Members of the Cancer Cell Biology (CB) Program study the cell cycle, signal transduction, apoptosis, cell development, cell differentiation, stem cell biology, immune and inflammatory responses and metastasis. They are engaged in determining the drivers of these processes in cancer and translating this knowledge into potential biomarkers and therapeutic approaches and targets for cancer patients. Novel technologies and approaches to address these areas developed by the program include facile animal models to study cancer stem cells, signaling and apoptosis, mass spectrometric analysis of unique tumor epigenetic modifications, functional genomic drug screens and cancer vaccine development. CB has four interconnected focus groups: 1) Signal Transduction and Apoptosis;2) Cell Cycle Regulation and Proliferation;3) Development, Stem Cells and Cancer;4) Inflammation, Immunity and Metastasis. In the prior funding period, CB made major contributions to the field, including: 1) Identified a novel oncogene using a frog model system (Repo-Man);2) Determined the mechanism of action of Silibinin (IP6) a chemopreventive compound;3) Developed novel therapeutics from knowledge of signal transduction, apoptosis and cell cycle pathways (e.g. Mer TK and p27 targets);4) Investigated IL-lb-mediated inflammation's role in melanoma metastasis;5) Discovered novel epigenetic markers (histone H3 K56);6) demonstrated the p53 gain of function mutations confer a worse prognosis than p53 deletion;and, 7) Tested the cancer stem cell hypothesis using novel animal models (BCR and MYC in skin). CB has 66 full members in 20 Departments and 6 schools on the University of Colorado Denver, University of Colorado Boulder, National Jewish Health, and the Colorado State University campuses holding $2.7 million direct costs in NCI grants and $23.7 million direct costs in other cancer-relevant support in the last budget year. Between 2005 and 2010, per capita cancer research funding increased by 40% from $286K to over $400K. CB produced 869 cancer-related publications from 2005 through 2010. Of these, 230 (26.5%) were inter-programmatic publications;66 (7.6%) were intra-programmatic publications;and 36 (4%) were both inter- and intra-programmatic. Thus, 332 (38%) of the total cancer-related publications by memtjers of this program were collaborative. Importantly, more than 2/3 of CB members published collaborative peer reviewed papers in the last funding period with other UCCC members.
The Cancer Cell Biology Program organizes UCCC researchers who study how cellular processes function in the development and progression of cancer. Understanding how cancer changes the way cells function can help biomedical researchers discover new ways to prevent and treat it.
|Saichaemchan, S; Ariyawutyakorn, W; Varella-Garcia, M (2016) Fibroblast Growth Factor Receptors: From the Oncogenic Pathway to Targeted Therapy. Curr Mol Med 16:40-62|
|Gillen, Austin E; Yamamoto, Tomomi M; Kline, Enos et al. (2016) Improvements to the HITS-CLIP protocol eliminate widespread mispriming artifacts. BMC Genomics 17:338|
|Justice, Cristina M; Bishop, Kevin; Carrington, Blake et al. (2016) Evaluation of IRX Genes and Conserved Noncoding Elements in a Region on 5p13.3 Linked to Families with Familial Idiopathic Scoliosis and Kyphosis. G3 (Bethesda) 6:1707-12|
|Eckwahl, Matthew J; Arnion, Helene; Kharytonchyk, Siarhei et al. (2016) Analysis of the human immunodeficiency virus-1 RNA packageome. RNA 22:1228-38|
|Iguchi, Nao; Malykhina, Anna P; Wilcox, Duncan T (2016) Inhibition of HIF Reduces Bladder Hypertrophy and Improves Bladder Function in Murine Model of Partial Bladder Outlet Obstruction. J Urol 195:1250-6|
|Seedorf, Gregory; Metoxen, Alexander J; Rock, Robert et al. (2016) Hepatocyte growth factor as a downstream mediator of vascular endothelial growth factor-dependent preservation of growth in the developing lung. Am J Physiol Lung Cell Mol Physiol 310:L1098-110|
|Agarwal, Neeraj; Dancik, Garrett M; Goodspeed, Andrew et al. (2016) GON4L Drives Cancer Growth through a YY1-Androgen Receptor-CD24 Axis. Cancer Res 76:5175-85|
|Helfrich, Barbara A; Kim, Jihye; Gao, Dexiang et al. (2016) Barasertib (AZD1152), a Small Molecule Aurora B Inhibitor, Inhibits the Growth of SCLC Cell Lines In Vitro and In Vivo. Mol Cancer Ther 15:2314-2322|
|Munson, Daniel J; Egelston, Colt A; Chiotti, Kami E et al. (2016) Identification of shared TCR sequences from T cells in human breast cancer using emulsion RT-PCR. Proc Natl Acad Sci U S A 113:8272-7|
|Scott, Aaron J; Lieu, Christopher H; Messersmith, Wells A (2016) Therapeutic Approaches to RAS Mutation. Cancer J 22:165-74|
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