Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/2026This study was truly a team effort! Thanks to all authors! We gratefully acknowledge support from the National Cancer Institute (NCI) and Mayo Clinic Breast Cancer SPORE for funding this project. A particularly meaningful milestone for our young lab—and hopefully the first of many! 010
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/2026Together, our results position FANCM at the intersection of replication-stress tolerance, structural genome evolution, and synthetic-lethal vulnerability in BRCA1-deficient breast cancer. 100
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/20265. BRCA1-altered human breast tumors with low FANCM expression recapitulate key features of the experimentally observed duplication phenotype. 110
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/20264. FANCM limits transcription–replication encounters in BRCA1-deficient breast cancer cells, with newly emerging tandem duplications preferentially associated with Pol II-occupied genomic regions. 110
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/20263. FANCM loss in BRCA1-mutant breast cancer cells drives genome-wide structural variation, amplifying short tandem duplications while enabling larger tandem duplications and diverse rearrangements. 110
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/20262. A temporally controlled FANCM-depletion system was developed to track genome evolution in BRCA1-mutant breast cancer over successive cell divisions under endogenous replication stress, before declining cellular fitness becomes limiting. 100
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/2026Key findings: 1. BRCA1 deficiency increases FANCM association with nascent replication forks, creating a synthetic-lethal dependency on FANCM across 2D and 3D breast cancer spheroid models. 100
Arvind Panday & Lab @arvindpanday.bsky.social · 10/09/2026🎉 Excited to share the first preprint from the Panday Lab! www.biorxiv.org/content/10.6... We identify FANCM as an adaptive genome-maintenance dependency in BRCA1-deficient breast cancer and uncover its role in restraining ongoing structural genome evolution. 231