The top priority of the Tumor Cell Biology Training (TCB) Grant is identification and training of the next generation of cancer biologists. Our goal is to provide trainees with the tools to be leaders in their prospective fields and to communicate in varied languages (pathology, oncology, molecular biology, engineering, chemistry, bioinformatics and biomathematics) related to modern medicine and biomedical research. The TCB Program focuses on training predoctoral and postdoctoral students in all aspects directly related to mechanisms of tumorigenesis. As such, supported training positions are focused on mechanisms of oncogenesis that evaluate oncogenes, tumor suppressor genes, dysregulated gene expression, aberrant signal transduction pathways, cell-of-origins for various cancers and so forth within the tumor cell population itself. We also have supported trainees with interests in the tumor cell microenvironment, such as in the area of abnormal angiogenesis, and in areas related to the interface of engineering and imaging with cancer. The development of cancer specialty tracks in brain and prostate cancers, cancer stem cells, tumor microenvironment and tumor epigenetics, offer fundamental new opportunities for Cancer training that will be highlighted in this renewal application. In addition, we highlight novel training structures developed at UCLA in order to foster more collaborative interactions in a multidisciplinary environment. In particular, the establishment of the Institute for Molecular Medicine (IMED) within the David Geffen School of Medicine at UCLA provides both infrastructure and a platform for multi-disciplinary training and team work in disease focused areas, including cancer. Expertise in the new area of cancer metabolomics, which offer opportunities for novel projects are now available in house, and provide opportunities for expansion of established projects that may gain added depth and breadth. Continued development of integrative technologies that facilitate high throughput screening for genetic polymorphisms and gene and protein expression on global scales are also supported and trainees that can communicate in all these approaches will support the promise for new advances in cancer research. Further developments require training of students who can increasingly bridge disciplines and communicate freely with experts in diverse areas of expertise. Our graduate student population for the TCB program is drawn from seven PhD-granting Departments and two multidepartmental umbrella organizations which support recruitment and admission mechanisms for 11 doctoral degree granting programs in the Molecular, Cellular and Integrated Life Sciences. Faculty of these degree granting entities currently train 351 doctoral students. These faculty also currently mentor and 387 postdoctoral fellows, creating a dynamic community and a diverse training environment in biomedical research. Collectively, our Program faculty are training a total of over 61 predoctoral and 73 postdoctoral trainees during the current year. Trainees in this program constitute approximately 5% of the predoctoral and 10% of the postdoctoral trainees of our mentors. Therefore, the training program plays an essential role in supporting the creativity and productivity of our key cancer research faculty.

Public Health Relevance

of the educational and research initiatives in this training program to the health of Americans encompasses the need to train the next generation of biomedical scientists and clinician scientists in i) the application of cutting edge conceptual and technical strategies to cancer biology and medicine and ii) the multidisciplinary, team approaches required to use those strategies from the laboratory to the bedside.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Institutional National Research Service Award (T32)
Project #
5T32CA009056-38
Application #
8687968
Study Section
Subcommittee B - Comprehensiveness (NCI)
Program Officer
Lim, Susan E
Project Start
1980-08-09
Project End
2017-06-30
Budget Start
2014-07-01
Budget End
2015-06-30
Support Year
38
Fiscal Year
2014
Total Cost
Indirect Cost
Name
University of California Los Angeles
Department
Other Basic Sciences
Type
Schools of Medicine
DUNS #
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
Mitra, Mithun; Johnson, Elizabeth L; Swamy, Vinay S et al. (2018) Alternative polyadenylation factors link cell cycle to migration. Genome Biol 19:176
Sullivan, William J; Mullen, Peter J; Schmid, Ernst W et al. (2018) Extracellular Matrix Remodeling Regulates Glucose Metabolism through TXNIP Destabilization. Cell 175:117-132.e21
Parvatiyar, Kislay; Pindado, Jose; Dev, Anurupa et al. (2018) A TRAF3-NIK module differentially regulates DNA vs RNA pathways in innate immune signaling. Nat Commun 9:2770
Gell, Joanna J; Zhao, Jasmine; Chen, Di et al. (2018) PRDM14 is expressed in germ cell tumors with constitutive overexpression altering human germline differentiation and proliferation. Stem Cell Res 27:46-56
Pasque, Vincent; Karnik, Rahul; Chronis, Constantinos et al. (2018) X Chromosome Dosage Influences DNA Methylation Dynamics during Reprogramming to Mouse iPSCs. Stem Cell Reports 10:1537-1550
Ohashi, Minori; Korsakova, Elena; Allen, Denise et al. (2018) Loss of MECP2 Leads to Activation of P53 and Neuronal Senescence. Stem Cell Reports 10:1453-1463
Momcilovic, Milica; Bailey, Sean T; Lee, Jason T et al. (2018) Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer. J Vis Exp :
Allison, Thomas F; Smith, Andrew J H; Anastassiadis, Konstantinos et al. (2018) Identification and Single-Cell Functional Characterization of an Endodermally Biased Pluripotent Substate in Human Embryonic Stem Cells. Stem Cell Reports 10:1895-1907
Youn, Minyoung; Wang, Nan; LaVasseur, Corinne et al. (2017) Loss of Forkhead box M1 promotes erythropoiesis through increased proliferation of erythroid progenitors. Haematologica 102:826-834
Williams, Carmen J; Chu, Alison; Jefferson, Wendy N et al. (2017) Epithelial membrane protein 2 (EMP2) deficiency alters placental angiogenesis, mimicking features of human placental insufficiency. J Pathol 242:246-259

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