temozolomide

[Acta Pharmacologica Sinica] Scientists investigated the role of forkhead box transcription factor 3a (FOXO3a) in regulating the sensitivity of glioma cells to temozolomide and its relationship with Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3)-mediated mitophagy.

[Proceedings of the National Academy of Sciences of the United States of America] Glioblastoma-associated microglia/macrophages secreted interleukin 11 activated STAT3-MYC signaling in glioblastoma cells. This signaling induced stem cell states that conferred enhanced tumorigenicity and resistance to the standard-of-care chemotherapy, temozolomide.

[Cell Death & Disease] Scientists discovered that glioblastoma cells exhibited features indicative of malignant progression and were present in a hypoxic environment.

[Proceedings of the National Academy of Sciences of the United States of America] The authors demonstrated increased binding of a specific GA binding protein B1L (GABPB1L)-isoform–containing complex to the mutant telomerase reverse transcriptase (TERT) promoter. They found that TERT promoter mutant glioblastoma cells, unlike wild-type cells, exhibited a critical near-term dependence on GABPB1L for proliferation.

[Cell Death Discovery] Investigators describe the antitumoral potential of selective cyclin-dependent kinase inhibitors on low-passage glioblastoma multiforme 2D- and 3D models, cultured as neurospheres or glioma stem-like cells.

[Scientific Reports] While cyclin-dependent kinase 1 (CDK1) phosphorylation is a well-described consequence of temozolomide (TMZ) treatment, researchers found that TMZ also robustly induced CDK1 expression.