Research & Publications
Overexpression of HER2, which occurs in ~30% of human breast cancers, correlates with enhanced tumor aggressiveness and decreased patient survival. Although Herceptin has significantly improved the treatment of HER2-positive tumors, drug resistance remains an obstacle in a high fraction of patients. The ability to target these cancers using antitumor agents with mechanisms of action that are independent of HER2 cellular growth function, represents a powerful tool to circumvent this form of resistance. Our lab is interested in the design of novel gene-targeted molecules that can be used in the treatment of both HER2-positive and Hercetin-resistant breast cancers.
Specialized Terms: Breast cancer; Drug design; Altered helical structures; Cancer and genomic instability; DNA repair and apoptosis
Biochemistry; Breast Neoplasms; DNA Repair; Nucleic Acids; Drug Design; Apoptosis; Radiation Oncology; Genomic Instability