The long-term goals of researchers studying molecular carcinogenesis and toxicology, part of NYU Langone’s Division of Environmental Medicine, are to elucidate the mechanisms of environmental agents that have adverse effects on human health, and to provide molecular rationales for the development of effective strategies for cancer prevention and intervention.

Our major area of focus is the genetic and epigenetic changes, including lifestyles and aging processes, elicited by environmental exposure. Our research teams are experts in using a combination of biochemical, molecular, and genetic approaches to perform these investigations.

Molecular carcinogenesis is a complex process in which the interactions between genetics and environmental factors result in a condition that is either more or less favorable for the transformation and subsequent development and progression of cancer.

Most human cancers are attributable to environmental factors and genetic susceptibility to those factors. It is imperative to gain a better understanding of the cellular and molecular mechanisms underlying the environmental origins of malignant transformation, as well as genetic and epigenetic factors affecting susceptibility of individuals to environmental toxicants or carcinogens.

Our Research

Led by Wei Dai, PhD, our program comprises independent research laboratories with principal investigators who have strong expertise in fields including biochemistry, cell biology, molecular biology, immunology, and oncology. Our scientists are actively engaged in research in areas such as cell signaling and DNA damage and repair in response to environmental exposure; chromatin structures and epigenetics on gene expression; mechanisms suppressing genomic instability; and molecular mode of actions that control cell division and cell death.

We are particularly strong in metal carcinogenesis studies, with an emphasis on inorganic compounds such as arsenic, nickel, chromium, and cadmium. Chronic and acute exposure to metal toxicants and other environmental factors interferes with the normal control mechanisms that regulate the levels of tissue-specific receptors, signal transducers, and effector molecules. Therefore, a major focus is on the identification of critical molecular circuits that are switched on and off by exposure to a particular environmental agent, resulting in modulation in cell proliferation and differentiation.

We study the molecular toxicologic effects of these metals and other agents by examining their functional interactions with DNA and gene products. The biochemistry of metal-mediated active oxygen species and the biological consequences that result from such reactive radicals are of great interest to many of us.

Components of the cellular machinery that respond to environmental factors are not only genetically determined but are also greatly influenced by epigenetic mechanisms. Several scientists also attempt to understand the mode of actions of many metal toxicants on the modification of chromatic structures, as well as other epigenetic factors, that cause individual variations in susceptibility or resistance to particular environmental agents.

We use a wide range of contemporary cellular and molecular approaches to study the mechanisms that suppress genomic instability and tumorigenesis in normal cells. Methodologies include genomics such as ChIP on Chip, DNA-Seq and RNA-Seq, proteomics, bioinformatics, and transgenic and recombinant inbred rodent models, as well as routine cellular and molecular biological approaches.