Activated Notch Signaling Pathway Suppresses Formation of Certain Gliomas; Inactivation of Pathway Leads to Accelerated Growth; Major Differences Seen in Molecular Requirements of Seemingly Similar Brain Tumors

Researchers at the University of Basel in Switzerland have taken a close look at a signaling pathway (Notch) present in most organisms and found that it suppresses the formation of specific types of brain tumor. Their results have been published online today (December 4, 2015) in an open-access article in Cancer Cell. The article is titled “A Tumor Suppressor Function for Notch Signaling in Forebrain Tumor Subtypes.” Gliomas are the most common brain tumors in adults and the prognosis for patients is, in many cases, very bad. Therefore, novel and effective therapies for glioma treatment are needed. In order to develop these, it is crucial to understand the biology of this type of tumor. So far, it has been highly debated as to which brain cells can form gliomas when they acquire gene mutations. However, researchers believe that brain stem cells might be a potential source of this type of cancer. Stem cells in the human brain can generate new nerve cells and, if something goes wrong in this process and uncontrolled proliferation or impaired differentiation occurs, this may lead to the formation of a brain tumor. A research team led by Professor Verdon Taylor from the Department of Biomedicine at the University of Basel has now studied whether one molecular mechanism that controls normal stem cell maintenance in the brain is hijacked and used by cancer cells during tumor formation. The researchers studied the so-called Notch pathway. This signaling pathway is central to brain stem cell activity and it has been proposed that it can, once aberrantly activated, contribute to the growth of gliomas. “In contrast to our expectations, we found that the opposite is the case: when activated, this pathway actually suppresses the formation of some types of glioma”, says Claudio Giachino, Ph.D., first author of the study.
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