This application is a request for continued funding of T32 CA080621 at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University, The Cancer Center is committed to promoting the highest caliber basic science and clinical science research. The Center has been supported by a support grant from the National Cancer Institute (NCI P30 CA60553) since 1993 and also has received support for SPORES in Prostate Cancer (P50 90386) and Breast Cancer (P50 CA89018). The Cancer Center is dedicated to preparing the next generation of research scientists through education and training programs. The Training Program in Oncogenesis and Developmental Biology has been preparing predoctoral and postdoctoral trainees to work at the interface of cancer biology and developmental biology through laboratory research, formal course work and participation in seminars, journal clubs and group meetings. Trainees learn how the gene networks controlling embryonic development play a central role in tumor formation and progression. In three and one half years, the Training Program in Oncogenesis and Developmental Biology has successfully trained five predoctoral students and six postdoctoral fellows, and five trainees are currently being supported (the sixth recently received her own funding). Of the eleven who completed the training program, seven have continued on in postdoctoral training and one accepted a senior scientist position in industry. Three students are still in the process of completing their Ph.D. training at Northwestern University. All trainees have remained in the field of cancer biology. Based on our expectation that we will continue to attract the same numbers of highly qualified candidates to Northwestern University, we request funding for two predoctoral students and four postdoctoral fellows per year for a period of five years in the current application. This will enable us to continue focused training in Oncogenesis and Developmental Biology.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Institutional National Research Service Award (T32)
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Study Section
Subcommittee G - Education (NCI)
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Damico, Mark W
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Northwestern University at Chicago
Internal Medicine/Medicine
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United States
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Pituch, Katarzyna C; Miska, Jason; Krenciute, Giedre et al. (2018) Adoptive Transfer of IL13R?2-Specific Chimeric Antigen Receptor T Cells Creates a Pro-inflammatory Environment in Glioblastoma. Mol Ther 26:986-995
Goretsky, Tatiana; Bradford, Emily M; Ye, Qing et al. (2018) Beta-catenin cleavage enhances transcriptional activation. Sci Rep 8:671
Suraneni, Praveen K; Corey, Seth J; Hession, Michael J et al. (2018) Dynamins 2 and 3 control the migration of human megakaryocytes by regulating CXCR4 surface expression and ITGB1 activity. Blood Adv 2:3540-3552
Volk, Andrew; Liang, Kaiwei; Suraneni, Praveen et al. (2018) A CHAF1B-Dependent Molecular Switch in Hematopoiesis and Leukemia Pathogenesis. Cancer Cell 34:707-723.e7
Miska, Jason; Lui, Jen Bon; Toomer, Kevin H et al. (2018) Initiation of inflammatory tumorigenesis by CTLA4 insufficiency due to type 2 cytokines. J Exp Med 215:841-858
Smith, Erica D; Garza-Gongora, Arturo G; MacQuarrie, Kyle L et al. (2018) Interstitial telomeric loops and implications of the interaction between TRF2 and lamin A/C. Differentiation 102:19-26
Chen, Jessie; Van Gulden, Stephanie; McGuire, Tammy L et al. (2018) BMP-Responsive Protease HtrA1 Is Differentially Expressed in Astrocytes and Regulates Astrocytic Development and Injury Response. J Neurosci 38:3840-3857
Hu, Deqing; Gao, Xin; Cao, Kaixiang et al. (2017) Not All H3K4 Methylations Are Created Equal: Mll2/COMPASS Dependency in Primordial Germ Cell Specification. Mol Cell 65:460-475.e6
Liang, Kaiwei; Volk, Andrew G; Haug, Jeffrey S et al. (2017) Therapeutic Targeting of MLL Degradation Pathways in MLL-Rearranged Leukemia. Cell 168:59-72.e13
Wang, Wei; Zhang, Honghong; Liu, Sali et al. (2017) Internalized CD44s splice isoform attenuates EGFR degradation by targeting Rab7A. Proc Natl Acad Sci U S A 114:8366-8371

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