The specific aims of the Cancer Epidemiology Program are to evaluate the following factors in relation to cancer risk and survival: 1. Hormonal markers and other intermediate markers (e.g., metabolomics) as well as energy balance. 2. Genetic and epigenetic markers, with an emphasis on their interaction with environmental factors. Chronic inflammatory processes, as assessed through lifestyle, molecular markers and use of anti-inflammatory drugs. 3. Diet, including vitamin D, folate and other nutritional contributors to one-carbon metabolism. The Program focuses on exposures over the life course, including childhood and adolescence. Further, exposures are evaluated in relation to specific molecular characteristics of the tumor, analyses that can greatly enhance the understanding of etiologic pathways and provide support for causality. Cancer Epidemiology has been a Program since the formation of DF/HCC. The Program is led by S. Hankinson BWH) and W. Willett(HSPH) and includes 59 members representing five of the Harvard member institutions and 11 departments across Harvard Medical School and Harvard School of Public Health. The Program was rated "outstanding" at its last review. Program members have $24.3 million in research funding (total costs), including $20.2 million in NCI funding and $3.7 million in other peer reviewed funding. Program members published 1,295 papers (2006 to 2010). Of these, ,30% were intra-programmatic, 43% of these were interprogrammatic collaborations and 35% were inter-institutional.
The Cancer Epidemiology Program focuses on determining and quantifying the role of lifestyle factors (such as diet and physical activity), other environmental factors, genetics and epigenetics in cancer incidence and survival. The overall goal of the Program is to find the means to reduce the occurrence of cancer and to improve the survival of patients with cancer.
|Hu, Yanhui; Comjean, Aram; Roesel, Charles et al. (2016) FlyRNAi.org-the database of the Drosophila RNAi screening center and transgenic RNAi project: 2017 update. Nucleic Acids Res :|
|Hong, Theodore S; Wo, Jennifer Y; Yeap, Beow Y et al. (2016) Multi-Institutional Phase II Study of High-Dose Hypofractionated Proton Beam Therapy in Patients With Localized, Unresectable Hepatocellular Carcinoma and Intrahepatic Cholangiocarcinoma. J Clin Oncol 34:460-8|
|Freedman, Rachel A; Gelman, Rebecca S; Wefel, Jeffrey S et al. (2016) Translational Breast Cancer Research Consortium (TBCRC) 022: A Phase II Trial of Neratinib for Patients With Human Epidermal Growth Factor Receptor 2-Positive Breast Cancer and Brain Metastases. J Clin Oncol 34:945-52|
|Mohr, Stephanie E; Hu, Yanhui; Ewen-Campen, Benjamin et al. (2016) CRISPR guide RNA design for research applications. FEBS J 283:3232-8|
|Brunner, Andrew M; Li, Shuli; Fathi, Amir T et al. (2016) Haematopoietic cell transplantation with and without sorafenib maintenance for patients with FLT3-ITD acute myeloid leukaemia in first complete remission. Br J Haematol 175:496-504|
|Cox, Andrew G; Hwang, Katie L; Brown, Kristin K et al. (2016) Yap reprograms glutamine metabolism to increase nucleotide biosynthesis and enable liver growth. Nat Cell Biol 18:886-96|
|McKay, Tina B; Hjortdal, Jesper; Sejersen, Henrik et al. (2016) Endocrine and Metabolic Pathways Linked to Keratoconus: Implications for the Role of Hormones in the Stromal Microenvironment. Sci Rep 6:25534|
|Nelms, Bradlee D; Waldron, Levi; Barrera, Luis A et al. (2016) CellMapper: rapid and accurate inference of gene expression in difficult-to-isolate cell types. Genome Biol 17:201|
|Tan, Justin L; Fogley, Rachel D; Flynn, Ryan A et al. (2016) Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma. Mol Cell 62:34-46|
|Johnson, Shawn F; Cruz, Cristina; Greifenberg, Ann Katrin et al. (2016) CDK12 Inhibition Reverses De Novo and Acquired PARP Inhibitor Resistance in BRCA Wild-Type and Mutated Models of Triple-Negative Breast Cancer. Cell Rep 17:2367-2381|
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