The Environmental and Molecular Carcinogenesis Program integrates 27 investigators (24 full members and 3 associate members) from several different departments on NYU campuses of Sterling Forest and the School of Medicine, sharing a common interest in understanding the Environmental causes of cancer. The overall goal of the Program is to understand the environmental etiology of cancer and to use this information for cancer prevention and early detection. The EMC Research Program focuses on the following goals: (1) Identifying the mechanisms of action for environmental carcinogens, with a strong focus on inorganic compounds, such as arsenic, nickel, chromium, and cadmium by investigating their effects on the structure and function of cellular macromolecules;(2) The formation of reactive oxygen species, their biochemistry, and the biological effects that might result from their cellular interactions;(3) The mutational specificity of carcinogens and the site-specific mutagenesis of particular DNA lesions, the molecular basis for genetic susceptibility to environmental agents, the effects of hormones on gene expression, carcinogenesis, and chemoprevention;and (4) Epigenetic mechanisms of carcinogenesis. To achieve these goals, research in this Program is divided thematically into four groups: 1) DNA adducts, DNA Damage and Repair;2) Carcinogenesis and Animal Models;3) Early Detection and Chemoprevention;and 4) Cell Signaling and Epigenetic Mechanisms of Carcinogenesis. Drs. Max Costa and William Rom are the Co-Leaders for this Program. Total funding decreased from $17,628,704 to $7,570,910 since the last competitive application. Membership has decreased from 47 to 28. Publications for the period total 323, of which 17% are intraprogrammatic, 16.1% are inter-programmatic, and 4% are both intra- and inter-programmatic collaborations.
The Environmental and Molecular Carcinogenesis Program integrates investigators whose research aims to understand the environmental etiology of cancer and to use this information for cancer prevention and early detection, with the ultimate goal of reducing the risk of cancer occurrence and death and improving the quality of life of cancer survivors.
|Puranik, Amrutesh S; Leaf, Irina A; Jensen, Mark A et al. (2018) Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney. Sci Rep 8:13948|
|Saint Fleur-Lominy, Shella; Maus, Mate; Vaeth, Martin et al. (2018) STIM1 and STIM2 Mediate Cancer-Induced Inflammation in T Cell Acute Lymphoblastic Leukemia. Cell Rep 24:3045-3060.e5|
|Cui, Xin; Morales, Renee-Tyler Tan; Qian, Weiyi et al. (2018) Hacking macrophage-associated immunosuppression for regulating glioblastoma angiogenesis. Biomaterials 161:164-178|
|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|
|Burgess, Hannah M; Pourchet, Aldo; Hajdu, Cristina H et al. (2018) Targeting Poxvirus Decapping Enzymes and mRNA Decay to Generate an Effective Oncolytic Virus. Mol Ther Oncolytics 8:71-81|
|Wong, Serre-Yu; Coffre, Maryaline; Ramanan, Deepshika et al. (2018) B Cell Defects Observed in Nod2 Knockout Mice Are a Consequence of a Dock2 Mutation Frequently Found in Inbred Strains. J Immunol 201:1442-1451|
|Handler, Jesse; Cullis, Jane; Avanzi, Antonina et al. (2018) Pre-neoplastic pancreas cells enter a partially mesenchymal state following transient TGF-? exposure. Oncogene 37:4334-4342|
|Diamond, Julie M; Vanpouille-Box, Claire; Spada, Sheila et al. (2018) Exosomes Shuttle TREX1-Sensitive IFN-Stimulatory dsDNA from Irradiated Cancer Cells to DCs. Cancer Immunol Res 6:910-920|
|Fan, Xiaozhou; Peters, Brandilyn A; Jacobs, Eric J et al. (2018) Drinking alcohol is associated with variation in the human oral microbiome in a large study of American adults. Microbiome 6:59|
|Chen, Danqi; Fang, Lei; Mei, Shenglin et al. (2018) Erratum: ""Regulation of Chromatin Assembly and Cell Transformation by Formaldehyde Exposure in Human Cells"". Environ Health Perspect 126:019001|
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