The primary goal of this NCI-funded T32 Cancer Biology Training Grant, CBTG (formally called the Research Oncology Training Grant), is to prepare postdoctoral and predoctoral Trainees for investigative careers in cancer research. The Training Program integrates the training of basic scientists (PhD) and physician scientists (MD/PhD) under the direction of a select faculty from the NCI-designated Case Comprehensive Cancer Center at Case Western Reserve University. These faculty mentors bridge traditional departmental boundaries to apply multidisciplinary approaches to fundamental problems in basic cancer biology. The CBTG Training Program provides a forum for training that emphasizes Cancer Research. Since our last competing renewal, we developed a new Cancer Biology Training Program, which trains predoctoral scientists who will advance research on the causes, diagnosis, progression and treatment of experimental and human cancer. To accomplish these training goals, the CBTP has been developed with didactic course work focused on cancer as an interdisciplinary track within the Pathology PhD Program and is jointly sponsored by the Cancer Center and the Department of Pathology. New to this application is a formalized Postdoctoral Program. Postdoctoral Trainees are required to participate in didactic coursework including the Cancer Biology Core Course and the scientific ethics course. We developed an innovative recruiting strategy called the Signaling in Cancer Symposium to attract regional trainees. Furthermore, each postdoctoral trainee is required to constitute a personal Mentoring Committee that meets every six months that is analogous to the thesis committee of predoctoral trainees. The chair of the three person postdoctoral mentoring committee will be a member of the CBTG steering committee and will serve as a "secondary mentor" for the postdoctoral trainee. Also new to this application is the establishment of Cancer Center Training Scholar positions, providing financial incentives to recruit and retain outstanding postdoctoral fellows who are committed to a cancer research career and whose research progress will be closely monitored by the mentoring committee. All trainees make oral presentations of their research at the monthly Cancer Trainee Seminar Series, which pairs off trainees whose basic research focuses on a particular cancer with an MD Hematology/Oncology Fellow who presents the clinical aspects of that type of cancer. The new seminar was designed to familiarize trainees with the translational aspects of cancer research. The Training Program is governed by a Steering Committee charged with responsibility for (i) active recruitment of trainees, with an emphasis on women and underrepresented minorities;(ii) selection of high caliber candidates who are fully committed to research careers;(iii) tracking the progress of trainees according to specified criteria and standards;(iv) evaluating the mentorship provided by individual faculty;and (v) tracking the success of trainees who have completed the training program.
An abnormally high cancer mortality rate afflicts the 3.9 million people throughout northeast Ohio. Therefore, it is imperative to train and develop the next generation of scientists with a focus on the fundamental problems in basic and translational cancer biology in order to improve cancer patient outcomes in this region and nationally. The Cancer Biology Training Program trains predoctoral and postdoctoral fellows in an NCI-designated Comprehensive Cancer Center at Case Western Reserve University. We request continued funding for years 15-20 of this NCI-supported T32 training grant.
|Ignatz-Hoover, J J; Wang, H; Moreton, S A et al. (2015) The role of TLR8 signaling in acute myeloid leukemia differentiation. Leukemia 29:918-26|
|Cipriano, R; Bryson, B L; Miskimen, K L S et al. (2014) Hyperactivation of EGFR and downstream effector phospholipase D1 by oncogenic FAM83B. Oncogene 33:3298-306|
|Cipriano, Rocky; Miskimen, Kristy L S; Bryson, Benjamin L et al. (2014) Conserved oncogenic behavior of the FAM83 family regulates MAPK signaling in human cancer. Mol Cancer Res 12:1156-65|
|Fecteau, Ryan E; Lutterbaugh, James; Markowitz, Sanford D et al. (2014) GNAS mutations identify a set of right-sided, RAS mutant, villous colon cancers. PLoS One 9:e87966|
|Junk, Damian J; Cipriano, Rocky; Stampfer, Martha et al. (2013) Constitutive CCND1/CDK2 activity substitutes for p53 loss, or MYC or oncogenic RAS expression in the transformation of human mammary epithelial cells. PLoS One 8:e53776|
|Cipriano, Rocky; Miskimen, Kristy L S; Bryson, Benjamin L et al. (2013) FAM83B-mediated activation of PI3K/AKT and MAPK signaling cooperates to promote epithelial cell transformation and resistance to targeted therapies. Oncotarget 4:729-38|
|Junk, Damian J; Cipriano, Rocky; Bryson, Benjamin L et al. (2013) Tumor microenvironmental signaling elicits epithelial-mesenchymal plasticity through cooperation with transforming genetic events. Neoplasia 15:1100-9|
|Shola, D T N; Wang, H; Wahdan-Alaswad, R et al. (2012) Hic-5 controls BMP4 responses in prostate cancer cells through interacting with Smads 1, 5 and 8. Oncogene 31:2480-90|
|Majumdar, Avijit; Petrescu, Anca D; Xiong, Yin et al. (2011) Nuclear translocation of cellular retinoic acid-binding protein II is regulated by retinoic acid-controlled SUMOylation. J Biol Chem 286:42749-57|
|Fishovitz, Jennifer; Li, Min; Frase, Hilary et al. (2011) Active-site-directed chemical tools for profiling mitochondrial Lon protease. ACS Chem Biol 6:781-8|
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