This application is a request for renewal funding for the Training Program in Signal Transduction and Cancer (T32 CA070085) at the Robert H. Lurie Comprehensive Cancer Center of Northwestern University. The Training Program in Signal Transduction and Cancer has been preparing postdoctoral trainees to work in the area of signal transduction and cancer through mentored laboratory research and a structured curriculum of seminars, journal clubs and program meetings. The preceptors are established NIH funded investigators who focus on translational research on signaling pathways in malignant cells. This training program complements the Lurie Cancer Center's existing Basic Science Program in Hormone Action and Signal Transduction in Cancer. The Training Program provides a training milieu that enables recent PhDs to spend two years in a structured mentored environment where they can acquire the skills and fundamental knowledge necessary before embarking on careers as independent investigators in cancer research laboratories, either in academia or in industry. Over the last ten years we have trained 26 postdoctoral fellows, several of whom have achieved successful academic faculty positions or senior scientist positions in industry. It is our expectation that our trainees will continue to be appropriately prepared to meet the challenges of biomedical research in the coming years and will contribute to seminal discoveries in signaling and cancer.
This Program trains postdoctoral fellows in the field of signal transduction and cancer and prepares them for careers as independent scientists. A group of highly qualified faculty at Northwestern University who work in different areas of signaling and cancer has been assembled to provide guidance and mentorship to postdoctoral trainees.
|Murmann, Andrea E; Gao, Quan Q; Putzbach, William E et al. (2018) Small interfering RNAs based on huntingtin trinucleotide repeats are highly toxic to cancer cells. EMBO Rep 19:|
|Putzbach, William; Gao, Quan Q; Patel, Monal et al. (2018) DISE: A Seed-Dependent RNAi Off-Target Effect That Kills Cancer Cells. Trends Cancer 4:10-19|
|Ladomersky, Erik; Zhai, Lijie; Lenzen, Alicia et al. (2018) IDO1 Inhibition Synergizes with Radiation and PD-1 Blockade to Durably Increase Survival Against Advanced Glioblastoma. Clin Cancer Res 24:2559-2573|
|Bell, Jonathan B; Eckerdt, Frank; Dhruv, Harshil D et al. (2018) Differential Response of Glioma Stem Cells to Arsenic Trioxide Therapy Is Regulated by MNK1 and mRNA Translation. Mol Cancer Res 16:32-46|
|Sang, Youzhou; Li, Yanxin; Song, Lina et al. (2018) TRIM59 Promotes Gliomagenesis by Inhibiting TC45 Dephosphorylation of STAT3. Cancer Res 78:1792-1804|
|Pangeni, Rajendra P; Zhang, Zhou; Alvarez, Angel A et al. (2018) Genome-wide methylomic and transcriptomic analyses identify subtype-specific epigenetic signatures commonly dysregulated in glioma stem cells and glioblastoma. Epigenetics 13:432-448|
|Wang, Lu; Ozark, Patrick A; Smith, Edwin R et al. (2018) TET2 coactivates gene expression through demethylation of enhancers. Sci Adv 4:eaau6986|
|Gilles, Laure; Arslan, Ahmet Dirim; Marinaccio, Christian et al. (2017) Downregulation of GATA1 drives impaired hematopoiesis in primary myelofibrosis. J Clin Invest 127:1316-1320|
|Wang, Lu; Collings, Clayton K; Zhao, Zibo et al. (2017) A cytoplasmic COMPASS is necessary for cell survival and triple-negative breast cancer pathogenesis by regulating metabolism. Genes Dev 31:2056-2066|
|Arslan, A D; Sassano, A; Saleiro, D et al. (2017) Human SLFN5 is a transcriptional co-repressor of STAT1-mediated interferon responses and promotes the malignant phenotype in glioblastoma. Oncogene 36:6006-6019|
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