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Molecular Mechanisms of Tumorigenesis and Cell Cycle Control My research is centered on understanding molecular mechanisms that control cell proliferation and checkpoint responses, and how those processes are disrupted during tumorigenesis. A principal focus of the lab is the ARF tumor suppressor, which is encoded by a gene (INK4a/ARF) that is inactivated in 40-50% of all human cancers. ARF inhibits tumorigenesis through p53-dependent and p53-independent signaling pathways that are complex and only partially defined. That is because ARF functions through numerous binding partners (at least 30) to promote apoptosis or senescence, inhibit migration/invasion and metastasis, sustain cell stress checkpoints and maintain chromosomal stability. Our goal is to define the critical regulators of ARF signaling and determine their significance to tumor suppression using molecular approaches and in vivo models of cancer. In so doing, we will advance our fundamental understanding of ARF-mediated tumor suppression and also identify novel regulators of growth (both positive and negative) whose characterization will likely contribute to new paradigms of carcinogenesis. Such knowledge is essential to providing new markers for tumor detection and developing useful, targeted anticancer strategies.
Molecular Mechanisms of Tumorigenesis and Cell Cycle Control My research is centered on understanding molecular mechanisms that control cell proliferation and checkpoint responses, and how those processes are disrupted during tumorigenesis. A principal focus of the lab is the ARF tumor suppressor, which is encoded by a gene (INK4a/ARF) that is inactivated in 40-50% of all human cancers. ARF inhibits tumorigenesis through p53-dependent and p53-independent signaling pathways that are complex and only partially defined. That is because ARF functions through numerous binding partners (at least 30) to promote apoptosis or senescence, inhibit migration/invasion and metastasis, sustain cell stress checkpoints and maintain chromosomal stability. Our goal is to define the critical regulators of ARF signaling and determine their significance to tumor suppression using molecular approaches and in vivo models of cancer. In so doing, we will advance our fundamental understanding of ARF-mediated tumor suppression and also identify novel regulators of growth (both positive and negative) whose characterization will likely contribute to new paradigms of carcinogenesis. Such knowledge is essential to providing new markers for tumor detection and developing useful, targeted anticancer strategies.
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