This is a competitive renewal of an application for postdoctoral training in cancer genetics at the Ohio State University Comprehensive Cancer Center (OSLJCCC). During the first funding period, the Advisory Committee and training faculty quickly realized the many strengths of the training program as well as some of the weaknesses. This application thus represents an evolving concept for training our new genre of cancer researchers that includes several new aspects to the training that we have implemented or plan to implement in the proposed Cancer Genetics Training Program (CG T32). The central theme and strength of the training program of having basic/translational co-mentoring of trainees in three cancer sites remains intact. Forty scientists at the OSUCCC will join forces to train the next generation of cancer geneticists, with an emphasis on multidisciplinary approaches to the study and treatment of breast, gastro-intestinal and hematopoietic cancers. We will use unique recruiting tools that were proven extraordinarily successful in the last funding period to attract and/or retain eight talented postdoctoral candidates each year of the program. Recognizing that a complete understanding of the basic mechanisms of cancer initiation and progression will be required for the efficient translation of knowledge to the treatment of patients, the training program has compiled a balanced group of investigators with expertise in genetics, cell signaling, cell biology and tumor models, and with an intense interest and a proven record in translational research. The commitment to coupling basic knowledge to translational and/or clinical research will continue to be realized by providing trainees with two co-mentors with strengths in basic and translational research and having divergent expertise, bridging the gap between these two areas. The main new aspects of the training program include 1. an annual postdoctoral symposium series, 2. a grant writing workshop that will be specific to each trainee and guide/evaluate applications aimed to help them transition into independent research positions (NIHK99/ROO, K01 or similar grants), and 3. the addition of new training faculty with strengths in translational and/or clinical cancer research. By maintaining the original strengths and focus of the CG T32 program and implementing novel targeted training approaches, the proposed training program will create a unique setting that strongly encourages basic scientists to venture into translational/clinical research.
!: Given the enormous gain of basic knowledge about the biology of cancer in recent years and the palpable excitement in cancer therapeutics, we feel an obligation to retool our strategies of training future cancer researchers to meet the expectation of eventually - sooner rather than later - eradicating cancer from society. We believe that this training program will help to also enhance the extensive ongoing collaborative studies that already exist between training faculty and foster further intellectual and practical exchange of basic and translational concepts to cancer genetics research.
|Larson, Jennifer R; Facemyer, Eric M; Shen, Kuo-Fang et al. (2014) Insights into dynamic mitotic chromatin organization through the NIMA kinase suppressor SonC, a chromatin-associated protein involved in the DNA damage response. Genetics 196:177-95|
|Arango, Daniel; Morohashi, Kengo; Yilmaz, Alper et al. (2013) Molecular basis for the action of a dietary flavonoid revealed by the comprehensive identification of apigenin human targets. Proc Natl Acad Sci U S A 110:E2153-62|
|Meng, Wei; McElroy, Joseph P; Volinia, Stefano et al. (2013) Comparison of microRNA deep sequencing of matched formalin-fixed paraffin-embedded and fresh frozen cancer tissues. PLoS One 8:e64393|
|Wenzel, Pamela L; Chong, Jean-Leon; Saenz-Robles, M Teresa et al. (2011) Cell proliferation in the absence of E2F1-3. Dev Biol 351:35-45|
|Yilmaz, Alper; Mejia-Guerra, Maria Katherine; Kurz, Kyle et al. (2011) AGRIS: the Arabidopsis Gene Regulatory Information Server, an update. Nucleic Acids Res 39:D1118-22|
|Trikha, Prashant; Sharma, Nidhi; Opavsky, Rene et al. (2011) E2f1-3 are critical for myeloid development. J Biol Chem 286:4783-95|
|Yilmaz, Alper; Grotewold, Erich (2010) Components and mechanisms of regulation of gene expression. Methods Mol Biol 674:23-32|
|Hertlein, Erin; Byrd, John C (2010) Signalling to drug resistance in CLL. Best Pract Res Clin Haematol 23:121-31|
|Chen, Shih-Shih; Raval, Aparna; Johnson, Amy J et al. (2009) Epigenetic changes during disease progression in a murine model of human chronic lymphocytic leukemia. Proc Natl Acad Sci U S A 106:13433-8|
|Chong, Jean-Leon; Wenzel, Pamela L; Saenz-Robles, M Teresa et al. (2009) E2f1-3 switch from activators in progenitor cells to repressors in differentiating cells. Nature 462:930-4|
Showing the most recent 10 out of 20 publications