The Population Science (PS) Program's overall goal is to reduce and prevent morbidity and mortality associated with cancer and its treatment, particularly through identification of genetic and modifiable factors that may influence adverse outcomes. To address this goal, our research is focused around four themes, each of which includes research along the cancer continuum ranging from cancer etiology to cancer treatment outcomes: Nutrition and Chemoprevention;Molecular Epidemiology of Cancer Risk and Prognosis;Cancer Health Disparities;and Tobacco Epidemiology and Translation into Policy. Molecular Epidemiology and Cancer Health Disparities particularly are critical and broadly considered concepts in all themes. The Program members seek to address cancer-related problems that are important to the community that we serve, with outreach, education and interventions to reduce cancer risk and morbidity within our catchment area. The PS program is co-led by Drs. Christine Ambrosone and James Marshall, who together facilitate research in discovery, to identify genetic and environmental causes of cancer and its outcomes; prevention interventions, particularly among those at greatest risk;translation and dissemination to the community;and to ultimately impact policy, particularly related to tobacco. PS seeks to translate basic and clinical science findings to human populations, integrating basic science with cancer epidemiology. PS members include scientists with expertise in each of these areas. Program themes have matured and expanded over the last funding cycle, enhanced by receipt of a number of ROl grants supporting molecular epidemiology of cancer risk and prognosis, disparities research, including POl and U54 grants, ROl and U01-funded dietary interventions, and continued NCI and FDA support for tobacco research. The PS Program is comprised of 22 members from 7 RPCI departments (Cancer Prevention and Control, Health Behavior, Medicine, Surgical !Oncology, Urology, and Dentistry), whose total peer-reviewed funding is $17.4M (NCI funding $12M) and total funding is $22.6M. This compares favorably to $11M peer reviewed/$17M total funding at the time of the last renewal. Of the 4g9 publications generated over the last funding cycle, 28% are intra-programmatic and 15% are inter-programmatic;40 publications were in journals with an Impact Factor >10.
The PS program conducts research to prevent cancer and its precursors, and to reduce morbidity and mortality associated with cancer and its treatment outcomes. Interventions among community and high-risk populations translate findings from the laboratory and observational studies to the community, with a focus on underserved populations in our catchment area.
|Goossens, Maria E; Isa, Fatima; Brinkman, Maree et al. (2016) International pooled study on diet and bladder cancer: the bladder cancer, epidemiology and nutritional determinants (BLEND) study: design and baseline characteristics. Arch Public Health 74:30|
|Clyde, Merlise A; Palmieri Weber, Rachel; Iversen, Edwin S et al. (2016) Risk Prediction for Epithelial Ovarian Cancer in 11 United States-Based Case-Control Studies: Incorporation of Epidemiologic Risk Factors and 17 Confirmed Genetic Loci. Am J Epidemiol 184:579-589|
|Wilton, John; Kurenova, Elena; Pitzonka, Laura et al. (2016) Pharmacokinetic analysis of the FAK scaffold inhibitor C4 in dogs. Eur J Drug Metab Pharmacokinet 41:55-67|
|Zhao, Zhiguo; Wen, Wanqing; Michailidou, Kyriaki et al. (2016) Association of genetic susceptibility variants for type 2 diabetes with breast cancer risk in women of European ancestry. Cancer Causes Control 27:679-93|
|Shafirstein, Gal; Battoo, Athar; Harris, Kassem et al. (2016) Photodynamic Therapy of Non-Small Cell Lung Cancer. Narrative Review and Future Directions. Ann Am Thorac Soc 13:265-75|
|Pharoah, Paul D P; Song, Honglin; Dicks, Ed et al. (2016) PPM1D Mosaic Truncating Variants in Ovarian Cancer Cases May Be Treatment-Related Somatic Mutations. J Natl Cancer Inst 108:|
|Austin, David C; Strand, Douglas W; Love, Harold L et al. (2016) NF-ÎºB and androgen receptor variant 7 induce expression of SRD5A isoforms and confer 5ARI resistance. Prostate 76:1004-18|
|Sexton, Sandra; Tulowitzki, Ryan; Jones, Craig A et al. (2016) Involvement of the renin-angiotensin system in the development of nephrogenic systemic fibrosis-like lesions in the RenTag mouse model. Clin Exp Nephrol 20:162-8|
|Chinnam, Meenalakshmi; Wang, Xiaoling; Zhang, Xiaojing et al. (2016) Evaluating Effects of Hypomorphic Thoc1 Alleles on Embryonic Development in Rb1 Null Mice. Mol Cell Biol 36:1621-7|
|Klinkebiel, David; Zhang, Wa; Akers, Stacey N et al. (2016) DNA Methylome Analyses Implicate Fallopian Tube Epithelia as the Origin for High-Grade Serous Ovarian Cancer. Mol Cancer Res 14:787-94|
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