11 months ago

2016 Scientific Report

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Prostate epithelial

Prostate epithelial cells expressing a Pten mutant (C124S) were differentiated for 18 days under suboptimal conditions. Androgen receptor (red) in the luminal cells and integrin α6 (green) in the basal cells were visualized by immunostaining and fluorescence microscopy. Image by Mclane Watson. 20 Van Andel Research Institute | Scientific Report

MATTHEW STEENSMA, M.D. Dr. Steensma received his B.A. from Hope College and his M.D. from Wayne State University School of Medicine in Detroit. Dr. Steensma is a practicing surgeon in the Spectrum Health Medical Group, and he joined VARI as an Assistant Professor in 2010. STAFF CURT ESSENBURG, B.S., LATG PATRICK DISCHINGER, B.S. DIANA LEWIS, A.S. MARIE MOONEY, M.S. MATT PRIDGEON, M.D. RESEARCH INTERESTS Our laboratory conducts research into new treatment strategies for sarcomas. Specifically, we are interested in determining the mechanisms underlying tumor formation in sporadic bone and soft tissue sarcomas and in neurofibromatosis type 1, a hereditary disorder caused by mutations in the neurofibromin 1 (NF1) gene. Neurofibromin is considered a tumor suppressor that suppresses Ras activity by promoting Ras GTP hydrolysis to GDP. People with mutations in the neurofibromin 1 gene develop benign tumors called neurofibromas and have an elevated risk of malignancies ranging from solid tumors to leukemia, including sarcomas. The disease affects 1 in 3000 people in the United States, of whom 8–13% will ultimately develop a neurofibromatosis-related sarcoma in their lifetime. These aggressive tumors typically arise from benign neurofibromas, but the process of benign-to-malignant transformation is not well understood, and treatment options are limited, leading to poor five-year survival rates. Our current sarcoma-related research efforts include the development of genetically engineered mouse models of neurofibromatosis type 1 tumor progression; the identification of targetable patterns of intratumoral and intertumoral heterogeneity through next-generation sequencing; genotype–phenotype correlations in neurofibromatosis type 1 and related diseases; and mechanisms of chemotherapy resistance in bone and soft-tissue sarcomas. RECENT PUBLICATIONS Foley, Jessica M., Donald J. Scholten, Noel R. Monks, David Cherba, David J. Monsma, Paula Davidson, Dawna Dylewski, Karl Dykema, Mary E. Winn, and Matthew R. Steensma. 2015. Anoikis-resistant subpopulations of human osteosarcoma display significant chemoresistance and are sensitive to targeted epigenetic therapies predicted by expression profiling. Journal of Translational Medicine 13: 110. Lane, Brian R., Jeffrey Bissonnette, Tracy Waldherr, Deborah Ritz-Holland, Dave Chesla, Sandra L. Cottingham, Sheryl Alberta, Cong Liu, Amanda Bartenbaker Thompson, et al. 2015. Development of a center for personalized cancer care at a regional cancer center. Journal of Molecular Diagnostics 17(6): 695–704. Peacock, Jacqueline D., Karl J. Dykema, Helga V. Toriello, Marie R. Mooney, Donald J. Scholten II, Mary E. Winn, Andrew Borgman, Nicholas S. Duesbery, Judith A. Hiemenga, et al. 2015. Oculoectodermal syndrome is a mosaic RASopathy associated with KRAS alterations. American Journal of Medical Genetics A 167(7): 1429–1435. CENTER FOR CANCER AND CELL BIOLOGY 21

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