Genome instability is a prominent hallmark of cancer, often associated with cancer heterogeneity, progression and poor survival. Indeed, nearly all forms of cancer (~90%) contain significant levels of genomic instability often driven by dysregulated DNA repair and/or DNA replication. Genomic DNA is packaged into chromatin, which has a profound, yet not well understood regulatory influence on DNA repair and replication. Determining the regulatory interplay between chromatin, DNA repair and replication is central to better understand cancer heterogeneity, progression and treatment opportunities. Our laboratory combines cross-disciplinary approaches in relevant epigenetic model organisms, human cell lines, and genomics into an integrative research program addressing multi-level epigenetic and chromatin-based regulation of DNA repair and genome stability. The key goal of our research is to advance current understanding of the epigenetic regulation and genome maintenance pathways as well as explore the functional interplay of these mechanisms with the immune system, to guide development of new approaches in cancer prevention, treatment and personalized medicine.
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