The University of Southern California (USC) Training Program in Cellular, Biochemical, and Molecular Sciences (CBM Training Program) prepares students for careers in interdisciplinary biomedical research and related occupations. Major goals of the Program are to promote interdisciplinary training and to make students aware of computational methods which will be useful for their current and future research and for their careers. Trainees are selected from 14 different Ph.D. programs at USC which span the entire spectrum of biomedical and biological sciences. This ensures that Trainees receive a multidisciplinary experience in the CBM Program and are the """"""""cream of the crop"""""""" at USC. CBM Trainees have diverse backgrounds and research interests, come from many parts of the U.S. and foreign countries, and include under-represented minority students. In addition to the requirements of their Ph.D. programs, Trainees benefit from Training Program-specific activities, including monthly Trainee research presentations, workshops with computational or career development themes, interactions with selected speakers from outside USC, participation in recruitment of new graduate students, training in ethical standards of research, and an annual retreat. The computational theme of the CBM Program takes advantage of areas of special strength at USC in computational genomics and cancer epidemiology, both of which emphasize quantitative treatments of complex data sets. Most CBM Trainees are supported during their second and third years of graduate school and continue to participate in the Program until completion of their Ph.D. degree. The CBM Program works closely with USC's outstanding graduate student recruitment mechanism, called Program in Biomedical and Biological Sciences (PIBBS). During their first year at USC, students in PIBBS rotate with several faculty, chosen from any biologically-oriented Ph.D. program at USC. The outstanding PIBBS web site attracts more than 100 U.S. and more than 500 total applicants per year. Faculty and staff attend national and regional recruitment fairs, including those targeted to under-represented minority students. We also have formal partnerships with BRIDGES-to-the-Ph.D. programs at local minority-serving institutions. These measures ensure that we will continue to attract a diverse group of high-quality trainees.

National Institute of Health (NIH)
National Institute of General Medical Sciences (NIGMS)
Institutional National Research Service Award (T32)
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National Institute of General Medical Sciences Initial Review Group (BRT)
Program Officer
Gindhart, Joseph G
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University of Southern California
Schools of Medicine
Los Angeles
United States
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Angell, Trevor E; Lechner, Melissa G; Smith, Alison M et al. (2016) Circulating Myeloid-Derived Suppressor Cells Predict Differentiated Thyroid Cancer Diagnosis and Extent. Thyroid 26:381-9
Gaddis, Malaina; Gerrard, Diana; Frietze, Seth et al. (2015) Altering cancer transcriptomes using epigenomic inhibitors. Epigenetics Chromatin 8:9
Kegulian, Natalie C; Sankhagowit, Shalene; Apostolidou, Melania et al. (2015) Membrane Curvature-sensing and Curvature-inducing Activity of Islet Amyloid Polypeptide and Its Implications for Membrane Disruption. J Biol Chem 290:25782-93
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Angell, Trevor E; Lechner, Melissa G; Jang, Julie K et al. (2014) BRAF V600E in papillary thyroid carcinoma is associated with increased programmed death ligand 1 expression and suppressive immune cell infiltration. Thyroid 24:1385-93
Wu, Dai-Ying; Ou, Chen-Yin; Chodankar, Rajas et al. (2014) Distinct, genome-wide, gene-specific selectivity patterns of four glucocorticoid receptor coregulators. Nucl Recept Signal 12:e002
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Angell, Trevor E; Lechner, Melissa G; Jang, Julie K et al. (2014) MHC class I loss is a frequent mechanism of immune escape in papillary thyroid cancer that is reversed by interferon and selumetinib treatment in vitro. Clin Cancer Res 20:6034-44
Chodankar, Rajas; Wu, Dai-Ying; Schiller, Benjamin J et al. (2014) Hic-5 is a transcription coregulator that acts before and/or after glucocorticoid receptor genome occupancy in a gene-selective manner. Proc Natl Acad Sci U S A 111:4007-12

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