Cancer is a complex disease with a range of genetic, genomic, and environmental factors that can impact disease development, progression, and response to therapy. These factors exhibit broad heterogeneity: large variations are seen between individuals in germline DNA sequence, tumor genetics, or histological subtypes, and environmental exposures. A high level of complexity is seen in the patterns of inherited genetic variants (SNPs) in the normal host DNA, and in the combinations of somatic genetic events and gene expression changes in tumors. In addition, complex interactions exist between the genetics of the host and environmental exposures that contribute to tumor susceptibility. The overall goal of the Cancer Genetics Program (Program) is to elucidate the genetics of tumor susceptibility, tumorigenesis, and progression;and to use this information clinically to improve cancer management. The central themes of the Program that we aim to further develop in the next five years are: (1) Genetics of Cancer Susceptibility, Progression, and Response;(2) Cancer Genome and Epigenome;(S) Functional Genomics;and (4) Systems Genetics of Cancer. The Program brings together experts in the application of advanced genomic and genetic analysis tools to identify abnormalities that contribute to cancer genesis and progression by utilizing the outstanding mouse and human genetic resources at UCSF. There are 24 members in the Program, and they represent 12 Departments from the Schools of Medicine and Pharmacy at UCSF. The NCI and other peer-reviewed support among Program members during the last budget year was $13,592,313, in total. Since 2007, 492 total papers were published by members of the Program, with 12 percent intra- and 33 percent interprogrammatic. Program members are fully integrated into the organ site-specific programs, and participate broadly in seminars, and discussion groups organized by the Program;and in conjunction with other research programs (e.g., the Cancer Genetics Risk Program, and the Human Genetics Program). Ultimately the Program aims to encourage and support cross-cutting research that encompasses both germline and somatic approaches to deciphering the genetic basis of cancer.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA082103-16
Application #
8693938
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
16
Fiscal Year
2014
Total Cost
$143
Indirect Cost
$53
Name
University of California San Francisco
Department
Type
DUNS #
094878337
City
San Francisco
State
CA
Country
United States
Zip Code
94143
John, Constance M; Phillips, Nancy J; Din, Richard et al. (2016) Lipooligosaccharide Structures of Invasive and Carrier Isolates of Neisseria meningitidis Are Correlated with Pathogenicity and Carriage. J Biol Chem 291:3224-38
Shatsky, Maxim; Dong, Ming; Liu, Haichuan et al. (2016) Quantitative Tagless Copurification: A Method to Validate and Identify Protein-Protein Interactions. Mol Cell Proteomics 15:2186-202
Nordström, Tobias; Van Blarigan, Erin L; Ngo, Vy et al. (2016) Associations between circulating carotenoids, genomic instability and the risk of high-grade prostate cancer. Prostate 76:339-48
Bulut-Karslioglu, Aydan; Biechele, Steffen; Jin, Hu et al. (2016) Inhibition of mTOR induces a paused pluripotent state. Nature 540:119-123
Akutagawa, J; Huang, T Q; Epstein, I et al. (2016) Targeting the PI3K/Akt pathway in murine MDS/MPN driven by hyperactive Ras. Leukemia 30:1335-43
Baeza-Raja, Bernat; Sachs, Benjamin D; Li, Pingping et al. (2016) p75 Neurotrophin Receptor Regulates Energy Balance in Obesity. Cell Rep 14:255-68
Ko, Andrew H; Bekaii-Saab, Tanios; Van Ziffle, Jessica et al. (2016) A Multicenter, Open-Label Phase II Clinical Trial of Combined MEK plus EGFR Inhibition for Chemotherapy-Refractory Advanced Pancreatic Adenocarcinoma. Clin Cancer Res 22:61-8
Nosbaum, Audrey; Prevel, Nicolas; Truong, Hong-An et al. (2016) Cutting Edge: Regulatory T Cells Facilitate Cutaneous Wound Healing. J Immunol 196:2010-4
Phan, An T; Fernandez, Samantha G; Somberg, Jessica J et al. (2016) Epstein-Barr virus latency type and spontaneous reactivation predict lytic induction levels. Biochem Biophys Res Commun 474:71-5
Chang, Matthew T; Asthana, Saurabh; Gao, Sizhi Paul et al. (2016) Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity. Nat Biotechnol 34:155-63

Showing the most recent 10 out of 135 publications