Mitochondrial morphology and reactive oxygen species production in supporting the tumorigenesis of malignant mesothelioma
I earned my BA from The Elms College in Chicopee, MA in 2007. In 2008 I began work at Baystate Medical Center in Springfield, MA as a Cytogenetics Technologist. I joined the CMB program in the fall of 2009 and am a PhD candidate in the lab of Dr. Nicholas Heintz. I love living in Vermont where incredible skiing, mountain biking and hiking are right around the corner!
My research is focused on how alterations in mitochondria architecture, reactive oxygen species (ROS) production, and changes in gene expression of mitochondria antioxidant enzymes supports tumorigenesis in malignant mesothelioma (MM). We utilize a number of ROS sensors, mitochondrial targeted drugs, and novel compounds to aid in our understanding of how mitochondria support MM tumor growth and survival. The overall theme of our research is to target alterations in the redox status of MM mitochondria as a means of therapy in MM.
Mitochondria of a mesothelial cell
Cunniff B, Snider GW, Fredette N, Stumpff J, Hondal RJ, Heintz NH (2014) Resolution of oxidative stress by thioredoxin reductase: Cysteine versus selenocysteine. Redox Biol 2: 475-84.
Cunniff B, Snider GW, Fredette N, Hondal RJ, Heintz NH (2013) A direct and continuous assay for the determination of thioredoxin reductase activity in cell lysates. Anal Biochem 443(1): 34-40.
Cunniff B, Benson K, Stumpff J, Newick K, Held P, Taatjes D, Joseph J, Kalyanaraman B, Heintz NH (2013) Mitochondrial-targeted nitroxides disrupt mitochondrial architecture and inhibit expression of peroxiredoxin 3 and FOXM1 in malignant mesothelioma cells. J Cell Physiol 228(4): 835-45.
Newick K, Cunniff B, Preston K, Held P, Arbiser J, Pass H, Mossman B, Shukla A, Heintz N (2012) Peroxiredoxin 3 is a redox-dependent target of thiostrepton in malignant mesothelioma cells. PLoS One 7(6): e39404.
Anathy V, Roberson E, Cunniff B, Nolin JD, Hoffman S, Spiess P, Guala AS, Lahue KG, Goldman D, Flemer S, van der Vliet A, Heintz NH, Budd RC, Tew KD, Janssen-Heininger YM (2012) Oxidative processing of latent Fas in the endoplasmic reticulum controls the strength of apoptosis. Mol Cell Biol 32(17): 3464-78.
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