Rachael Rose Parisi

I was a lifeguard at the Mohawk Golf Club, which entailed personal responsibility for the safety of the members at the country club and pool.

I was hired as a electrocardiogram technician and medical assistant by the Cardiology Associates of Schenectady.

After reading fascinating research publications from Dr. Stewart Sell’s laboratory in Wadsworth Center, a division of the New York State Department of Health, in Albany, I took a personal initiative to join its team of research physicians. I contacted Dr. Sell in hopes of volunteering and performing my own independent research projects under his mentorship and that of his colleagues. I began working year-round on my two independent research projects during my sophomore year in high school. Breast Cancer Stem Cell Line: A genetically modified transgenic mouse spontaneously grows mammary gland tumors through the FVB/N-Tg (MMTV-PyVT) strain and is therefore affected by the mouse mammary tumor virus. I studied and cultured stem cell line 419, which was extracted from the tumor, and used immunohistochemistry and quantitative morphometry to find an explanation for infinite cell division. My theory is that the initial trigger for uncontrolled cell division is not mutation, but is rather caused by an antigen. I tried to detect antigens such as the Sox 2 and Nanog by blocking nonspecific antigen sites, testing primary antibodies, testing secondary antibodies and staining the cell line. I utilized the concept that specific antibodies will bind to their antigen counterpart if they are present. I had success with the Sox 2 staining experiment because I found that the antigen was present in the stem cell line. This key discovery verifies my hypothesis that antigens are present and can cause unhindered cell division. Liver Cancer Stem Cell Line: I analyzed, cultured and inhibited the Morris hepatoma 7777 liver cancer stem cell line that was extracted from an infected rat. The goal is to stop or slow down liver cancer cell division. I studied the cell cycle to know when to begin inhibition trials. In the beginning of the experiments, I carefully observed the stem cell line’s growth pattern by counting cells every day for weeks using the hemocytometer chamber. With this information, I constructed a graph of the cell’s growth before and after testing compounds. The compounds tested acted as growth inhibitors for this experiment, these include Mtol, IGF/IGFR, and EGFR. I had the most success with the Mtol inhibitor because it inhibited cell growth 50%. This important discovery proves that liver cancer can be dramatically slowed and leaves hope that there is an inhibitor that could hinder growth even more or stop it completely. I will continue to test more growth inhibitors in hopes of hindering growth over 50% and will continue more trials with the Mtol to confirm the discovery.