B. ENVIRONMENTAL HEALTH IDENTITY AND IMPACT OF THE RESEARCH BASE An important strength of this Center is its interdisciplinary capability, which permits the evolution of new fields and disciplines that are at the cutting-edge interface of traditional disciplines including epidemiology, molecular biology, cardiopulmonary toxicology, environmental toxicology, and exposure assessment with emerging disciplines such as bioinformatics. Collectively, the previous research cores and now the newly formed Focus Groups in the Center cover a broad spectrum spanning the field of environmental health science as it exists today, ranging from basic studies of reaction mechanisms of chemicals with DNA and other macromolecules in the test tube, to epigenetic, human exposure assessment and environmental epidemiology. Center research also extends from simple yeast and bacterial models to higher organisms, and utilizes cell systems, whole animals, and human subjects, with whole animal studies mirroring, and relevant to, the studies of human exposures and responses. Our recently formed Focus Groups are also quite broad in the environmental health arena, and foster translational applications of basic science discoveries with biomarker development and epidemiological studies. The research of the Center is directed towards detecting, understanding, and preventing injury produced by environmentally hazardous agents, with a strong focus on heavy metals, air pollution, and the role of radiation, dietary and hormonal factors, and occupational exposures in human diseases. The Center brings together investigators from a wide variety of scientific and public health disciplines to focus their research efforts in the area of environmental health sciences. Our broad-based Center has well-established research strengths in the following areas: 1) cardiopulmonary toxicology;2) environmental carcinogenesis;3) metal toxicology;4) exposure assessment;and 5) environmental epidemiology, with epigenetic becoming an important new focus within many of these areas. All Center members have research interests in one or more of these areas, and the majority of funding is from agencies that classically fund this type of research, including the NIEHS, NCI, NHLBI, NIAID, NIOSH, U.S. EPA, Health Effects Institute, U.S. Department of Defense, and U.S. Department of Energy. In addition, the Center currently has two other Centers/Programs associated with it: the Superfund Research Program Project and the Health Effects Institute Program Project grant on the health effects of particulate air pollution. The NYU NIEHS Center, from its inception in 1963, has been one of the leaders in the area of environmental health research, and continues to be at the forefront of environmental health research by focusing on the molecular and epigenetic mechanisms of toxicity, carcinogenesis, and disease. Currently, we have substantially expanded our leadership role in the elucidation of the mechanisms that account for the very large public health impacts of ambient air particulate matter (PM), and of the chemical and physical properties that account for its toxicity. The Center, through its past support of our programs and facilities in exposure assessment, controlled inhalation in humans, animals and cells in vitro, analytical chemistry, histopathology, and data processing, has made it possible for us to remain at the cutting edge of research in high impact areas of concern to environmental health. To further the impact of the Center in developing new investigators who can apply to the NIEHS for funding, the Center has had, and will continue to have, several strategic planning sessions per year on topics that are timely and lie within the mission of the NIEHS. Faculty members at NYU School of Medicine (NYUSOM) who are not currently members of the Center will continue to be invited to these strategic planning sessions. We feel that this pro-active strategic planning effort, combined with our active Pilot Project Program, which is open to the entire NYU community, will serve to enhance Environmental Health Sciences research at NYUSOM and to increase our NIEHS grant application pool.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Center Core Grants (P30)
Project #
5P30ES000260-49
Application #
8554435
Study Section
Environmental Health Sciences Review Committee (EHS)
Project Start
Project End
Budget Start
2013-04-01
Budget End
2014-03-31
Support Year
49
Fiscal Year
2013
Total Cost
$169,821
Indirect Cost
$63,494
Name
New York University
Department
Type
DUNS #
121911077
City
New York
State
NY
Country
United States
Zip Code
10016
Chen, Danqi; Fang, Lei; Li, Hongjie et al. (2018) The effects of acetaldehyde exposure on histone modifications and chromatin structure in human lung bronchial epithelial cells. Environ Mol Mutagen 59:375-385
Hua, Xiaohui; Xu, Jiheng; Deng, Xu et al. (2018) New compound ChlA-F induces autophagy-dependent anti-cancer effect via upregulating Sestrin-2 in human bladder cancer. Cancer Lett 436:38-51
Choi, Byeong Hyeok; Philips, Mark R; Chen, Yuan et al. (2018) K-Ras Lys-42 is crucial for its signaling, cell migration, and invasion. J Biol Chem 293:17574-17581
Peng, Minggang; Wang, Jingjing; Zhang, Dongyun et al. (2018) PHLPP2 stabilization by p27 mediates its inhibition of bladder cancer invasion by promoting autophagic degradation of MMP2 protein. Oncogene :
Jose, Cynthia C; Jagannathan, Lakshmanan; Tanwar, Vinay S et al. (2018) Nickel exposure induces persistent mesenchymal phenotype in human lung epithelial cells through epigenetic activation of ZEB1. Mol Carcinog 57:794-806
Choi, Byeong Hyeok; Chen, Changyan; Philips, Mark et al. (2018) RAS GTPases are modified by SUMOylation. Oncotarget 9:4440-4450
Li, Xin; Tian, Zhongxian; Jin, Honglei et al. (2018) Decreased c-Myc mRNA Stability via the MicroRNA 141-3p/AUF1 Axis Is Crucial for p63? Inhibition of Cyclin D1 Gene Transcription and Bladder Cancer Cell Tumorigenicity. Mol Cell Biol 38:
Jung, Seungyoun; Allen, Naomi; Arslan, Alan A et al. (2018) Anti-Müllerian hormone and risk of ovarian cancer in nine cohorts. Int J Cancer 142:262-270
Guo, Xirui; Huang, Haishan; Jin, Honglei et al. (2018) ISO, via Upregulating MiR-137 Transcription, Inhibits GSK3?-HSP70-MMP-2 Axis, Resulting in Attenuating Urothelial Cancer Invasion. Mol Ther Nucleic Acids 12:337-349
Weng, Mao-Wen; Lee, Hyun-Wook; Park, Sung-Hyun et al. (2018) Aldehydes are the predominant forces inducing DNA damage and inhibiting DNA repair in tobacco smoke carcinogenesis. Proc Natl Acad Sci U S A 115:E6152-E6161

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