CANCER CELL BIOLOGY PROGRAM (Project-113) ABSTRACT Overview and Goals: Accumulation of defects in the regulation of cell behavior results in uncontrolled proliferation, immune evasion, invasiveness and metastasis. Understanding these mechanisms will provide new diagnostic markers and therapeutic targets. The major goal of the Cancer Cell Biology (CCB) Program is to foster and improve research focused on dissecting the cellular regulatory functions that establish and maintain this malignant phenotype and to apply this knowledge to translational and clinical investigations. CCB members have expertise in many areas and disciplines: Cell Cycle Regulation, Apoptosis and Autophagy, Developmental Biology and Stem Cells, Immunotherapy/Immunology, Signal Transduction and Tumor Microenvironment and Metastasis. This deep and diverse expertise results in collaborations, enhanced training and facilitation of technological innovations through UCCC Shared Resources (SR). Research Highlight: A multidisciplinary team including members at the UCB consortium site mapped the cell cycle phosphoproteome of the yeast centrosome. This molecular resource will provide foundational knowledge about the cell cycle in cancer and other diseases (Science, 20111). Program Activities: To accomplish its goal, the CCB program co-leaders employ resources provided by the UCCC to foster interactions by organizing retreats, mentoring programs, and weekly seminars attended by program members, students, fellows, and non-program faculty. Our collaborative publications and grants demonstrate the success of our endeavors. Furthermore, key members of the CCB Program have collaborated effectively with other programs, resulting in joint grant awards and submissions. Members: The program has 43 Full members with $2.2M in grant funding from NCI and $5.9M in other peer-reviewed research grant funding in 2015. Members are from 5 basic science (21%) and 7 clinical (51%) departments in the SOM, from the School of Dental Medicine (5%), and the School of Public Health (1%) at AMC; and the College of Liberal Arts and Sciences (2%) at the downtown campus. Thirteen percent of members are at UCB; 2% at CSU; and 5% are at non-consortium institutions. Program members published 690 cancer-relevant publications in the previous grant period of which 41% were inter- and 17% were intra-programmatic. Future Directions: We will enhance our high degree of productivity and collaborative science by continuing to support fundamental research in cell biology, by guiding these fundamental discoveries into the clinic and by leveraging the scientific strengths found in the consortium institutions unique to the State of Colorado. Specifically, we will accomplish this goal by enhancing the training and mentoring of students, fellows and junior faculty, by increasing the number of novel cancer biology and mechanism discoveries that lead to collaborative scientific studies and are translated into clinical applications, and by providing access to new technologies and innovative experimental models of cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA046934-30
Application #
9429061
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
Project End
Budget Start
2018-02-01
Budget End
2019-01-31
Support Year
30
Fiscal Year
2018
Total Cost
Indirect Cost
Name
University of Colorado Denver
Department
Type
DUNS #
041096314
City
Aurora
State
CO
Country
United States
Zip Code
80045
Sanchez, Gilson J; Richmond, Phillip A; Bunker, Eric N et al. (2018) Genome-wide dose-dependent inhibition of histone deacetylases studies reveal their roles in enhancer remodeling and suppression of oncogenic super-enhancers. Nucleic Acids Res 46:1756-1776
Witt, Davis A; Donson, Andrew M; Amani, Vladimir et al. (2018) Specific expression of PD-L1 in RELA-fusion supratentorial ependymoma: Implications for PD-1-targeted therapy. Pediatr Blood Cancer 65:e26960
McCoach, Caroline E; Le, Anh T; Gowan, Katherine et al. (2018) Resistance Mechanisms to Targeted Therapies in ROS1+ and ALK+ Non-small Cell Lung Cancer. Clin Cancer Res 24:3334-3347
Abraham, Christopher G; Ludwig, Michael P; Andrysik, Zdenek et al. (2018) ?Np63? Suppresses TGFB2 Expression and RHOA Activity to Drive Cell Proliferation in Squamous Cell Carcinomas. Cell Rep 24:3224-3236
Lyu, Hui; Wang, Shuiliang; Huang, Jingcao et al. (2018) Survivin-targeting miR-542-3p overcomes HER3 signaling-induced chemoresistance and enhances the antitumor activity of paclitaxel against HER2-overexpressing breast cancer. Cancer Lett 420:97-108
Noonan, Sinead A; Patil, Tejas; Gao, Dexiang et al. (2018) Baseline and On-Treatment Characteristics of Serum Tumor Markers in Stage IV Oncogene-Addicted Adenocarcinoma of the Lung. J Thorac Oncol 13:134-138
Guarnieri, A L; Towers, C G; Drasin, D J et al. (2018) The miR-106b-25 cluster mediates breast tumor initiation through activation of NOTCH1 via direct repression of NEDD4L. Oncogene 37:3879-3893
Davies, Kurtis D; Le, Anh T; Sheren, Jamie et al. (2018) Comparison of Molecular Testing Modalities for Detection of ROS1 Rearrangements in a Cohort of Positive Patient Samples. J Thorac Oncol 13:1474-1482
Wu, Xiaorong; An, Xiuxiang; Zhang, Caiguo et al. (2018) Clb6-Cdc28 Promotes Ribonucleotide Reductase Subcellular Redistribution during S Phase. Mol Cell Biol 38:
Lee-Sherick, Alisa B; Jacobsen, Kristen M; Henry, Curtis J et al. (2018) MERTK inhibition alters the PD-1 axis and promotes anti-leukemia immunity. JCI Insight 3:

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