Evidence map›Paper›PMID 42760358›Full record

ReviewNature reviews. Molecular cell biology2026

Mechanisms and disease relevance of DNA break repair pathway choice.

Michelle L Swift, Cody M Rogers, Hardeep Kaur, Dipanjan Chowdhury, Patrick Sung

Abstract readReview
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In one paragraph

Review in Nature reviews. Molecular cell biology, 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

5 authors.

Michelle L Swift *Division of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0003-3645-1308
Cody M Rogers *Department of Biochemistry and Structural Biology and Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.ORCID http://orcid.org/0000-0001-6499-1390
Hardeep Kaur *Department of Biochemistry and Structural Biology and Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.ORCID http://orcid.org/0000-0002-6385-8413
Dipanjan ChowdhuryDivision of Radiation and Genome Stability, Department of Radiation Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA. dipanjan_chowdhury@dfci.harvard.edu.ORCID http://orcid.org/0000-0001-5645-3752
Patrick SungDepartment of Biochemistry and Structural Biology and Greehey Children's Cancer Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA. sungp@uthscsa.edu.ORCID http://orcid.org/0000-0003-1396-9040

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Understanding what drives the choice between homologous recombination (HR) and non-homologous end joining (NHEJ) as the DNA double-strand break (DSB) repair pathway can help to elucidate mechanisms of genome repair and acquired drug resistance in cancer cells. This choice is intimately linked with a highly regulated process of DNA end resection, mediated by several nuclease entities. Concerted efforts by many laboratories have identified several factors involved in DNA end resection, but we are only beginning to appreciate the mechanisms that underpin DSB repair pathway choice. In this Review, we highlight how DSB repair factors, DSB repair regulators and chromatin modifications determine whether HR or NHEJ is engaged as the repair pathway, with a focus on the antagonistic roles of the tumour suppressor complex BRCA1-BARD1 and the 53BP1 axis in repair pathway choice. How RNA-DNA hybrids affect HR execution and how they are processed by helicases and HR factors is also discussed. Moreover, we describe how dysfunction in repair pathway choice affects tumorigenesis and drives chemotherapeutic resistance.

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