The mission of the Cancer Risk and Disparities Program is to support research that will lead to a reduction of cancer risk and disparities across society. To achieve this goal, the Program has the following four specific aims: 1. Understand the individual, psychosocial, organizational and community-level factors that determine differences in cancer risk across the life course and population groups. 2. Develop, test and evaluate interventions to reduce cancer risk across the life course and population groups. 3. Advance the science of communication and knowledge translation to promote dissemination of evidence-based interventions to reduce cancer risk. 4. Examine causes of disparities in cancer risk and incidence and Identify interventions to redress these disparities. The Program was initially funded in 2000 when the Dana-Farber/Harvard Cancer Center was established as a consortium Center, and received a merit score of "excellent to outstanding" at the time of the last renewal in 2005. The Program Is led by L. Frazier(DFCI). There are two Co-Leaders: K. Viswanath (DFCI) and D. Williams(HSPH). During the current project period, the goals of the Program were substantially revised to include new research foci including: 1) the individual and societal factors that predispose to cancer risk, 2) the science of dissemination and 3) an explicit focus on cancer disparities, all of which represent expanded and vibrant strengths within the Program. The expertise of the 49 members spans epidemiology, molecular epidemiology, behavioral science, communication science, intervention science, health policy and dissemination. In 2009, the Program received $19.7 million in cancer-relevant funding (total costs), which included over $11.9 million in NCI funding and $6.5 million in other federal, peer-reviewed funding. Attesting to the productivity and interactivity of the Program are the 903 publications authored by members of the Program during the project period (2006 to 2010), of which 15.5% were Intra-programmatic ,18% were inter-programmatic and 16% were inter-institutional collaborations.
The Cancer Risk and Disparities Program seeks to identify the causes of increased risk of cancer, to design interventions to address these causes and to disseminate this knowledge effecfively into the community by advancing the methodologies of communication science and knowledge translafion. The Program is committed to reducing the incidence of cancer and its unequal distribution in the US population through its research and involvement in health and social policy.
|Chen, Yi-Bin; Batchelor, Tracy; Li, Shuli et al. (2015) Phase 2 trial of high-dose rituximab with high-dose cytarabine mobilization therapy and high-dose thiotepa, busulfan, and cyclophosphamide autologous stem cell transplantation in patients with central nervous system involvement by non-Hodgkin lymphoma. Cancer 121:226-33|
|Waldron, Levi; Haibe-Kains, Benjamin; Culhane, Aedín C et al. (2014) Comparative meta-analysis of prognostic gene signatures for late-stage ovarian cancer. J Natl Cancer Inst 106:|
|Yilmazel, Bahar; Hu, Yanhui; Sigoillot, Frederic et al. (2014) Online GESS: prediction of miRNA-like off-target effects in large-scale RNAi screen data by seed region analysis. BMC Bioinformatics 15:192|
|Mazzola, Emanuele; Chipman, Jonathan; Cheng, Su-Chun et al. (2014) Recent BRCAPRO upgrades significantly improve calibration. Cancer Epidemiol Biomarkers Prev 23:1689-95|
|Zhao, Sihai Dave; Parmigiani, Giovanni; Huttenhower, Curtis et al. (2014) Más-o-menos: a simple sign averaging method for discrimination in genomic data analysis. Bioinformatics 30:3062-9|
|Parkhitko, Andrey A; Priolo, Carmen; Coloff, Jonathan L et al. (2014) Autophagy-dependent metabolic reprogramming sensitizes TSC2-deficient cells to the antimetabolite 6-aminonicotinamide. Mol Cancer Res 12:48-57|
|Cheng, Long; Desai, Jigar; Miranda, Carlos J et al. (2014) Human CFEOM1 mutations attenuate KIF21A autoinhibition and cause oculomotor axon stalling. Neuron 82:334-49|
|Akbay, Esra A; Moslehi, Javid; Christensen, Camilla L et al. (2014) D-2-hydroxyglutarate produced by mutant IDH2 causes cardiomyopathy and neurodegeneration in mice. Genes Dev 28:479-90|
|Brunner, Andrew M; Blonquist, Traci M; Sadrzadeh, Hossein et al. (2014) Population-based disparities in survival among patients with core-binding factor acute myeloid leukemia: a SEER database analysis. Leuk Res 38:773-80|
|Karamichos, D; Hutcheon, A E K; Rich, C B et al. (2014) In vitro model suggests oxidative stress involved in keratoconus disease. Sci Rep 4:4608|
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