The Translational and Clinical Research (TACR) Program was established in early 2016 as a forward-looking, proactive response to an ongoing shift in translational and clinical cancer research away from disease-centric paradigms, and toward cross-disease site innovation and development. TACR represents the interface between basic science Programs and the clinic-based, disease-specific research groups and is designed to expedite the translation of innovative clinical approaches developed by University of Michigan Comprehensive Cancer Center (UMCCC) researchers to the clinic. The program is comprised of 69 members from 24 different departments representing 6 different schools and colleges. In 2016, TACR members had a total of $28.8M in annual (DC) cancer grant funding, of which $7M (24.3%) is from NCI, $2.7M (9.4%) is from other NIH, and $12.6M (43.7%), is total peer-reviewed. In addition, TACR members are supported by grants from drug and device companies with total funding of $14.5M (50.4%). Investigators are involved in intra- and inter-programmatic interactions and actively collaborate with researchers in the other UMCCC programs within most of the Basic Science and Cancer Control and Population Sciences Programs. Members have a total of 1423 publications, of which 31.1% are intra-programmatic and 50.6% are inter-programmatic. The TACR program has three main Specific Aims: I) use state-of-the-art genomic approaches to make discoveries that advance patient care; II) Advance novel UMCCC concepts and agents into human trials to expedite the translation of laboratory discoveries to the clinic; and III) Develop and test new predictive biomarker and disease monitoring strategies for improving patient care.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
3P30CA046592-29S1
Application #
9756972
Study Section
Subcommittee I - Transistion to Independence (NCI)
Program Officer
Belin, Precilla L
Project Start
Project End
Budget Start
2018-06-01
Budget End
2019-05-31
Support Year
29
Fiscal Year
2018
Total Cost
Indirect Cost
Name
University of Michigan Ann Arbor
Department
Type
DUNS #
073133571
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109
Feng, Mary; Suresh, Krithika; Schipper, Matthew J et al. (2018) Individualized Adaptive Stereotactic Body Radiotherapy for Liver Tumors in Patients at High Risk for Liver Damage: A Phase 2 Clinical Trial. JAMA Oncol 4:40-47
Xiong, Yi; Torsoni, Adriana Souza; Wu, Feihua et al. (2018) Hepatic NF-kB-inducing kinase (NIK) suppresses mouse liver regeneration in acute and chronic liver diseases. Elife 7:
El Kadi, Najwa; Wang, Luo; Davis, April et al. (2018) The EGFR T790M Mutation Is Acquired through AICDA-Mediated Deamination of 5-Methylcytosine following TKI Treatment in Lung Cancer. Cancer Res 78:6728-6735
Namkoong, Sim; Ho, Allison; Woo, Yu Mi et al. (2018) Systematic Characterization of Stress-Induced RNA Granulation. Mol Cell 70:175-187.e8
Thomas, Tina T; Chukkapalli, Sahiti; Van Noord, Raelene A et al. (2018) Utilization of Ultrasound Guided Tissue-directed Cellular Implantation for the Establishment of Biologically Relevant Metastatic Tumor Xenografts. J Vis Exp :
Eisenberg, Marisa C; Campredon, Lora P; Brouwer, Andrew F et al. (2018) Dynamics and Determinants of HPV Infection: The Michigan HPV and Oropharyngeal Cancer (M-HOC) Study. BMJ Open 8:e021618
Boonstra, Philip S; Barbaro, Ryan P (2018) Incorporating historical models with adaptive Bayesian updates. Biostatistics :
Johnson, Allison M; Roach, James P; Hu, Anna et al. (2018) Connexin 43 gap junctions contribute to brain endothelial barrier hyperpermeability in familial cerebral cavernous malformations type III by modulating tight junction structure. FASEB J 32:2615-2629
Feinberg, Tamar Y; Zheng, Huarui; Liu, Rui et al. (2018) Divergent Matrix-Remodeling Strategies Distinguish Developmental from Neoplastic Mammary Epithelial Cell Invasion Programs. Dev Cell 47:145-160.e6
Hrycaj, Steven M; Marty-Santos, Leilani; Cebrian, Cristina et al. (2018) Hox5 genes direct elastin network formation during alveologenesis by regulating myofibroblast adhesion. Proc Natl Acad Sci U S A 115:E10605-E10614

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