Overview:
Our knowledge of cancer progression has grown exponentially by our ability to model cancer initiation. Still the major challenge faced by physicians is the prevention and treatment of metastasis, the main reason for cancer related deaths.
Our understanding of metastasis has lagged behind that of primary tumor biology resulting in limited metastasis preventive therapies. Our work focuses on understanding the biology of residual cancer cells that persist in a dormant state
after initial therapy. This knowledge will allow targeting minimal residual disease before it becomes clinically detectable and thus preventing recurrences. Our research is revealing ways to maintain residual cancer dormancy, kill dormant
cancer cells and markers to determine the dormant or active state of disseminated disease.
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Surprisingly, cancer patients presumed cured after primary tumor removal and therapy, can carry non-proliferating ‘dormant’ disseminated tumor cells (DTCs) for years before reactivating to form incurable metastasis. Thus, despite cancer cells carrying
genetic alterations micro-environmental and epigenetic mechanisms appear to induce tumor cell dormancy. My lab focuses on understanding the biology of dormant DTCs and their reactivation, to target them and prevent relapse. This contrasts
to the vast majority of cancer research, which is aimed at understanding constant cancer growth. My team led a paradigm shift that is revealing novel cancer biology. We integrated mechanisms of basic stress and mitogenic signaling, adult
stem cell and micro-environmental biology and discovered that a reciprocal crosstalk between DTCs and the microenvironment regulates the inter-conversion between dormancy and proliferation.
