. Article
  5. Review
  6. Article
  7. PathogenicThe journal of physical chemistry. B · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. DOT1L-mediated RAP80 methylation promotes BRCA1 recruitment to elicit DNA repair.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. R-loop functions inProceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

32 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

2 authors at 1 institution in 1 country.

Daniel P SilverDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
David M Livingston
Dana-Farber Cancer Institute · US

Funding

Use of Organotypic and Mammary Gland Models to Investigate the Outcomes of ClonalP01CA080111 · NCI · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI DILLON, DEBORAH · 1999 to 2018
$36.0M
Variation in Receptor Tyrosine Kinases and Breast Cancer RiskP50CA089393 · NCI · DANA-FARBER CANCER INSTITUTE · PI HARRIS, LYNDSAY NORINE · 2000 to 2009
$28.8M
BRCA1 Function in Post-Damage Nuclear FociR01CA136512 · NCI · DANA-FARBER CANCER INST · PI LIVINGSTON, DAVID MORSE · 2009 to 2019
$4.6M
ROLES OF BRCA1 AND BRCA2 IN BREAST CARCINOGENESISK08CA082572 · NCI · DANA-FARBER CANCER INSTITUTE · PI SILVER, DANIEL P · 1999 to 2003
$528k
NCI NIH HHS CA089393NCI NIH HHS K08 CA082572NCI NIH HHS P01 CA080111NCI NIH HHS P50 CA089393NCI NIH HHS R01 CA136512
6 · The paper itself

Abstract

unlabelledThe p220 BRCA1 tumor suppressor protein has been implicated in multiple biochemical and biologic functions since its molecular cloning 18 years ago. Here, we discuss those functions most relevant for its tumor-suppressing activities with an emphasis on new findings. In particular, this review focuses on what is known of the activities of those BRCA1-binding partners that have tumor suppressor functions, on the reversion of mutant BRCA1 alleles concomitant with therapy resistance, on insights gained from studies of BRCA1 structure-function relationships, recent findings from animal models, and the potential role of BRCA1 in some nonhereditary tumors. From this information, a more detailed and refined picture of BRCA1 tumor suppression is beginning to emerge. Although key mysteries remain--such as why BRCA1 tumor suppression is focused on carcinomas of the breast and ovary--the pace of discovery is increasing. SIGNIFICANCE: BRCA1 functions as a clinically important classical tumor suppressor in hereditary breast and ovarian cancer; here, we review progress in understanding how BRCA1 operates to suppress tumor formation.

Indexed as

Genes, BRCA1AnimalsBRCA1 ProteinBreast NeoplasmsFemaleHumansMutationOvarian NeoplasmsBRCA1 Protein

Identifiers

PMID22843421
PMCPMC3437262
OpenAlexW2156001194

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.