The Cancer Genetics Program (CGP) is an interdisciplinary research group of 37 investigators from 13 departments and three different schools/colleges, Since the past funding cycle, tine research base of the Cancer Genetics Program has increased 180% from $3,866,370 to $10,978,820 total annual direct support, of which $1,132,859 is from the NCI. Over this last grant period, there were 472 publications of Cancer Genetics Program members, of which 8.4% are intra-programmatic and 31.9% are Inter-programmatic. The CGP pursues laboratory and translational research, emphasizing genetic and genomics approaches, with the overarching goal of advancing knowledge of the nature and role of mutations and gene expression changes In the development and altered phenotypic traits of cancer. Investigatory in the CGP are committed to the pursuit of research that will not only inform understanding of the origins and nature of cancer but that will also lead to novel diagnostic approaches for cancer and improved clinical management of cancer patients. Investigators in the Program collaborate with investigators in other University of Michigan Comprehensive Cancer Center (UMCCC) programs in the Basic Science, Clinical Science and Population Sciences Divisions, including Cancer Cell Biology, Radiation Sciences, Experimental Therapeutics, Breast Oncology, GI Oncology, Prostate Oncology, and Biomedical Prevention. The CGP has four major research themes: I) Defining oncogene and tumor suppressor gene network defects and gene expression signatures in cancers of various types. II) Characterization of mechanisms of gene regulation by transcription factor complexes and chromatin modification factors in cancer cells. III) Elucidation of genetic and epigenetic mechanisms contributing to genomic instability in cancer. IV) Development of genetically engineered mouse models for investigating the role of recurrent gene defects in cancer pathogenesis.
Cancer Genetics Program members conduct research to identify the many types of genetic and epigenetic alterations that occur in various human cancers and aim to utilize the knowledge gained from such studies to develop more effective ways to detect, prognosticate, and treat cancer. Members also develop genetically engineered mouse models of cancer and cell-based systems to better understand the factors and mechanisms that influence cancer development, progression, and metastasis.
|Verhaegen, Monique E; Mangelberger, Doris; Harms, Paul W et al. (2015) Merkel cell polyomavirus small T antigen is oncogenic in transgenic mice. J Invest Dermatol 135:1415-24|
|Chinn, Steven B; Darr, Owen A; Owen, John H et al. (2015) Cancer stem cells: mediators of tumorigenesis and metastasis in head and neck squamous cell carcinoma. Head Neck 37:317-26|
|Vainshtein, Jeffrey M; Spector, Matthew E; Stenmark, Matthew H et al. (2014) Reliability of post-chemoradiotherapy F-18-FDG PET/CT for prediction of locoregional failure in human papillomavirus-associated oropharyngeal cancer. Oral Oncol 50:234-9|
|Castro, Maria G; Candolfi, Marianela; Wilson, Thomas J et al. (2014) Adenoviral vector-mediated gene therapy for gliomas: coming of age. Expert Opin Biol Ther 14:1241-57|
|Vainshtein, Jeffrey M; Spector, Matthew E; McHugh, Jonathan B et al. (2014) Refining risk stratification for locoregional failure after chemoradiotherapy in human papillomavirus-associated oropharyngeal cancer. Oral Oncol 50:513-9|
|Grogan, Patrick T; Sarkaria, Jann N; Timmermann, Barbara N et al. (2014) Oxidative cytotoxic agent withaferin A resensitizes temozolomide-resistant glioblastomas via MGMT depletion and induces apoptosis through Akt/mTOR pathway inhibitory modulation. Invest New Drugs 32:604-17|
|VanderVeen, Nathan; Paran, Christopher; Appelhans, Ashley et al. (2014) Marmosets as a preclinical model for testing "off-label" use of doxycycline to turn on Flt3L expression from high-capacity adenovirus vectors. Mol Ther Methods Clin Dev 1:|
|Krook, Melanie A; Nicholls, Lauren A; Scannell, Christopher A et al. (2014) Stress-induced CXCR4 promotes migration and invasion of ewing sarcoma. Mol Cancer Res 12:953-64|
|Ro, Seung-Hyun; Semple, Ian A; Park, Haewon et al. (2014) Sestrin2 promotes Unc-51-like kinase 1 mediated phosphorylation of p62/sequestosome-1. FEBS J 281:3816-27|
|Stenmark, Matthew H; McHugh, Jonathan B; Schipper, Matthew et al. (2014) Nonendemic HPV-positive nasopharyngeal carcinoma: association with poor prognosis. Int J Radiat Oncol Biol Phys 88:580-8|
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