GBM is a fast-growing malignant brain tumor. It accounts for about 17% of adult brain tumors, making it the most common, as well as the most invasive, type of brain tumor occurring in adults. A Glioblastoma multiform is considered a stage IV astrocytoma - a glioma that develops from star-shaped glial cells that supports nerve cells. Although treatment exists for GBM - usually surgery succeeded by chemotherapy and/or radiation - most GBM patients do not survive more than 15 months post diagnosis.
GBM may seem like the kiss of death, but do not lose hope...
A molecule that targets glioblastoma has been discovered...
LXY1 is a molecule that can be injected into the bloodstream and transport high concentrations of medications and radionuclides directly to brain tumor cells and more importantly, it is able to avoid normal tissues along the way.
How it works:
LXY1 has a high affinity for the cell surface protein known as alpha-3 integrin - an overexpressed protein in cancer cells - and is thus able to bind to its receptor. By binding to alpha-3 integrin, LXY1 inhibits its signaling capabilities and thus decreases the expression of cancerous glioma cells.
Note: Alpha-3 integrin is a signaling molecule that phosporylates SRC (a tumor suppressor gene) - lowering expression levels of alpha-3 integrin inhibits glioma cell adhesion.
Testing:
Mice injected with a radiolabeled version of LXY1 --> IR fluorescence imaging confirmed LXY1's specificity to bind to glioblastoma cells
What this means for glioblastoma's future:
Treating glioblastoma with targeted therapies does not harm normal brain tissues, as surgery, radiation and chemotherapy do. Such treatments are only temporary when it comes to GBM and survival rate increases insignificantly. Therefore, targeted therapy is not only a safer method but its effects appear to be much more long-term and even permanent.
Below is a representation of the pathway and function of SRC similar to what we have seen in class:
Why I'm somewhat sceptical:
Although the LXY1 molecule inhibits transcription by binding to alpha-3 integrin and serves as targeted glioblastoma treatment, it only does so by binding to the apha-3 integrin protein. There are numerous proteins involved in glioblastoma expression, for example CD95, that would also have to be bound by an alternate, but LXY1-like molecule, in order to prevent SRC phosphorylation. Moreover, many more molecules must be discovered before targeted therapies become the "go-to" treatment for glioblastoma patients.
