Our Research

Our laboratory is interested in understanding the molecular mechanisms of cancer development and progression. Another line of research focuses on the molecular events that determine the outcome of patients to targeted therapies such as imatinib mesylate (GleevecTM).

These two research areas are grouped around a common theme: genomic instability.

We are focusing on two model systems for our studies:

Human papillomavirus (HPV)-induced carcinomas of the anogenital tract and the oropharynx are used to determine how genomic instability promotes tumor progression. Current projects include:

· CDK2 and the mechanisms of centriole overduplication induced by the HPV-16 E7 oncoprotein

· The role of proteolysis in centriole overduplication

· Causes and consequences of genomic instability in tumor cells with a focus on factors that determine cell viability

· High-risk HPV infection in Fanconi Anemia patients.

· Genomic instability in HPV-associated anal carcinomas.

Gastrointestinal stromal tumors (GISTs), which are caused by mutations in the KIT or PDGFRA receptor tyrosine kinases, are used to exploit signaling pathways involved in genomic instability for cancer therapy and prevention. Current projects include:

· Identification of mechanisms that mediate the cytotoxic response of GIST cells to imatinib mesylate

· Mechanisms of resistance to small molecule inhibitor therapy

· Profiling of GISTs using a tissue array

Smaller subprojects are available for individuals interested in a lab rotation/internship/volunteer position.

Our Research