This application requests funds to continue the highly successful Radiation Sciences program at the Stanford University School of Medicine, entitled "Postdoctoral Training In The Radiation Sciences." This training program meets a crucial need in providing training for the next generation of researchers investigating this critical element of clinical cancer therapy. No other training program at Stanford, and indeed few around the country, addresses the radiation sciences. This program provides our faculty, especially those in non-degree granting departments (e.g., Radiation Oncology and Pathology), the opportunity to recruit and mentor top-notch postdoctoral fellows. The goal of this program is to provide the very best training for its postdoctoral trainees so that they may become successful and independent leaders in the field of radiation and cancer research. The program accomplishes this goal by providing each postdoctoral trainee with a broad and comprehensive curriculum, a vast array of educational resources including seminars, lectures, conferences and workshops specifically geared towards radiation biology, physics, and oncology, a faculty comprised of 16 exceptional preceptors spanning 7 departments with extensive experience in mentoring, and an unparalleled research environment within the Stanford School of Medicine. In addition, postdoctoral trainees audit courses that will aid them in their research and achieving their career goals. Our postdoctoral trainees become independent scientists. They learn to write grants effectively and to obtain their own individual funding. They also learn extensive professional skills such as lab management and mentoring to more successfully compete in today's job market. A key strength of the program is its true multidisciplinary approach to the radiation sciences incorporating such fields as molecular biology, genetics, cell biology, computational biology and bioinformatics, comparative oncology, developmental biology, and tumor biology, as well as biotechnology development for use in cancer diagnosis and therapeutics.
This is a resubmitted application for the T32 postdoctoral training grant in Radiation Sciences at Stanford University. The program has created a thriving and innovative training environment as well as an effective administrative infrastructure, which have been very successful in attracting highly qualified postdoctoral fellows to Stanford University. In this next funding period, we intend to build on this success and to further refine te program to prepare our postdoctoral trainees to become independent and self-reliant scientists, who take positions as junior faculty in academic or research institutions, biotechnology industries, or government laboratories.
|Finger, E C; Cheng, C-F; Williams, T R et al. (2014) CTGF is a therapeutic target for metastatic melanoma. Oncogene 33:1093-100|
|Razorenova, Olga V; Castellini, Laura; Colavitti, Renata et al. (2014) The apoptosis repressor with a CARD domain (ARC) gene is a direct hypoxia-inducible factor 1 target gene and promotes survival and proliferation of VHL-deficient renal cancer cells. Mol Cell Biol 34:739-51|
|Taniguchi, Cullen M; Finger, Elizabeth C; Krieg, Adam J et al. (2013) Cross-talk between hypoxia and insulin signaling through Phd3 regulates hepatic glucose and lipid metabolism and ameliorates diabetes. Nat Med 19:1325-30|
|Bonnet, Muriel; Flanagan, Jack U; Chan, Denise A et al. (2011) SAR studies of 4-pyridyl heterocyclic anilines that selectively induce autophagic cell death in von Hippel-Lindau-deficient renal cell carcinoma cells. Bioorg Med Chem 19:3347-56|
|Chan, Denise A; Sutphin, Patrick D; Nguyen, Phuong et al. (2011) Targeting GLUT1 and the Warburg effect in renal cell carcinoma by chemical synthetic lethality. Sci Transl Med 3:94ra70|
|Finger, Elizabeth C; Giaccia, Amato J (2010) Hypoxia, inflammation, and the tumor microenvironment in metastatic disease. Cancer Metastasis Rev 29:285-93|
|Schiffman, Joshua D; Hodgson, J Graeme; VandenBerg, Scott R et al. (2010) Oncogenic BRAF mutation with CDKN2A inactivation is characteristic of a subset of pediatric malignant astrocytomas. Cancer Res 70:512-9|