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.
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.
|Brown, Nicholas E; Paluch, Andrew M; Nashu, Madison A et al. (2018) Tumor Cell Autonomous RON Receptor Expression Promotes Prostate Cancer Growth Under Conditions of Androgen Deprivation. Neoplasia 20:917-929|
|Feng, Xuyang; Hsu, Shih-Jui; Bhattacharjee, Anukana et al. (2018) CTC1-STN1 terminates telomerase while STN1-TEN1 enables C-strand synthesis during telomere replication in colon cancer cells. Nat Commun 9:2827|
|Morrison, Brian J; Steel, Jason C; Morris, John C (2018) Reduction of MHC-I expression limits T-lymphocyte-mediated killing of Cancer-initiating cells. BMC Cancer 18:469|
|Bylund, Jeffery B; Trinh, Linh T; Awgulewitsch, Cassandra P et al. (2017) Coordinated Proliferation and Differentiation of Human-Induced Pluripotent Stem Cell-Derived Cardiac Progenitor Cells Depend on Bone Morphogenetic Protein Signaling Regulation by GREMLIN 2. Stem Cells Dev 26:678-693|
|Fang, Jing; Bolanos, Lyndsey C; Choi, Kwangmin et al. (2017) Ubiquitination of hnRNPA1 by TRAF6 links chronic innate immune signaling with myelodysplasia. Nat Immunol 18:236-245|
|Feng, Xuyang; Hsu, Shih-Jui; Kasbek, Christopher et al. (2017) CTC1-mediated C-strand fill-in is an essential step in telomere length maintenance. Nucleic Acids Res 45:4281-4293|
|Kattamuri, Chandramohan; Nolan, Kristof; Thompson, Thomas B (2017) Analysis and identification of the Grem2 heparin/heparan sulfate-binding motif. Biochem J 474:1093-1107|
|Ruiz-Torres, Sasha J; Benight, Nancy M; Karns, Rebekah A et al. (2017) HGFL-mediated RON signaling supports breast cancer stem cell phenotypes via activation of non-canonical ?-catenin signaling. Oncotarget 8:58918-58933|
|Oben, Karine Z; Alhakeem, Sara S; McKenna, Mary K et al. (2017) Oxidative stress-induced JNK/AP-1 signaling is a major pathway involved in selective apoptosis of myelodysplastic syndrome cells by Withaferin-A. Oncotarget 8:77436-77452|
|Zhou, Zilan; Kennell, Carly; Jafari, Mina et al. (2017) Sequential delivery of erlotinib and doxorubicin for enhanced triple negative Breast cancer treatment using polymeric nanoparticle. Int J Pharm 530:300-307|
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