|massachusetts institute of technology|
There is now overwhelming evidence that inflammation causes cancer. Despite that knowledge, we still have incomplete understanding of the underlying mechanism(s) by which inflammation initiates or affects the progression of the disease, and we are consequently ill- equipped to plot a rational path forward toward preventing cancer or delaying its progression. The overarching goal of our research is to reveal the molecular basis by which exposure to inflammatory chemicals leads to genetic alterations that give rise to cancer. We examine the roles of infiltrating macrophages and neutrophils in exposing the normal resident cells of tissues to the many reactive chemical species that lead to DNA damage, protein modification, mutation, and to cell death from apoptosis and necrosis.
The focus of our work is on nitric oxide (NO ⋅) and the related reactive species that are formed in biological systems. Depending on the dose rate, total dose, and cell-type, this battery of compounds may either drive cells into apoptosis or inhibit apoptosis and enhance mutation through formation of base damage, strand breaks and DNA cross-links. We study these processes at every level, from individual chemical reactions to effects in cells, tissues, organs, and animals (including, eventually, humans). This will lead to a better understanding of these processes and to a rational approach to their prevention, and will provide biomarkers to analyze and quantitate the chemical origins of lesions in the human population.
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