Glioblastoma Spread Slowed in Mouse Model by Cutting Off Communication Mechanism of Cancer Cells; Gap Junction Targeting May Be Effective Approach to Treatment

The rapid spread of a common and deadly brain tumor has been slowed down significantly in a mouse model by cutting off the way some cancer cells communicate, according to a team of researchers that includes University of Florida (UF) Health faculty. The technique improved survival time by 50 percent when tested in a mouse model, said Loic P. Deleyrolle, Ph.D., a Research Assistant Professor of Neurosurgery in the UF College of Medicine. Researchers focused on disrupting the cell-to-cell communication that allows cancer stem cells to spread. To do that, they targeted a channel that cancer cells use to transfer molecules. By cutting off their communications pathway, it is possible to keep the deadly cells in check, Dr. Deleyrolle said. Eight UF Health researchers took part in the study, which was co-authored by Dr. Deleyrolle and published in an open-access article in the May 19, 2015 issue of Cell Reports. The article is titled “Differential Connexin Function Enhances Self-Renewal in Glioblastoma.” The UF scientists collaborated with researchers at the Cleveland Clinic and the University of California, Berkeley in this research effort. Glioblastoma is the most common brain tumor in adults and there is no effective long-term treatment. Patients usually live for just 12 to 15 months after diagnosis, according to the National Cancer Institute. Glioblastoma tumors, which are highly malignant, typically start in the largest part of the brain and can spread rapidly. The current research focused on connexin 46, a protein that is an essential component of cancer stem cells. Connexin 46 is part of intercellular channels known as a gap junctions. Those intercellular channels, which allow cells to exchange molecules and ions, are crucial to the growth of a glioblastoma tumor, researchers found.
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