Characterizing and establishing effects of L1CAM on patient-derived glioblastoma stem cells
Date
2020
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Publisher
University of Delaware
Abstract
Glioblastoma Multiforme (GBM) is the most common and malignant brain tumor with a median survival time of 12-14 months. The prognosis of the patient is bleak due to subsequent relapse after treatment because of Glioblastoma’s invasive behavior through the axon tracts, blood vessels, and diffusely through the parenchyma. Many point to GBM relapse being so prevalent due to the Cancer Stem Cell (CSC) theory phenomenon. This theory states that neural stem cell like cancer cells compose a percentage of the tumor and contribute to the tumors self-renewal and invasive characteristics. This theory suggests that this small subpopulation of tumor cells is both resistant to chemo-/radio-therapy and are extremely invasive. Unfortunately, the CSC theory is relatively new knowledge, and many believe that experiments involving long-established commercial gliomas due to it not accurately representing the disease. In the past, lab members have shown L1CAM influence crucial cancer cell mechanisms in vitro (i.e. increase in motility and proliferation rates) and in vivo (i.e. tumor formation and invasion) in long-established commercial gliomas. However, with the CSC theory gaining traction in the GBM model our lab looked to obtain a more accurate representation of the disease. By collaborating with the Helen F. Graham Cancer Center & Research Institute I successfully characterized patient derived GBM samples for stem cell markers. Furthermore, my primary goal was to determine if the effects L1CAM has in vitro and in vivo could be seen in our Glioblastoma Stem Cells (GSCs). Here I present identification of glioblastoma stem cell lines using Flow Cytometry and confirmed with Western Blot and immunofluorescence. I also demonstrate effects of L1CAM on motility in L1-Fc Super scratch velocity assays and its role in tumor formation in our in vivo chick embryo model.
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Keywords
Glioblastoma multiforme, L1CAM, Stem cell markers, Tumor formation, Velocity assays, Xenograft models