- The most common types of brain cancer are meningiomas, those of the pituitary gland, and glioblastomas.
- Although all of them have a low incidence, the biggest problem is their high mortality.
- A drug could fight brain tumors by targeting cancer cells’ fat production.
It is seldom talked about brain cancer due to its low incidence. Only in Mexico it occupies the 18th place with respect to the most frequent. A little over 3,000 cases are detected annually, although the biggest problem is its high mortality because 80% of patients die.
For its part, there is a wide variety of tumors that can develop in the brain. The most common are meningiomasfollowed by pituitary gland and in third place are the glioblastomasalso considered the most lethal.
The deadliest brain tumor
Since glioblastoma, a brain cancer highly aggressive and lethal, resistant to conventional therapies, researchers are looking for cell characteristics that may point to promising drug targets.
One of these features is the cells’ reliance on what is called “de novo lipid synthesis” – or conversion of carbohydrates to fat – to meet their energy needs.
New research led by scientists from Massachusetts General Hospital reveals that a drug that inhibits the enzyme stearoyl CoA desaturase 1 (ECD) interferes with this process, and when given to mice with glioblastoma, the drug slows tumor growth and increases the sensitivity of glioblastoma cells to anticancer therapies . The results, published in Science Translational Medicinecould lead to new therapeutic options for patients.
How does it work?
During one step of de novo lipid synthesis, ECD converts saturated fatty acids to monounsaturated fatty acids. Previously, Christian Badr, Assistant Professor of Neuroscience at Mass General and Associate Professor of Neurology at Harvard Medical School, and his colleagues demonstrated that glioblastoma cells depend on ECD activation and the availability of monounsaturated fatty acids. .
In this new research, the team tested the potential antiglioblastoma of an ECD inhibitor, YTX-7739, which can cross the blood-brain barrier and is being evaluated as an oral drug in phase I clinical trials for the treatment of patients with Parkinson’s disease.
The researchers found that YTX-7739 was toxic to patient-derived glioblastoma stem cells. By blocking ECD, the cells accumulated too many saturated fatty acids, a process called lipotoxicity.
In addition, when given to mice with tumors, the drug inhibited processes involved in fatty acid metabolism in glioblastoma cells and increased the cells’ sensitivity to conventional glioblastoma chemotherapy.
By examining the detailed mechanisms underlying the drug’s effects on cells, the scientists discovered that the MEK/ERK signaling pathway makes glioblastoma cells especially vulnerable, while the AMPK signaling pathway works to protect the cells. glioblastoma and may render them resistant to de novo loss of lipid synthesis.
“Based on our results, we propose that MEK/ERK and AMPK activities, which can be detected in tumor biopsies, could be predictive biomarkers to guide patient selection and stratification.”
In other words, patients whose tumors have robust MEK/ERK activity would likely benefit from therapies like YTX-7739, while those with high AMPK activity probably would not.
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