“MTK1 Regulates Extracellular Acidification and Cell Migration through the HER2 Breast Cancer Receptor"
Year Graduated: 2014
Career Type: Academia
Postdoctoral Fellow, University of North Carolina at Chapel Hill
Academic & Professional Updates
As a Postdoctoral Research Associate at the University of North Carolina, I am investigating how environmental heavy metal exposures such as arsenic (As), and cadmium (Cd) alter immune related gene expression in the human placenta. The placenta is an organ that forms during pregnancy and serves two primary functions. First, the placenta acts as a barrier between maternal and fetal blood, so they do not mix. Second, the placenta facilitates nutrient and oxygen exchange between the mother and the fetus. In diseases such as preeclampsia, the placenta development is impaired which can lead to a decrease in nutrient and gas exchange between the mother and fetus resulting in birth related complications such as low birth weight. Cadmium is known to accumulate in the placenta and is associated with low birth weight. Additionally, cadmium is known to alter immune responses in mouse models. The primary focus of this research is to identify how cadmium exposure effects immune related gene expression in human placenta.
Honors & Achievements
1. Graduate College Fellowship, 2010. 2. NIEHS Training Grant - Environmental Toxicology of Human Diseases, 2011 (31). 3. NIEHS Training Grant - Environmental Toxicology of Human Diseases, 2012 (32).
1. Sollome, J.J., Thavathiru, E., Camensich, T.D. and R.R. Vaillancourt (2013). HER2/HER3 Regulates Extracellular Acidification and Cell Migration through MTK1 (MEKK4). Cell Signal. 26:70-82. 2. Sollome, J.J., Thavathiru, E., Camensich, T.D. and R.R. Vaillancourt (2014). The Role of MTK1 in the GIT1-Associated ERK1/2 MAPK Pathway in Response to Heregulin in T-47D and MCF-7 Breast Cancer Cells.