Our research focuses on understanding how genetic diversity provides insights into the predisposition to cancer and how somatic genomic aberrations contribute to tumor progression. As we learn more about the complexity of the human genome from programs like the HapMap and ENCODE projects, it becomes evident that our understanding of genetic diversity is incomplete. Structural variants, specifically in the form of Copy Number Variants (CNVs), add to the genomic diversity encoded in single DNA base-pair difference (Single Nucleotide Polymorphism, SNPs) and may contribute to cancer susceptibility. Genetic diversity and somatic mutations provide cancer a selective advantage to develop and progress.
In a highly interdisciplinary and systems biology
framework, our group contributes to the understanding of the
genomic complexity, which defines human tumors and of the
involvement of inherited genetic make-up through the development
and application of computational tools. Our group is
currently working on Whole Genome and Whole Exome Sequencing data
of prostate cancer in collaboration with Weill Cornell Medical
College and the Broad Institute and Weill Cornell Medical College.
Methodological work is dedicated to the assessment of tumor
evolution through clonality and sub-clonality quantification.
We are also designing, implementing and analyzing validation studies using human samples collected from the Harvard/Michigan/Cornell Early Detection Research Network clinical trial (U.S.A.) and the Tyrol Prostate Specific Antigen Screening Trial (Austria).
Specific projects include:
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