My research has consistently uncovered fundamental mechanisms of genome maintenance and cancer metabolism. Early work identified novel nucleotide excision repair factors in yeast (PMID: 11920679) and revealed that H2AX phosphorylation after UV irradiation functions beyond double-strand break signaling (PMID: 16788066). I helped to demonstrate that short-term starvation protects healthy tissue but sensitizes tumors to chemotherapy (PMID: 23211021). In NSCLC, we showed that pretreatment with pemetrexed augments DNA-damaging therapies and that resistant A549 subpopulations harbor distinct metabolic states linked to tumor initiation and therapy response (PMID: 30591423, 31798346). Building on this, I identified lactate dehydrogenase B (LDHB) as a metabolic gatekeeper: its silencing induces mitochondrial DNA damage, disrupts nucleotide metabolism, and reduces tumorigenesis in KRAS^mut/TP53^loss mice (PMID: 35877003). Most recently, we uncovered the underlying mechanism—LDHB transfers reducing equivalents from NADH to ubiquinone, sustaining mitochondrial ubiquinol pools that suppress ferroptosis independently of lactate metabolism. This discovery positions LDHB as a novel anti-ferroptosis factor acting in parallel with GPX4 and DHODH, highlighting its potential as a therapeutic target to enhance radiotherapy and ferroptosis-based therapies (PMID: 40090955)