The core of my research is divided into two scientifically complementary strategies: the genomic and proteomic analysis of patient samples that can be hypothesis-generating for the identification of gene/pathways associated with therapy sensitivity, and the biochemical validation of these hypotheses in the laboratory to dissect the molecular mechanisms and validating the causative role of potential players of drug resistance. Ideally, these findings will translate into more efficacious and safe antitumor treatments.
Identify the distinct genomic alterations that mediate acquired resistance in patients who initially respond to but eventually fail on targeted therapy.
Analyze tumors from patients who are exquisitely sensitive to targeted therapy (outliers).
Study the early molecular mechanisms of tumor adaptation following treatment that can limit the sensitivity to the targeted agents.