The overall goal of the Ivy Neurological Science Internship Program is to inspire high school and undergraduate students to pursue a career in bioscience, particularly in the areas of glioma research, neuroscience or neurogenomics, by providing an opportunity to conduct hands-on biomedical research under the direct mentorship of a TGen investigator.
Modeled after the Helios Scholars Program, the Ivy Neurological Sciences Internship Program replicates three key features that we have found instrumental to that training program’s success:
- Fully-funded research internships for promising high school and undergraduate students
- Exposure to translational/clinical medicine leveraging existing community based partnerships
- Presentation of research results at the end of the program to faculty, peers, parents and community members
Ivy Neurological Science Internship Program
Junior at BASIS Mesa
Mentored by Angela Baker, Ph.D.
Brain Tumor Unit, Cancer and Cell Biology Division
Inhibiting the Proliferation of Patient-Derived Glioblastoma Multiforme (GBM) cells by activating Estrogen Receptor beta using estradiol and IGF-1
Glioblastoma multiforme (GBM) is the most aggressive and common type of primary brain tumor. Patients with GBM have a median survival rate between 12-14 months. There are sex-based differences that exist in the occurrence of GBM with men having a 60% higher chance of developing a tumor indicating that differences in the function of Estrogen Receptor Beta (ERβ), a known tumor suppressor, may influence tumor progression in GBM. Considering ERβ function, it was hypothesized that 17β-estradiol and IGF-1, estrogen receptor agonists, may promote ERβ function and inhibit the proliferation of GBM cells in vitro. 17β-estradiol and IGF-1 were applied to a patient-derived GBM cell line and MDA-MB-453, breast cancer cell line, in-vitro. The concentrations tested ranged from 2 to 20 nM of 17β-estradiol and IGF-1. After 48 hours of exposure, GBM cell proliferation was analyzed through a trypan blue exclusion assay. The results revealed that cell proliferation was inhibited by the estrogen receptor agonists in the patient-derived GBM cells and promoted in the MDA-MB-453 cell line which served as a positive control. In conclusion, this study presents evidence that ERβ function may indeed inhibit GBM proliferation. This study presents a potential approach to the treatment of GBM. As this study continues, more steroid hormone receptors will be tested like the Androgen Receptor which may also cause the inhibition of cell proliferation in GBM.