The Lantern Vol. 24, No. 3, May 1956

• Wedding Week in East Pookins • Playground • When the Moon • Love Song • Balladier • Soliloquy • The Search for Alfie Patch • How I Learned to Drive • The Hard-Backed Chair • Amicus • A Strange Experiencehttps://digitalcommons.ursinus.edu/lantern/1069/thumbnail.jp

The Lantern Vol. 23, No. 2, March 1955

• Roy Blakesee on Mt. Washington • The Sound of the Bell • A City Dog • Why of Course I Still Read Comic Books, She Said • The Challenge • Thanks for the Ride • Tableau • On Necking • Be Gone With You O Pestilence of Mine • Turning the Pages • Now Showing • Spinning the Plattershttps://digitalcommons.ursinus.edu/lantern/1065/thumbnail.jp

The Lantern Vol. 23, No. 3, May 1955

• Les Assassins • Golf • The Dance • Philosophy for the Beginner • Spelling - Why Bother • The Hooded Paperweight • The Wonderful Gizmo • The Accident • What Happened • Old Dog Tilts Her Head • Interlude • The Monastery Mouse • Study in Rhime Royalhttps://digitalcommons.ursinus.edu/lantern/1066/thumbnail.jp

EXO1 protects BRCA1-deficient cells against toxic DNA lesions

Inactivating mutations in the BRCA1 and BRCA2 genes impair DNA double-strand break (DSB) repair by homologous recombination (HR), leading to chromosomal instability and cancer. Importantly, BRCA1/2 deficiency also causes therapeutically targetable vulnerabilities. Here, we identify the dependency on the end resection factor EXO1 as a key vulnerability of BRCA1-deficient cells. EXO1 deficiency generates poly(ADP-ribose)-decorated DNA lesions during S phase that associate with unresolved DSBs and genomic instability in BRCA1-deficient but not in wild-type or BRCA2-deficient cells. Our data indicate that BRCA1/EXO1 double-deficient cells accumulate DSBs due to impaired repair by single-strand annealing (SSA) on top of their HR defect. In contrast, BRCA2-deficient cells retain SSA activity in the absence of EXO1 and hence tolerate EXO1 loss. Consistent with a dependency on EXO1-mediated SSA, we find that BRCA1-mutated tumors show elevated EXO1 expression and increased SSA-associated genomic scars compared with BRCA1-proficient tumors. Overall, our findings uncover EXO1 as a promising therapeutic target for BRCA1-deficient tumors