Shaina Hasan is 16 years old and a junior at Hamilton High School in Chandler, Arizona. She regularly visits the Arizona Biomedical Collaborative in Phoenix to conduct research with her mentor, Dr. Sourav Ghosh, and actively participates in science fairs held locally and statewide. Shaina aspires to continue research and one day have a lab where she can conduct her own experiments and contribute to medicine.

Glioma Mutations and Differential Sensitivity to Erlotinib
The purpose of this project was to find out how the increased concentration of erlotinib affected the amount of cell growth in two different glioblastoma cell lines. The hypothesis was that erlotinib would better decrease the number of cells in cell line SF763 than in cell line U87vIII. This is because SF763 only has a mutation in EGFR, but U87vIII has mutations in EGFR and in PI3K. Erlotinib will prevent EGFR from functioning in both cell lines, but since PI3K is mutated and overactivated in U87vIII, cell growth will still continue in the line, contributing to cell proliferation. The differential sensitivity to erlotinib in the two cell lines was determined by conducting a cell viability assay to measure the number of cells present when the concentration of erlotinib was increase, conducting a BrdU proliferation assay to compare the rates of proliferation between the two cell lines as erlotinib concentration was increased, and finally conducting a crystal violet assay to visually compare the amount of live cells present after the lines were treated with erlotinib. The results collected in the cell viability assay demonstrated that as the concentration of erlotinib increased, the amount of cells in cell line SF763 decreased while the cell number in U87vIII remained constant. The results from the BrdU assay showed that the amount of cell proliferation decreased in SF763 and was constant in U87vIII as erlotinib concentration increased. Statistical analysis of the BrdU results with a t-test revealed that p=0.05. Overall, the hypothesis was supported. Future research includes the differential effect of BEZ235 with erlotinib on cell proliferation in glioblastoma cell lines.

Stanley Palasek is a 15-year-old freshman from the Sonoran Science Academy in Tucson, Arizona. In 2009 he received the Grand Award in the Arizona State Science and Engineering Fair, earning a trip to Intel ISEF. This year he explores his scientific interests in the classroom with AP Biology and AP Calculus. In addition, his Advanced Research Methods class and the opportunity to conduct his research at the University of Arizona have further rounded out his science education. Stan looks forward to pursuing a scientific career and exploring his many options throughout high school.

Heat Stress Reveals Hexose Transport Rates in Saccharomyces cerevisiae
The overall rate of hexose metabolism may be highly dependent on the rate at which a hexose is transported across the cellular membrane. A correlation between these processes would suggest, in an evolutionary context, the structural aspects of a carbohydrate that maximize the rate of metabolism. This knowledge would make it possible to compile these optimal properties in a synthetic molecule. In this study, heat stress was utilized to destroy plasma membrane integrity in Saccharomyces cerevisiae cultures. The amount of metabolism that took place was represented by the amount of carbon dioxide in the system, measured by means of infrared absorption. Algebraic characterization and manipulation of the amount of metabolism in stressed and non-stressed cells and high and low activity hexoses yields the metabolic activity due to increased transport rate for hexoses of various metabolic activities. This result is confirmed using graphical and statistical analysis (P<.05).

Madeleine Scott is a 16 year old junior at Berkeley High School in Berkeley, California. I love science, especially biology, and my lifelong dream has always been, at least as long as I can remember, to participate in the creation of a drug. To watch each clinical trial go through, knowing that I will no doubt encounter a variety of obstacles, but persevering anyway: this is my ideal future. Recently I interned at the Buck Institute of Age Research, a beautiful science research center in Novato, California. As a member of the Berkeley High science club we work hard to tutor struggling students in science courses and try not to fail our own AP science classes.

TAL1: A Novel Gene in Neurodegenerative Disease
T-cell acute lymphocytic leukemia protein 1 (TAL1), a basic helix loop helix (bHLH) transcription factor, is known to have a very important role both in leukemia and in immune cell development, such as microglial development. Microglia cells, the macrophages of the brain, perform a variety of immunological functions in the brain. Microglia activation has been linked to neurodegenerative diseases, such as Parkinson’s Disease, where neuronal death in the basal ganglia leads to degeneration of motor function. I both measured TAL1 expression levels in microglia cell line BV2 and determined TAL1’s role in influencing cellular response to the inflammation caused by lipopolysaccharide (LPS), a microglial activator. I have used a siRNA knockdown TAL1 to determine TAL1’s role in microglia activation as characterized by the production of inflammatory neurodegenerative molecules such as IL6. TAL1 proved to have a critical negative regulatory role of inflammation in microglia; knockdown cells had a marked increase in inflammatory molecules. Interestingly, TAL1 was quickly degraded after microglial stimulation with LPS, suggesting that TAL1 performs a key repressive function. This data implicates that TAL1 is in part necessary for microglia to cause neuronal death. Overexpression of TAL1 has the potential to reduce neuronal death, without side effects to other cell lines, as TAL1 both plays a critical regulatory role and is not expressed in any other cell line in the brain.