To improve cancer therapy, it is increasingly critical that advances in basic cancer research be translated to the clinic. In the Training Program in Cancer Therapeutics, the goal is to provide training to cancer researchers in the action of therapeutic agents used in the treatment of cancer. This Training Program will be multi-disciplinary and expose the trainees to both basic research involving cancer therapeutic agents and the clinical utilization of therapeutics. A particular emphasis will be placed on the mechanisms through which basic scientific discovery is brought into the clinic through clinical trials. To facilitate this training, a team of mentoring faculty and ancillary clinical faculty hasbeen recruited into the Training Program from the University of Cincinnati and Cincinnati Children's Hospital Medical Center. Mentors on this training program are independently funded, have experience in mentoring, and work on projects related to cancer therapy. The ancillary faculty are clinical partners on this proposal, who will educate on the clinical utilization of specific therapeutic modalities. Together, the mentors and ancillary faculty will provide training both through direct interactions and through specialized educational activities and course work for the Training Program. This Program will provide outstanding career development for trainees, as more emphasis is placed on translating basic scientific discovery into improved patient care. Logistically, the Training Program in Cancer Therapeutics has 17 mentors and 6 ancillary faculty. It is administered by the Principal Investigators and Administrative Committees, which are directed at training excellence and providing an ethnically and scientifically diverse group of trainees. The Training Program requests support for 6 postdoctoral and 2 predoctoral trainees. The program will be evaluated regularly through both internal and external review to ensure that the trainees are receiving the best possible training.

Public Health Relevance

The purpose of The Training Program in Cancer Therapeutics is to provide predoctoral and postdoctoral scientists training and mentorship on the action of therapeutic agents for use in the treatment of cancer. The training program will place emphasis on translating basic scientific discoveries into improved patient care and will incorporate mentors with expertise in the clinical and basic aspects of the use of therapeutic modalities.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Institutional National Research Service Award (T32)
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Study Section
Subcommittee B - Comprehensiveness (NCI)
Program Officer
Damico, Mark W
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University of Cincinnati
Anatomy/Cell Biology
Schools of Medicine
United States
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Yuan, Zhenyu; Praxenthaler, Heiko; Tabaja, Nassif et al. (2016) Structure and Function of the Su(H)-Hairless Repressor Complex, the Major Antagonist of Notch Signaling in Drosophila melanogaster. PLoS Biol 14:e1002509
Chlon, Timothy M; Ruiz-Torres, Sonya; Maag, Logan et al. (2016) Overcoming Pluripotent Stem Cell Dependence on the Repair of Endogenous DNA Damage. Stem Cell Reports 6:44-54
Du, Wei; Amarachintha, Surya; Erden, Ozlem et al. (2016) The Fanconi anemia pathway controls oncogenic response in hematopoietic stem and progenitor cells by regulating PRMT5-mediated p53 arginine methylation. Oncotarget :
Watts, Nelson B; Bilezikian, John P; Usiskin, Keith et al. (2016) Effects of Canagliflozin on Fracture Risk in Patients With Type 2 Diabetes Mellitus. J Clin Endocrinol Metab 101:157-66
Link, Kevin A; Lin, Shan; Shrestha, Mahesh et al. (2016) Supraphysiologic levels of the AML1-ETO isoform AE9a are essential for transformation. Proc Natl Acad Sci U S A 113:9075-80
Oswald, Franz; Rodriguez, Patrick; Giaimo, Benedetto Daniele et al. (2016) A phospho-dependent mechanism involving NCoR and KMT2D controls a permissive chromatin state at Notch target genes. Nucleic Acids Res 44:4703-20
Goyama, S; Schibler, J; Gasilina, A et al. (2016) UBASH3B/Sts-1-CBL axis regulates myeloid proliferation in human preleukemia induced by AML1-ETO. Leukemia 30:728-39
Sampson, Leesa L; Davis, Ashley K; Grogg, Matthew W et al. (2016) mTOR disruption causes intestinal epithelial cell defects and intestinal atrophy postinjury in mice. FASEB J 30:1263-75
Benight, Nancy M; Wagh, Purnima K; Zinser, Glendon M et al. (2015) HGFL supports mammary tumorigenesis by enhancing tumor cell intrinsic survival and influencing macrophage and T-cell responses. Oncotarget 6:17445-61
Johnson, Abby L; Zinser, Glendon M; Waltz, Susan E (2015) Vitamin D3-dependent VDR signaling delays ron-mediated breast tumorigenesis through suppression of β-catenin activity. Oncotarget 6:16304-20

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