- PROFESSOR Preventive Medicine
- PROFESSOR Medicine, Hematology and Medical Oncology
- PROFESSOR Pediatrics
- PROFESSOR Oncological Sciences
B.S., Beijing (Peking) University
M.A., College of William and Mary
Sc.D., Massachusetts Institute of Technology
Toxicology Civil Environmental Engineering
Brigham and Women's Hospital
Harvard School of Public Health
- Training Area(s)
Visiting Scientist Award
International Agency for Reserch on Cancer (IARC/WHO)
American Cancer Society Research Award
American Cancer Society
NCI Career Development Award
AACR-Phone-Poulenc Rorer Young Investigator Award
American Association of Cancer Research
1993, 1994 -
Arthur T. Ippen Travel Fellowship
Massachusetts Institute of Technology
1983, 1985 -
Student Merit Award
Molecular and genetic epidemiology: genetic susceptibility; gene-environment interactions in human diseases
The focus of our molecular epidemiology laboratory is to understand complex interactions between environment and genome/epigenome in contribution to human diseases. We are performing functional epi/genetic analyses in population studies to elucidate disease mechanism and to identify/validate biomarkers for disease risk or prognosis. Such work is of great importance in identifying disease-causing exposure, clarifying disease etiology, designing prevention strategies through lifestyle modifications, and even assisting disease treatment and management.
We have three active research tracks in the lab:
(1) Environmental epi/genetics in breast cancer.
We have been working extensively to elucidate the effects of environment (endocrine disruptors) and lifestyle (dietary intake) on breast cancer via epigenetic mechanisms. We incorporate environmental measurements (questionnaire, biomarkers), genomic/epigenomic tools (gene expression, SNPs, methylation, and microRNAs), and bioinformatics into large epidemiologic studies. Given that cancer is considered a “developmental disease”, we are using a translational approach, combining animal and population studies, to systematically evaluate the role of endocrine disruptors (chemicals found ubiquitously in the environment) in breast cancer etiology during different stage (windows of susceptibility) of breast development.
(2) Environmental Epi/genetics in Reproductive Health and Child Development.
We use placenta as our model system. As an interface between maternal and fetal environment, placenta is the source of fetal nutrients and immune regulation as well as a barrier for environmental toxins; these effects are modulated by simultaneous production of many pregnancy related hormones, proteins and growth factors thereby fulfilling a critical role in proper intrauterine development. Thus placenta plays a vital role in productive health as well as fetal growth and neurodevelopment. We are actively studying the role of placental genome and epigenome, such as genomic imprinting, in birth outcomes and child neurodevelopment. We are also studying the environmental influences, such as maternal stress, nutrition and chemical exposure, on the placental epigenome. Utilizing resources of several birth cohorts, we are trying to build a comprehensive model to examine the inter-relationships among in utero environment, placental epigenome, and fetal growth and neurobehavioral outcomes.
(3) Developmental Origins of Human Diseases.
The Developmental Origins and Health and Disease (DOHaD) hypothesis posits that lifelong health is partially shaped by the environment experienced during early developmental period. We are investigating this hypothesis in two exposure - disease models. The first model is endocrine disruptors and breast cancer in which are conducting trans-disciplinary studies combining animal and human studies to systematically evaluate the role of endocrine disruptors in breast cancer etiology during different stage of breast development. The second focuses on adverse maternal environment during pregnancy (maternal stress, toxin exposure) and neurodevelopment of the children in which we are conducting genetic and epigenetic profiling of the placentas and cord bloods.
Chen J, Giovannucci E, Kelsey K, Rimm EB, Stampfer MJ, Colditz GA, Spiegelman DA, Willett WC, Hunter DJ. A methylenetetrahydrofolate reductase polymorphism and the risk of colorectal cancer. Cancer Research 1996; 56: 4862-4864.
Chen J, Stampfer MJ, Hough HL, Garcia-Closas ML, Willett WC, Hennekens CH, Kelsey KT, Hunter DJ. A prospective study of N-acetyltransferase genotype, red meat intake, and risk of colorectal cancer. Cancer Res 1998 Aug 1; 58(15): 3307-11.
Chen J, Stampfer MJ, Ma J, Selhub J, Malinow MR, Hennekens CH, Hunter DJ. Influence of a methionine synthase (D919G) polymorphism on plasma homocysteine and folate levels and relation to risk of myocardial infarction. Atherosclerosis 2001 Feb 15; 154(3): 667-72.
Chen J, Germer S, Higuchi R, Berkowitz GS, Godbold JH, Wetmur JG. Kinetic polymerase chain reaction on pooled DNA: a high-throughput, high-efficiency alternative in genetic epidemiological studies. Cancer Epidemiol Biomarkers Prev 2002 Jan; 11(1): 131-6.
Chen J, Hunter DJ, Stampfer MJ, Kyte CJ, Chan WJ, Wetmur JG, Selhub JG, Ma JG. Polymorphism in the thymidylate synthase promoter enhancer region modifies the risk and survival of colorectal cancer. Cancer Epidemiol Biomarkers Prev 2003 Oct; 12(10): 958-62.
Chen J, Kumar M, Chan W, Berkowitz G, James GW. Increased influence of genetic variation on paraoxonase-1 enzymatic activity in neonates. Environ Health Perspect 2003; 111: 1403-09.
Chen J, Kyte C, Valcin M, Chan W, Wetmur JG, Selhub JG, Hunter DJ, Ma JJ. Polymorphisms in the one-carbon metabolic pathway, serum folate levels and colorectal cancer in a prospective study. Int J Cancer 2004; 110: 617-20.
Chen J, Kyte C, Chan W, Wetmur JG, Fuchs CS, Giovannucci E. Polymorphism in the thymidylate synthase promoter enhancer region and risk of colorectal adenomas. CancerEpidemiol Biomarkers Prev 2004 Dec; 13(12): 2247-50.
Chen J, Gammon MD, Chan W, Palomeque C, Wetmur JG, Kabat GC, Teitelbaum SL, Britton JA, Terry MB, Neuqut AI, Santella RM. One-carbon metabolism, MTHFR polymorphisms, and risk of breast cancer. Cancer Res 2005 Feb 15; 65(4): 1606-14.
Chen J, Chan W, Wallenstein S, Berkowitz G, Wetmur JG. Haplotype-phenotype relationships of paraoxonase-1. Cancer Epidemiol Biomarkers Prev 2005 Mar; 14(3): 731-4.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Dr. Chen did not report having any of the following types of financial relationships with industry during 2012 and/or 2013: consulting, scientific advisory board, industry-sponsored lectures, service on Board of Directors, participation on industry-sponsored committees, equity ownership valued at greater than 5% of a publicly traded company or any value in a privately held company. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
Mount Sinai's faculty policies relating to faculty collaboration with industry are posted on our website at http://icahn.mssm.edu/about-us/services-and-resources/faculty-resources/handbooks-and-policies/faculty-handbook. Patients may wish to ask their physician about the activities they perform for companies.
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