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.
|Mathewson, Nathan D; Jenq, Robert; Mathew, Anna V et al. (2016) Gut microbiome-derived metabolites modulate intestinal epithelial cell damage and mitigate graft-versus-host disease. Nat Immunol 17:505-13|
|Owen, John Henry; Graham, Martin P; Chinn, Steven B et al. (2016) Novel method of cell line establishment utilizing fluorescence-activated cell sorting resulting in 6 new head and neck squamous cell carcinoma lines. Head Neck 38 Suppl 1:E459-67|
|Lee, Alice W; Ness, Roberta B; Roman, Lynda D et al. (2016) Association Between Menopausal Estrogen-Only Therapy and Ovarian Carcinoma Risk. Obstet Gynecol 127:828-36|
|Boonstra, Philip S; Mukherjee, Bhramar; Gruber, Stephen B et al. (2016) Tests for Gene-Environment Interactions and Joint Effects With Exposure Misclassification. Am J Epidemiol 183:237-47|
|Peng, Dongjun; Tanikawa, Takashi; Li, Wei et al. (2016) Myeloid-Derived Suppressor Cells Endow Stem-like Qualities to Breast Cancer Cells through IL6/STAT3 and NO/NOTCH Cross-talk Signaling. Cancer Res 76:3156-65|
|Kadakia, Kunal C; Snyder, Claire F; Kidwell, Kelley M et al. (2016) Patient-Reported Outcomes and Early Discontinuation in Aromatase Inhibitor-Treated Postmenopausal Women With Early Stage Breast Cancer. Oncologist 21:539-46|
|Boonstra, Philip S; Taylor, Jeremy M G; Smolska-Ciszewska, Beata et al. (2016) Alpha/beta (Î±/Î²) ratio for prostate cancer derived from external beam radiotherapy and brachytherapy boost. Br J Radiol 89:20150957|
|Amin, Nisar A; Malek, Sami N (2016) Gene mutations in chronic lymphocytic leukemia. Semin Oncol 43:215-21|
|Hardiman, Karin M; Ulintz, Peter J; Kuick, Rork D et al. (2016) Intra-tumor genetic heterogeneity in rectal cancer. Lab Invest 96:4-15|
|Zhao, Ende; Maj, Tomasz; Kryczek, Ilona et al. (2016) Cancer mediates effector T cell dysfunction by targeting microRNAs and EZH2 via glycolysis restriction. Nat Immunol 17:95-103|
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