Evidence map›Paper›PMID 41495480›Full record

ReviewNature genetics2026

Insights from three decades of BRCA1/2 modeling in mice.

Julia-Star Darnold, Jos Jonkers

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Julia-Star DarnoldDivision of Molecular Pathology, Netherlands Cancer Institute, Amsterdam, the Netherlands.ORCID http://orcid.org/0009-0003-9744-3114
Jos JonkersDivision of Molecular Pathology, Netherlands Cancer Institute, Amsterdam, the Netherlands. j.jonkers@nki.nl.ORCID http://orcid.org/0000-0002-9264-9792

Funding

KWF Kankerbestrijding (Dutch Cancer Society) 14516KWF Kankerbestrijding (Dutch Cancer Society) 14949Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) 320030M_219453
6 · The paper itself

Abstract

Since the discovery of the BRCA1 and BRCA2 (hereafter referred to as BRCA1/2) hereditary breast and ovarian cancer genes three decades ago, genetically engineered and patient-derived mouse models have been instrumental in advancing our understanding of BRCA1/2 biology, particularly their roles in normal development, tumor suppression and therapy response. Brca1/2-mutant mouse models and derivative cell lines have facilitated in vivo dissection of BRCA1/2 functions and identification of the cellular origin and (epi)genetic drivers of BRCA1/2-associated cancer. Genetically engineered and patient-derived mouse tumor models have also been instrumental in developing new (combination) therapies for patients with BRCA1/2-mutated cancers and to study mechanisms of therapy resistance. In this Perspective, we highlight the crucial insights into the complex biology of BRCA1/2 these models have afforded and emphasize those aspects that remain to be elucidated. We also propose next-generation mouse models to further advance our understanding of BRCA1/2 and improve the quality of life of mutation carriers.

Indexed as

BRCA1 ProteinBRCA2 ProteinBreast NeoplasmsDisease Models, AnimalGenes, BRCA1Genes, BRCA2Ovarian NeoplasmsAnimalsFemaleHumansMiceMutationBRCA1 ProteinBRCA2 Protein

Identifiers

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.