This application seeks continuation of our T32 Cancer Cell Biology Training Program (CCBTP), now in its 19th year. This exclusively predoctoral training program, together with the long-standing exclusively postdoctoral Integrated Training in Cancer Model Systems (ITCMS) T32, comprise the training component of the Lineberger Comprehensive Cancer Center (LCCC) at UNC-Chapel Hill. LCCC is one of only 45 NCI-designated Comprehensive Cancer Centers. The CCTP premise is that cancer cell biology is a distinct, interdisciplinary biomedical science that encompasses experimental approaches and didactic knowledge from fields as diverse as biochemistry, cell biology, epidemiology, genetics, immunology, microbiology, molecular biology, pathology, pharmacology, physiology and toxicology. The CCBTP mission has been, and continues to be, training the next generation of basic and translational cancer biologists. Since ours is not a degree-granting program, we seek to provide our students with unique opportunities beyond their departmental requirements. In this renewal application, the CCBTP seeks to build on its past success, while also recognizing that the landscape of cancer research and training has entered a new era of very dynamic change. With the approach of precision medicine, and the genomic era of cancer research continuing at warp speed, these are now some of the best of times for cancer research. Conversely, these are also challenging times. We are faced with information overload and must ensure that our trainees can leverage this information to advance their own research studies. Grant funding continues to challenge the research community. Issues of reproducibility dog this and other research fields. The pharmaceutical industry is no longer able to sustain its own research capabilities, changing the dynamics between industry and academia. To keep the CCBTP program fresh and to address the needs of future cancer biology trainees, we have critically evaluated the program and remodeled some aspects to keep abreast of this changing landscape. The core mission remains to ensure that we provide the best training for our cancer biology students. We also now focus on preparing our trainees for both academic and non-academic careers. In the past cycle, we have added novel interactions with faculty mentors, improved our diversity pipeline, and obtained enhanced institutional support. Going forward, in addition to our continued emphasis on translational cancer biology, we will provide our trainees with new opportunities to develop their knowledge of state-of-the-art methodologies to profile and dissect the cancer genome, bioinformatics and computational biology, the emerging areas of immunotherapy and epigenetics, the best model systems to study cancer, and reproducibility in research. The CCBTP serves a vital role in the mission of training to support the pipeline of future cancer biologists, preparing them to serve leading roles in the NCI Cancer Moonshot Initiative, and to accelerate progress in the prevention, diagnosis and treatment of cancer.

Public Health Relevance

As cancer overtakes cardiovascular disease as the number-one cause of deaths in the US, the need for well- trained cancer biologists is now more acute than ever. The landscape in cancer research and training continues to evolve rapidly. In this renewal application of our long-standing interdisciplinary Cancer Cell Biology Training Program for predoctoral students at the University of North Carolina at Chapel Hill, we propose our vision for the future training of cancer biologists for both academic and non-academic career paths, to position them well to contribute to the Moonshot Initiative to ?eliminate cancer as we know it?. !

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Institutional National Research Service Award (T32)
Project #
2T32CA071341-21
Application #
9280400
Study Section
Subcommittee I - Transistion to Independence (NCI)
Program Officer
Perkins, Susan N
Project Start
1996-09-30
Project End
2022-08-31
Budget Start
2017-09-01
Budget End
2018-08-31
Support Year
21
Fiscal Year
2017
Total Cost
Indirect Cost
Name
University of North Carolina Chapel Hill
Department
Radiation-Diagnostic/Oncology
Type
Schools of Medicine
DUNS #
608195277
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599
Runge, John S; Raab, Jesse R; Magnuson, Terry (2018) Identification of Two Distinct Classes of the Human INO80 Complex Genome-Wide. G3 (Bethesda) 8:1095-1102
Siegel, Marni B; He, Xiaping; Hoadley, Katherine A et al. (2018) Integrated RNA and DNA sequencing reveals early drivers of metastatic breast cancer. J Clin Invest 128:1371-1383
Vaseva, Angelina V; Blake, Devon R; Gilbert, Thomas S K et al. (2018) KRAS Suppression-Induced Degradation of MYC Is Antagonized by a MEK5-ERK5 Compensatory Mechanism. Cancer Cell 34:807-822.e7
Raab, Jesse R; Runge, John S; Spear, Camarie C et al. (2017) Co-regulation of transcription by BRG1 and BRM, two mutually exclusive SWI/SNF ATPase subunits. Epigenetics Chromatin 10:62
Vitucci, Mark; Irvin, David M; McNeill, Robert S et al. (2017) Genomic profiles of low-grade murine gliomas evolve during progression to glioblastoma. Neuro Oncol 19:1237-1247
Irvin, David M; McNeill, Robert S; Bash, Ryan E et al. (2017) Intrinsic Astrocyte Heterogeneity Influences Tumor Growth in Glioma Mouse Models. Brain Pathol 27:36-50
Bailey, Sean T; Smith, Aleisha M; Kardos, Jordan et al. (2017) MYC activation cooperates with Vhl and Ink4a/Arf loss to induce clear cell renal cell carcinoma. Nat Commun 8:15770
McNeill, Robert S; Canoutas, Demitra A; Stuhlmiller, Timothy J et al. (2017) Combination therapy with potent PI3K and MAPK inhibitors overcomes adaptive kinome resistance to single agents in preclinical models of glioblastoma. Neuro Oncol 19:1469-1480
Kechele, Daniel O; Blue, R Eric; Zwarycz, Bailey et al. (2017) Orphan Gpr182 suppresses ERK-mediated intestinal proliferation during regeneration and adenoma formation. J Clin Invest 127:593-607
Pattenden, Samantha G; Simon, Jeremy M; Wali, Aminah et al. (2016) High-throughput small molecule screen identifies inhibitors of aberrant chromatin accessibility. Proc Natl Acad Sci U S A 113:3018-23

Showing the most recent 10 out of 87 publications