The Cancer Biology Training Grant (CBTG) at the University of Minnesota Masonic Cancer Center combines rigorous training in laboratory-based cancer research with interdisciplinary and translational perspectives that prepares CBTG trainees for independent research careers in cancer biology. Now in its 35th year of NCI support, the CBTG supports 4 predoctoral and 4 postdoctoral trainees. All trainees are selected on a competitive basis using clearly-defined criteria. The 39 preceptors provide research training in four areas of research strength at the Masonic Cancer Center: tumor biology and progression, cancer immunology, cancer genetics, and cancer therapy. The training program consists of intensive one-on-one research mentoring, didactic training in cancer biology, regular CBTG-specific meetings where trainees obtain feedback, develop critical presentation skills and establish new research collaborations, networking opportunities with prominent external cancer biology scientists, and formal career development activities. Enhanced monitoring and evaluation of trainee progress, and participation of the CBTG Director and Steering Committee members in key leadership positions associated with graduate education and trainee recruitment at the University of Minnesota, have enhanced the CBTG applicant pool and improved the career outcomes of CBTG trainees. These efforts have also enhanced our success at recruiting individuals from under-represented groups. New initiatives during the next funding period include the establishment of a new required graduate-level course in translational cancer research that will expose trainees to clinical issues in cancer biology research and to the realities of cancer patient treatment and care, establishment of an External Advisory Board and formal exit interviews with trainees to enhance CBTG program evaluation and development, and re-organization of CBTG leadership responsibilities to more effectively administer the various components of the CBTG program. The CBTG is central to the Masonic Cancer Center's mission of educating and training the next generation of scientific leaders pursuing research into the etiology and treatment of cancer.
This goal of this program at the University of Minnesota Masonic Cancer Center is to train a diverse group of highly qualified individuals to become future scientific leaders working in basic laboratory research to address fundamental problems in cancer biology.
|Van Etten, Jamie L; Nyquist, Michael; Li, Yingming et al. (2017) Targeting a Single Alternative Polyadenylation Site Coordinately Blocks Expression of Androgen Receptor mRNA Splice Variants in Prostate Cancer. Cancer Res 77:5228-5235|
|Knutson, Todd P; Truong, Thu H; Ma, Shihong et al. (2017) Posttranslationally modified progesterone receptors direct ligand-specific expression of breast cancer stem cell-associated gene programs. J Hematol Oncol 10:89|
|Brady, Nicholas J; Farrar, Michael A; Schwertfeger, Kathryn L (2017) STAT5 deletion in macrophages alters ductal elongation and branching during mammary gland development. Dev Biol 428:232-244|
|Van Etten, Jamie L; Nyquist, Michael; Li, Yingming et al. (2017) Targeting a single alternative polyadenylation site coordinately blocks expression of androgen receptor mRNA splice variants in prostate cancer. Cancer Res :|
|Hanse, E A; Ruan, C; Kachman, M et al. (2017) Cytosolic malate dehydrogenase activity helps support glycolysis in actively proliferating cells and cancer. Oncogene 36:3915-3924|
|Baxley, Ryan M; Bielinsky, Anja-Katrin (2017) Mcm10: A Dynamic Scaffold at Eukaryotic Replication Forks. Genes (Basel) 8:|
|Matson, Jacob Peter; Dumitru, Raluca; Coryell, Philip et al. (2017) Rapid DNA replication origin licensing protects stem cell pluripotency. Elife 6:|
|Du, Jing; Paz, Katelyn; Flynn, Ryan et al. (2017) Pirfenidone ameliorates murine chronic GVHD through inhibition of macrophage infiltration and TGF-? production. Blood 129:2570-2580|
|Du, Jing; Paz, Katelyn; Thangavelu, Govindarajan et al. (2017) Invariant natural killer T cells ameliorate murine chronic GVHD by expanding donor regulatory T cells. Blood 129:3121-3125|
|Regan Anderson, Tarah M; Ma, Shi Hong; Raj, Ganesh V et al. (2016) Breast Tumor Kinase (Brk/PTK6) Is Induced by HIF, Glucocorticoid Receptor, and PELP1-Mediated Stress Signaling in Triple-Negative Breast Cancer. Cancer Res 76:1653-63|
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