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Associate Professor of PharmacologyAssociate Professor of
Primary Office: 2-570 Bowen Science BuildingIowa City, IA 52242
Lab: 2-551 Bowen Science BuildingIowa City, IA 52242
BS, Biochemistry, University of Maine, OronoPhD, Molecular & Cell Biology, The Pennsylvania State University, University Park
Fellowship, The Pennsylvania State UniversityFellowship, Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, TN
Interdisciplinary Graduate Program in Molecular and Cellular BiologyInterdisciplinary Graduate Program in Translational BiomedicineMedical Scientist Training Program
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.
p53 Acetylation: Regulation and consequences.
2014 December 23. 7(1):30-69.
RABL6A promotes G1-S phase progression and pancreatic neuroendocrine tumor cell proliferation in an Rb1-dependent manner.
2014 November 15. 74(22):6661-6670.
NIAM-deficient mice are predisposed to the development of proliferative lesions including B-cell lymphomas.
2014 November 13. 9(11):e112126.
Van Rheeden R,
Development and translational imaging of a TP53 porcine tumorigenesis model.
J of Clinical Investigation.
2014 September. 124(9):4052-4066.
ARF sees Pdgfrβ through the miR.
Nuclear Interactor of ARF and Mdm2 regulates multiple pathways to activate p53.
RABL6A promotes oxaliplatin resistance in tumor cells and is a new marker of survival for resected pancreatic ductal adenocarcinoma patients.
Genes & Cancer.
Van Rheeden R,
RABL6A, a novel RAB-like protein, controls centrosome amplification and chromosome instability in primary fibroblasts.
The ARF tumor suppressor inhibits tumor cell colonization independent of p53 in a novel mouse model of pancreatic ductal adenocarcinoma metastasis.
Molecular Cancer Research.
Date Last Modified: 06/06/2016 -
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