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.

Public Health Relevance

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.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Center Core Grants (P30)
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Subcommittee G - Education (NCI)
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Dana-Farber Cancer Institute
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Lin, Ruei-Zeng; Lee, Chin Nien; Moreno-Luna, Rafael et al. (2017) Host non-inflammatory neutrophils mediate the engraftment of bioengineered vascular networks. Nat Biomed Eng 1:
Wang, Meng; Han, Jing; Marcar, Lynnette et al. (2017) Radiation Resistance in KRAS-Mutated Lung Cancer Is Enabled by Stem-like Properties Mediated by an Osteopontin-EGFR Pathway. Cancer Res 77:2018-2028
Ignatius, Myron S; Hayes, Madeline N; Lobbardi, Riadh et al. (2017) The NOTCH1/SNAIL1/MEF2C Pathway Regulates Growth and Self-Renewal in Embryonal Rhabdomyosarcoma. Cell Rep 19:2304-2318
Nugent, Alicia A; Park, Jong G; Wei, Yan et al. (2017) Mutant ?2-chimaerin signals via bidirectional ephrin pathways in Duane retraction syndrome. J Clin Invest 127:1664-1682
Breitkopf, Susanne B; Taveira, Mateus De Oliveira; Yuan, Min et al. (2017) Serial-omics of P53-/-, Brca1-/- Mouse Breast Tumor and Normal Mammary Gland. Sci Rep 7:14503
Bowden, John A; Heckert, Alan; Ulmer, Candice Z et al. (2017) Harmonizing lipidomics: NIST interlaboratory comparison exercise for lipidomics using SRM 1950-Metabolites in Frozen Human Plasma. J Lipid Res 58:2275-2288
Lindsley, R Coleman; Saber, Wael; Mar, Brenton G et al. (2017) Prognostic Mutations in Myelodysplastic Syndrome after Stem-Cell Transplantation. N Engl J Med 376:536-547
Mita, Monica M; Mita, Alain C; Moseley, Jennifer L et al. (2017) Phase 1 safety, pharmacokinetic and pharmacodynamic study of the cyclin-dependent kinase inhibitor dinaciclib administered every three weeks in patients with advanced malignancies. Br J Cancer 117:1258-1268
Hu, Yuebi; Alden, Ryan S; Odegaard, Justin I et al. (2017) Discrimination of Germline EGFR T790M Mutations in Plasma Cell-Free DNA Allows Study of Prevalence Across 31,414 Cancer Patients. Clin Cancer Res 23:7351-7359
Lam, Hilaire C; Liu, Heng-Jia; Baglini, Christian V et al. (2017) Rapamycin-induced miR-21 promotes mitochondrial homeostasis and adaptation in mTORC1 activated cells. Oncotarget 8:64714-64727

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