How Blocking DNA-Repairing Mechanisms Could Combat Glioblastomas

Glioblastomas — the most common and aggressive brain tumors in adults — can be difficult to treat because therapies only affect a proportion of tumor cells, which in turn leads to a poor survival rate in the patient population. It is hypothesized that a subgroup of cells within these tumors, identified as Glioblastoma Stem Cells (GSCs), reproduce making identical drug-resistant copies of themselves.

Researchers at the University of Leeds have found that a vast amount of the protein RAD51 is located in the GSCs population, and that when RAD51 is inhibited there is a suppression of tumor cell replication upon radiotherapy. The team validated this hypothesis by harvesting tumor cells from glioblastoma patients and examining them using immunofluorescence microscopy. Upon evaluation, the tumor cells yielded higher levels of RAD51 in comparison to the normal controls. Subsequent treatment of the malignant samples with a RAD51 inhibitor and radiation made the cells more sensitive to radiotherapy. The exact mechanism by which RAD51 is increased in cells that survive radiotherapy is not yet known, but this study provides strong evidence that RAD51 is a target in the development of treatment of glioblastoma.

Does this finding impact current studies being conducted at your organization or are you in need of samples with notated presence of specific proteins? BIOIVT offers FFPE and frozen tumor specimens of which we test for markers relevant to cancer research. Furthermore, donor-matched serum and plasma are also available. Contact us to see how we can help.