It is widely accepted that genetic mutation plays an important role in the development of cancers. However, accumulating evidence suggests that more than 60% of human cancers are attributable to environment and lifestyles, including air pollution, drinking water contamination, some special work settings, and smoking. Even for some types of cancers that have strong association with genetic abnormalities, such as BRCA1 or BRCA2 gene mutations for breast cancer and ovarian cancer, certain environmental factors had been viewed as environmental modifiers that alter the metabolisms of hormone and DNA repair capacity of the cells to trigger or facilitate tumorigenesis, which explains why only certain portion of the people with inherited genetic mutation developed cancers. Accordingly, it is very likely that cancers are caused by a web of interacting factors, including environmental exposure, genetic predisposition and lifestyle.
The state of Michigan, especially in the Detroit tri-county area of Macomb, Oakland and Wayne, exhibits a unique cancer epidemiological pattern, which provides the strongest support for the importance of environmental exposure on the increased or sustained cancer incidence and mortality rates. During the past three decades, the lung cancer incidence rate in Michigan is above the national average, while the prevalence of tobacco smoking is comparable to the national average at the same or the previous period. In the Detroit tri-county area, the Wayne County, in which the air quality is the poorest due to the presence of many chemical, refinery and manufacture industries, shows the highest rate of lung cancer, colorectal cancer and prostate cancer relative to Macomb county and Oakland County in the past several years.
The members in this focused group are leaders in their field and actively involved in cutting edge projects that range from discovery of basic biological mechanisms to clinical concepts and application of healthcare on cancers associated with environmental exposure. The objectives of this research interest group is to determine whether a given environmental factor is able to activate a specific carcinogenic or tumorigenic process in addition to DNA damage, such as altering the epigenetic landscape of the genome to reduce the genomic stability, inducing self-renewal and clone expansion of the cancer stem cells, preventing apoptosis of the transformed or tumor cells, and enhancing angiogenesis and tumor cell metastasis. Additional objectives include but not limited to translating knowledge of a carcinogenic effect of environmental risk factors into preventive strategies for the exposed population; assessing carcinogenic potentials for those newly identified environmental risk factors through both epidemiological and laboratory settings; determining the key windows of vulnerability of individuals in response to environmental exposure; and developing new research tools or methodologies in assessing cancer risk associated with multiple environmental exposures.
|Fei Chen, Ph.D., GXE Cancer Leader||Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University||Cancer epigenetics, metabolism, metal carcinogenesis, non-coding RNAs.|
|Jennifer Beebe-Dimmer, Ph.D., MPH||Department of Oncology and Karmanos Cancer Institute, Wayne State University||Population Sciences, Epidemiology, Cancer genetics|
|Michele Cote, Ph.D.||Department of Oncology and Karmanos Cancer Institute, Wayne State University School of Medicine||Cancer disparities, Lung cancer genetics|
|Christine Neslund-Dudas, Ph.D.||Department of Public Health Sciences, Henry Ford Health System||Biostatistics, Clinical Trials, Race Disparities, Lung cancer, Prostate Cancer|
|Benjamin Rybicki, Ph.D.||Department of Public Health Sciences, Henry Ford Health System||Genetic Epidemiology, Biostatistics, Prostate Cancer|
|Ann Schwartz, Ph.D., MPH||Department of Oncology and Karmanos Cancer Institute, Wayne State University||Cancer Risk Factors, Molecular Epidemiology, Cancer Disparities|
Li L, Chen F. Oxidative stress, epigenetics and cancer stem cells in arsenic carcinogenesis and prevention. Curr Pharmacol Rep. 2016, 2:57-63
Beebe-Dimmer JL, Yee C, Cote ML, Petrucelli N, Palmer N, Bock C, Lane D, Agalliu I, Stefanick ML, Simon MS. Familial Clustering of breast and prostate cancer and risk of postmenopausal breast cancer in the women's health initiative study. Cancer. 2015, 121: 1265-72
Holowatyj AN, Ruterbusch JJ, Ratnam M, Gorski DH, Cote ML. Her2 status and disparities in luminal breast cancers. Cancer Med. 2016, doi: 10.2002 [Epub ahead of print]
Howard JL, Orlicki KM. Effects of anthropogenic microparticles on the chemical and geophysical properties of urban soils, Detroit, Michigan. Soil Science. 2016, 180:154-66
Schwartz AG, Lusk CM, Wenzlaff AS, Watza D, Pandolfi S, Mantha L, Cote ML, Soubani AO, Walworth G, Wozniak A, Neslund-Dudas C, Ardisana AA, Flynn MJ, Song T, Spizarny DL, Kvale PA, Chapman R, Gadgeel SM. Risk of lung cancer associated with COPD phenotype based on quantitative image analysis. Cancer Epidemiol Biomarkers Prev. 2016, July 6, [Epub ahead of print]
Rybicki BA, Rundle A, Kryvenko ON, Mitrache N, Do KC, Jankowski M, Chitale DA, Trudeau S, Belinsky SA, Tang D. Methylation in benign prostate and risk of disease progression in men subsequently diagnosed with prostate cancer. Int J Cancer. 2016, 138:2884-93
Lusk CM, Wenzlaff AS, Dyson G, Purrington KS, Watza D, Land S, Soubani AO, Gadgeel SM, Schwartz AG. Whole-exome sequencing reveals genetic variability among lung cancer cases subphenotyped for emphysema. Carcinogenesis. 2016, 37: 139-44.