Katherine M. Aird

The paper identifies altered Golgi morphology as a vulnerability in CDKN2A/p16-Low melanoma and shows that Golgi disruption via lipid peroxidation sensitizes these cells to treatment.

This study shows that chemotherapy-induced senescence-associated secretome promotes metastasis in ovarian cancer by reprogramming metabolism and increasing cell detachment.

This study shows that αKG-mediated carnitine synthesis supports HR proficiency by promoting histone acetylation, which enhances DNA repair.

This study identifies RHOV as a detachment-sensitive Rho GTPase critical for ovarian cancer peritoneal metastasis by enhancing anoikis resistance and cytoskeletal remodeling.

This study shows that UNG deficiency in tumor cells reduces intrinsic inflammatory signaling and alters interferon sensitivity, leading to a modified tumor microenvironment.

This study shows that loss of MPZL3 promotes EMT and chemoresistance in ovarian cancer by reducing adhesion and increasing drug resistance.

This study shows ATR enhances mTORC1 activity through cholesterol synthesis via LSS, independent of CHK1 and TSC, and this effect is amplified in p16-deficient cells.

This study shows that zinc availability in the tumor microenvironment affects anti-PD1 therapy response in CDKN2A-low tumors through macrophage phagocytosis.

This study shows that ACSS2-mediated acetate conversion to acetyl-CoA promotes quiescence in ovarian cancer cells, linking metabolic reprogramming to therapeutic resistance.

This study identifies an alternative splice variant of Drp1 in ovarian cancer that promotes metastasis and chemoresistance by altering mitochondrial dynamics.

The paper shows that dU-rich cytoplasmic DNA inhibits STING-dependent immune responses and enhances anti-PD-L1 therapy efficacy in tumors.

This study shows GPX3 is necessary for ovarian cancer growth in vivo and promotes GDF15 expression, linking it to immune checkpoint inhibitor response.