Raquel Buj

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

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 identifies de novo purine metabolism as a vulnerability in cancers with low p16 expression, showing sensitivity to anti-folate drugs like methotrexate.

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 that tumor-associated macrophages (TAMs) enhance ovarian cancer stem-like cell (OvCSC) proliferation and survival, contributing to chemotherapy resistance and relapse.