Defining mechanisms of genomic evolution in cancer
Sarah McClelland, PhD
Barts Cancer Institute, Queen Mary University of London
Aneuploidy and DNA copy number variations are defining features of nearly all cancer types. Despite this, very little is known about the mechanisms that cause these aberrations to accumulate, and what their functional significance is to cancer development and therapy resistance. To tackle these two fundamental challenges, we combine approaches from cell biology and genomics: First, we define the mechanisms that cause chromosomal instability and aneuploidy in cancer by characterising the acute genomic alterations that occur as a result of specific chromosomal instability mechanisms after one cell cycle. Second, we track the genomic alterations at the single cell level as the cancer cells grow – giving insights into patterns of ongoing genome evolution beyond traditional static sequencing approaches. Lastly, we employ a recently developed Cas9-based experimental tool, that induces chromosomal missegregation during mitosis, to study the impact of specific chromosomal alterations on cellular behaviour.
BIOSKETCH
Sarah McClelland is Professor in Cancer Genomics and Cancer Cell Biology at the Barts Cancer Institute, Queen Mary University of London and deputy Centre lead for Cancer Genomics and Computational Biology. Sarah studied Biochemistry and obtained her PhD in Biochemistry from the University of Bristol. Her lab aims to understand the mechanisms that underlie numerical and structural chromosome aberrations in cancer at a molecular level, which also involves understanding how normal cells replicate and segregate their genomes.