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Anti-Diarrheal Drug Shows Potential for Treating Glioblastoma

A cancer research team sourced at Goethe University found startling results on the effects of an anti-diarrheal drug, loperamide, on cell deaths in glioblastoma cells in culture. Glioblastoma, a fatal form of cancer that forms in the brain and/or spinal cord, is being evaluated as a target for the loperamide drug, whose mechanisms may prove effective against this lethal cancer.


But how in the world would a medication that fights disturbed stool movements have anything to do with an aggressive, malignant cancer that stems and grows in the brain? Analyzing the composition of loperamide and its methods, it activates a cascade of stress responses in some cancer cells that causes the degradation of the Endoplasmic Reticulum, triggering self-destruction in a process known as autophagy-dependent cell death. Thus, the concentration of ATF4, Activating Transcription Factor, exponentially increases due to Endoplasmic Reticulum stress as well as the result of loperamide-induced autophagy.


This autophagy channel of cell death from the anti-diarreal drug could be implemented in the same course for Glioblastoma cells in tumor cell culturing. Loperamide's debilitating effect would be to alter the course of ATF4 blockage in the tumor cells to contain the aggressive characteristics of glioblastoma.


This discovery has broadened the scope and universality of cross treatment, in which a single medication may be useful for treating multiple diseases. In this case, there was deliberative study on how a pill for fighting diarrhea could also be used to fight a malignant tumor in the brain. This flexibility of treatments opens up the potential for not only cancer, but neurodegenerative diseases because of its correlative causes in ER degradation and transfusion through the blood brain barrier.




Works Cited

Goethe University Frankfurt. "Anti-diarrhea drug drives cancer cells to cell death." ScienceDaily. ScienceDaily, 22 December 2020 <www.sciencedaily.com/releases/2020/12/201222101455.htm>.




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