The overall mission of the Cancer Genetics Program is to expand our understanding of the genetic basis of cancer development and to use this knowledge to improve the care of cancer patients. To advance this mission, the Program has assembled a large and vibrant membership, including investigators with a broad range of scientific interests in all major aspects of cancer genetics. Particular areas of focus include: 1) cancer gene discovery and functional characterization (in both human cancers and model organisms), 2) technology development and application (e.g., massively parallel sequencing, emerging genomic technologies, and single cell analyses), 3) computational analysis (e.g., algorithm development, bioinformatics methods, and genome annotation approaches), 4) genetic and molecular studies of cancer progenitor cells, 5) analysis of mechanisms of cancer targeted therapy resistance, 6) clinical cancer genetics, including risk counseling, and 7) delivery of state-of-the-art CLIA-certified testing of both cancer gene panels and of whole exomes for cancer precision medicine. The program has 111 members, representing seven DF/HCC institutions and 14 academic departments. In 2014 peer-reviewed grant funding attributed to the Program was $8.2 million in total costs from the NCI and $25.1 million from other sponsors. During the current funding period, Cancer Genetics Program members published 2,332 cancer-relevant papers. Of these 31% were inter-institutional, 15% were intra- programmatic, and 48% were inter-programmatic collaborations between two or more DF/HCC members. Overall, when counted once, 27% of DF/HCC publications were inter-programmatic collaborations.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA006516-53
Application #
9405396
Study Section
Subcommittee I - Transistion to Independence (NCI)
Project Start
Project End
Budget Start
2017-12-01
Budget End
2018-11-30
Support Year
53
Fiscal Year
2018
Total Cost
Indirect Cost
Name
Dana-Farber Cancer Institute
Department
Type
DUNS #
076580745
City
Boston
State
MA
Country
United States
Zip Code
Yao, Lina; Seaton, Sarah Craven; Ndousse-Fetter, Sula et al. (2018) A selective gut bacterial bile salt hydrolase alters host metabolism. Elife 7:
Jalbut, Marla M; Brunner, Andrew M; Amrein, Philip C et al. (2018) Early infectious complications among patients treated with induction compared to hypomethylating therapy for acute myeloid leukemia. Leuk Lymphoma 59:988-991
Tapela, Neo M; Peluso, Michael J; Kohler, Racquel E et al. (2018) A Step Toward Timely Referral and Early Diagnosis of Cancer: Implementation and Impact on Knowledge of a Primary Care-Based Training Program in Botswana. Front Oncol 8:187
Roemer, Margaretha G M; Redd, Robert A; Cader, Fathima Zumla et al. (2018) Major Histocompatibility Complex Class II and Programmed Death Ligand 1 Expression Predict Outcome After Programmed Death 1 Blockade in Classic Hodgkin Lymphoma. J Clin Oncol 36:942-950
Francini, Edoardo; Gray, Kathryn P; Xie, Wanling et al. (2018) Time of metastatic disease presentation and volume of disease are prognostic for metastatic hormone sensitive prostate cancer (mHSPC). Prostate 78:889-895
Hu, Yanhui; Vinayagam, Arunachalam; Nand, Ankita et al. (2018) Molecular Interaction Search Tool (MIST): an integrated resource for mining gene and protein interaction data. Nucleic Acids Res 46:D567-D574
Mohr, Stephanie E; Rudd, Kirstin; Hu, Yanhui et al. (2018) Zinc Detoxification: A Functional Genomics and Transcriptomics Analysis in Drosophila melanogaster Cultured Cells. G3 (Bethesda) 8:631-641
Odiaka, Emeka; Lounsbury, David W; Jalloh, Mohamed et al. (2018) Effective Project Management of a Pan-African Cancer Research Network: Men of African Descent and Carcinoma of the Prostate (MADCaP). J Glob Oncol :1-12
Mills, Evanna L; Pierce, Kerry A; Jedrychowski, Mark P et al. (2018) Accumulation of succinate controls activation of adipose tissue thermogenesis. Nature 560:102-106
Oser, Matthew G; Fonseca, Raquel; Chakraborty, Abhishek A et al. (2018) Cells Lacking the RB1 Tumor Suppressor Gene are Hyperdependent on Aurora B Kinase for Survival. Cancer Discov :

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