ArticleThe EMBO journal2026
The BRCA1 coiled-coil domain is dispensable for suppression of tandem duplications and tolerance of FANCM loss.
Namrata M Nilavar, Alberto Marin-Gonzalez, Francesca Menghi, Daniel Nguyen, Nicholas A Willis, Ellen Wientjens, Bing Xia, Jos Jonkers, Edison T Liu, Ralph Scully
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In one paragraphArticle in The EMBO journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 · Who and what moneyAuthors and funding
10 authors.
Namrata M NilavarDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0001-6081-0513 Alberto Marin-GonzalezDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Francesca MenghiThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Daniel NguyenDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Nicholas A WillisDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Ellen WientjensDivision of Molecular Pathology, Netherlands Cancer Institute, Amsterdam, The Netherlands.
Edison T LiuThe Jackson Laboratory for Genomic Medicine, Farmington, CT, USA.
Ralph ScullyDepartment of Medicine, Division of Hematology-Oncology and Cancer Research Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. rscully@bidmc.harvard.edu.ORCID http://orcid.org/0000-0002-5064-0175 Funding
Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI Paul Robson · 1985 to 2026
$61.9MProject 4: The BRCA Network in Medulloblastoma Responses to Replication StressP01CA250957 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI DE, SUBHAJYOTI · 2021 to 2025
$11.3MRole of PALB2 in the DNA Damage Response and Cancer SuppressionR01CA138804 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI XIA, BING · 2009 to 2024
$5.5MStalled replication fork repair in cancer predisposition and cancertherapyR35CA263813 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI Ralph Scully · 2022 to 2026
$5.1MGenomic Biology of the Tandem Duplicator Phenotype in Mouse and Human CancersR01CA255705 · NCI · JACKSON LABORATORY · PI LIU, EDISON TAK-BUN · 2021 to 2025
$3.5MTargeting Autophagy in Hereditary Breast CancerR01CA188096 · NCI · RBHS -CANCER INSTITUTE OF NEW JERSEY · PI WHITE, EILEEN P., XIA, BING · 2015 to 2019
$2.4MRegulation of DNA replication kinetics by BRCA2 after DNA damageR01CA262227 · NCI · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI XIA, BING · 2021 to 2025
$1.7MAmerican Cancer Society (ACS) PF-24-1321213-01-DMCHHS | NIH | National Cancer Institute (NCI) P01CA250957HHS | NIH | National Cancer Institute (NCI) P30CA034196HHS | NIH | National Cancer Institute (NCI) R01CA138804HHS | NIH | National Cancer Institute (NCI) R01CA255705HHS | NIH | National Cancer Institute (NCI) R01CA262227HHS | NIH | National Cancer Institute (NCI) R35CA263813KWF Kankerbestrijding (KWF) NKI 2015-7877Lundbeck Foundation (Lundbeckfonden) R223-2016-8NCI NIH HHS R01 CA138804NCI NIH HHS R01 CA188096NCI NIH HHS R01 CA262227
6 · The paper itselfAbstract
BRCA1-linked cancers contain abundant ~10 kb 'Group 1' tandem duplications (TDs). Group 1 TDs form at a Tus/Ter replication-fork barrier in DNA-end resection-defective mouse embryonic stem (mES) cells lacking Brca1 exon 11. To elucidate how BRCA1 suppresses Group 1 TDs, we analyzed Brca1 coiled-coil (CC)-domain mutants-separation-of-function alleles impaired for homologous recombination (HR) through loss of PALB2-binding and RAD51-loading functions but competent for DNA-end resection. Notably, Brca1 CC mutants retain the ability to suppress Group 1 TDs in the Tus/Ter system and in a mouse model of Brca1-linked mammary tumorigenesis. These data suggest that Brca1 CC domain-mutant cancers follow a path of tumorigenesis distinct from that of other Brca1-linked cancers. FANCM is a TD co-suppressor, loss of which is synthetic lethal/sick in Brca1 exon 11-deleted cells. In contrast, Fancm deletion unexpectedly improves the growth of Brca1 CC mutant and Brca2 mutant mES cells. Thus, Group 1 tandem duplication formation and Fancm synthetic lethality are linked phenotypes, potentially related to defective BRCA1-mediated DNA end resection but genetically separable from BRCA1/PALB2-mediated RAD51 loading.
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