The Cancer Genetics Program's overall mission is to expand the understanding of the genetic underpinnings of cancer development, and to use this information 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, such as: cancer gene discovery in both human cancer samples and model organisms, technology development and efficient application of high throughput DNA sequencing, detailed cancer genome analysis, high throughput approaches to cancer gene analysis and annotation, identification and analysis of both cancer initiating cells and induced pluripotent stem cells, clinical cancer genetics and risk counseling, and development and use of CLIA-certified testing for clinically relevant cancer diagnostics.
The specific aims of the Program are to: 1. Support the discovery of new genes and cellular pathways implicated in cancer. 2. Enhance identification and understanding of the germline genetic variations that influence cancer risk and response to therapy. 3. Increase the understanding of the full spectrum of somatic mutation that occurs in cancer and how it contributes to the genesis and progression of cancer. 4. Support the translation of these research findings to both clinical research in oncology and routine cancer patient care. The Program has been funded by the CCSG since 2000 when DF/HCC was established, and received an Outstanding merit score at the last renewal in 2005. The Program's membership includes 100 investigators, representing all seven institutions in the consortium, 14 departments of HMS, and one department of HSPH. In 2009, the Program received $52.5 million in cancer-relevant funding (total costs), which includes $18.5 million from NCI and $25 million from other peer-reviewed sponsors. Program members have published 1,630 publications over the project period (2006 to 2010), of which 9% were intra-programmatic, 44% were inter-programmatic and 32% were inter-institutional.
The Cancer Genetics Program aims to expand the understanding of the genetic underpinnings of cancer development, and to use this information to improve the care of cancer patients. The Program brings together laboratory and clinical scientists to accelerate the translation of basic discoveries in genetics to the improvement of patient outcomes.
| Santana-Codina, Naiara; Roeth, Anjali A; Zhang, Yi et al. (2018) Oncogenic KRAS supports pancreatic cancer through regulation of nucleotide synthesis. Nat Commun 9:4945 |
| Cox, Andrew G; Tsomides, Allison; Yimlamai, Dean et al. (2018) Yap regulates glucose utilization and sustains nucleotide synthesis to enable organ growth. EMBO J 37: |
| Oxnard, Geoffrey R; Hu, Yuebi; Mileham, Kathryn F et al. (2018) Assessment of Resistance Mechanisms and Clinical Implications in Patients With EGFR T790M-Positive Lung Cancer and Acquired Resistance to Osimertinib. JAMA Oncol 4:1527-1534 |
| Patil, Prasad; Parmigiani, Giovanni (2018) Training replicable predictors in multiple studies. Proc Natl Acad Sci U S A 115:2578-2583 |
| Agoston, Agoston T; Pham, Thai H; Odze, Robert D et al. (2018) Columnar-Lined Esophagus Develops via Wound Repair in a Surgical Model of Reflux Esophagitis. Cell Mol Gastroenterol Hepatol 6:389-404 |
| Barber, Lauren; Gerke, Travis; Markt, Sarah C et al. (2018) Family History of Breast or Prostate Cancer and Prostate Cancer Risk. Clin Cancer Res 24:5910-5917 |
| Kwee, Brian J; Budina, Erica; Najibi, Alexander J et al. (2018) CD4 T-cells regulate angiogenesis and myogenesis. Biomaterials 178:109-121 |
| Madsen, Thomas; Braun, Danielle; Peng, Gang et al. (2018) Efficient computation of the joint probability of multiple inherited risk alleles from pedigree data. Genet Epidemiol 42:528-538 |
| Chen, Jingjing; Guccini, Ilaria; Di Mitri, Diletta et al. (2018) Compartmentalized activities of the pyruvate dehydrogenase complex sustain lipogenesis in prostate cancer. Nat Genet 50:219-228 |
| Li, Andrew G; Murphy, Elizabeth C; Culhane, Aedin C et al. (2018) BRCA1-IRIS promotes human tumor progression through PTEN blockade and HIF-1? activation. Proc Natl Acad Sci U S A 115:E9600-E9609 |
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