Associate Professor in Surgery
My research has been focusing on the development of methodologies and strategies to address the general question of human cancer heterogeneity and complexity, recognizing that clinical outcomes reflect a combination of contribution from the actual tumor but also the environment in which the tumor resides. By understanding who is at risk for recurrence, who is likely to respond to a given agent or regimen, and who is likely to exhibit an adverse event associated with a particular therapy, it will be possible to tailor therapeutic strategies to the characteristics of the individual patient as opposed to relying on the results of studies with heterogeneous populations of patients.
I made the original observation that gene copy number alterations (CNAs) in malignant cells can quantitatively affect gene function (Nat Genet 2005), and the contribution of this work to the field of cancer pharmacogenomics and personalized medicine was highly recognized by a "NEWS AND VIEWS" paper of Nature Genetics, in 2005. I demonstrated that clinical phenotypes can be affected by multiple forms of alterations (methylation, mutation, CNA) (Am J Hum Genet 2006), and genome-scan of CNAs followed by pathway analysis could uncover the novel gene interactions (Nat Med 2011). We developed a methodology that compiled a large collection of genomic data (Breast Cancer Res 2012) and demonstrated that uniquely characteristic of a clinical phenotype, such as dormancy, could be accessed using gene signature, a collection of multiple genetic alterations (Breast Cancer Res 2014).
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