Gene-deleted glioblastoma is more vulnerable to cell death

the study was announced in cancer cell We found that glioblastoma (GBM) is associated with deletions. CDKN2A Genes make them more susceptible to being killed. Researchers at UCLA Johnson Comprehensive Cancer Center CDKNA Present in approximately 60% of glioblastoma tumors, this gene alters the way lipids are distributed within cancer cells, making them more likely to be targeted and destroyed by targeted therapies.

The research team performed lipidomic, transcriptomic and genomic analyzes from 156 molecularly diverse GBM tumors, including 84 human glioblastoma tumors, 42 human cell lines, and 30 mouse GBM models. Data were collected and analyzed.

“We identified CDKN2A Deletions remodel the GBM lipidome, redistributing particularly oxidizable polyunsaturated fatty acids into separate lipid compartments,” the authors write. especially, CDKN2A Deletions have been demonstrated in human brain, as mouse brain xenografts, and CDKN2A This deletion indicates that this metabolic vulnerability may be a therapeutic target for glioblastoma patients.

Investigators also found that CDKN2A– Deleted GBM differs from deleted GBM in the way it processes fat. CDKN2A gene. They selectively stimulate tumors for ferroptosis, a form of controlled cell death characterized by the accumulation of iron and the generation of reactive oxygen species that attack and damage lipids. Ferroptosis is triggered by depletion of molecules, especially lipids, that protect cells from oxidative damage and represents a new therapeutic target in several cancers.

Researchers evaluated drugs that induce ferroptosis by inhibiting GPX4, an enzyme that prevents lipid peroxidation. They observed that glioblastoma cells carry genetic mutations. CDKN2A Glioblastoma cells without genetic mutations were insensitive to GPX4 inhibition but highly sensitive to cell death.

“We discovered that CDKN2A “It may be a key regulator of cancer cell metabolism and has never been shown in cancer, despite being deleted in other types of cancer.” and co-senior author, David Nathanson, Associate Professor of Molecular Medicine and Pharmacology. UCLA’s David Geffen School of Medicine.

The research team’s results provide proof-of-concept evidence that GPX4 may be a relevant therapeutic target for a large, genetically stratified subset of GBM patients. CDKN2A-erase. Although there are currently no pharmacological GPX4 inhibitors suitable for use in the brain, the research team believes that these new results may help induce GBM cell death through inhibition of GPX4 or other ferroptotic targets through brain penetration. We believe that it provides a strong rationale for the development of toxic small molecules.

A database of 156 glioblastoma samples analyzed by researchers is available to researchers worldwide. The team also expanded the number of samples in the database to over 500 of his.

“This dataset will allow investigation of genetic influences and the potential influence of the tumor environment on GBM lipid metabolism,” the authors wrote, revealing other potential therapies for glioblastoma. I encourage others to use this dataset to

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