Evidence map›Paper›PMID 26775620›Full record

ReviewNature reviews. Cancer2016

BRCAness revisited.

Christopher J Lord, Alan Ashworth

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 798 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
798citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

798 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Multilevel Mechanisms of Cancer Drug Resistance.International journal of molecular sciences · 2024
    Pooled it
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  16. Targeting CDKs in the RNAPII transcription cycle.Nature reviews. Drug discovery · 2026
    Review
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  18. Article
  19. Review
  20. Article

738 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.

Christopher J LordCancer Research UK Gene Function Laboratory and Breast Cancer Now Research Centre, The Institute of Cancer Research, London SW3 6JB, UK.
Alan AshworthUCSF Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, California 94158, USA.

Funding

Cancer Research UK 14276
6 · The paper itself

Abstract

Over the past 20 years, there has been considerable progress in our understanding of the biological functions of the BRCA1 and BRCA2 cancer susceptibility genes. This has led to the development of new therapeutic approaches that target tumours with loss-of-function mutations in either BRCA1 or BRCA2. Tumours that share molecular features of BRCA-mutant tumours - that is, those with 'BRCAness' - may also respond to similar therapeutic approaches. Several paradigm shifts require a reassessment of the concept of BRCAness, how this property is assayed and its relevance to our understanding of tumour biology and the treatment of cancer.

Indexed as

Antineoplastic AgentsBiomarkers, TumorBRCA1 ProteinBRCA2 ProteinDrug Resistance, NeoplasmFemaleGenetic Predisposition to DiseaseGerm-Line MutationHumansMutationNeoplasmsPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsRad51 RecombinaseAntineoplastic AgentsBiomarkers, TumorBRCA1 ProteinBRCA1 protein, humanBRCA2 ProteinBRCA2 protein, humanolaparibPhthalazinesPiperazinesPoly(ADP-ribose) Polymerase InhibitorsRAD51 protein, humanRad51 Recombinase

Identifiers

PMID26775620

What OpenQuestion holds

Textmetadata
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.