My research focuses on understanding the molecular mechanisms underlying the DNA damage response (DDR) to develop innovative therapeutic strategies that target cancer-specific vulnerabilities. I have examined the role of Ku and DNA-PK in DNA double-strand break repair, leading to the discovery and optimization of first-in-class small molecule inhibitors that block the Ku-DNA interaction and modulate DDR, thereby sensitizing cancer models to DNA-damaging agents. These efforts have integrated medicinal chemistry, biochemistry, and cellular biology to define structure–activity relationships, validate on-target efficacy in vitro and in vivo, and uncover synergistic interactions with ionizing radiation and standard chemotherapeutics.
Through these initiatives, my main goal is to translate DDR-targeted approaches into clinically viable therapies that overcome resistance and improve outcomes for patients with lung and esophageal cancers. Building on this foundation, my research interests focus on the epidermal growth factor receptor (EGFR) axis, which drives a significant subset of non-small cell lung cancers (NSCLC) to uncover novel vulnerabilities in the context of DDR. A key aspect of my interest involves dissecting the mechanistic interactions that influence therapeutic responses and resistance in EGFR-driven cancers. I am especially focused on how replication stress and DDR modulation impact EGFR signaling and sensitivity to EGFR tyrosine kinase inhibitors (TKIs), aiming to develop new therapeutic interventions with direct clinical relevance for patients with EGFR-driven NSCLC cancers and related malignancies.
Post-doctoral Fellowship - Indiana University, Indianapolis, IN 2020, 2025
Ph.D. - University of Concepcion, Chile 2018
