AI Article Synopsis

  • Abnormal changes in a specific protein called histone can influence the development of brain tumors known as gliomas, but how useful this is for doctors is still unclear.
  • Researchers studied 73 glioma patients to see how levels of a specific type of histone called H3K36me2 relate to the tumor's severity and patients' survival chances.
  • The study found that higher levels of H3K36me2 are linked to more serious tumors and worse outcomes, suggesting it could help doctors with the diagnosis and treatment of gliomas, but more research is needed.

Article Abstract

Abnormal histone methylation plays a key role in glioma development but the clinical value of specific alterations is still unclear. Here, the potential significance of histone H3 lysine 36 dimethylation (H3K36me2) was investigated as a biomarker for glioma. Seventy-three glioma patients were included in the study and the level of H3K36me2 in the tumor tissues was determined by immunohistochemistry. The χ2 test was used to explore the influence of clinical and pathological characteristics on H3K36me2 levels. The Kaplan-Meier method was used to estimate progression-free survival (PFS) and overall survival (OS). COX regression was used to explore the relationship between H3K36me2 levels and glioma prognosis. The results indicated that the H3K36me2 level increases with glioma grade. The proportion of high H3K36me2 levels was lower in glioma patients under the age of 52 years. H3K36me2 levels were negatively correlated with IDH1 mutation and MGMT promoter methylation, and positively correlated with p53 expression. Thus, high H3K36me2 levels positively correlated with poor prognosis of gliomas. In conclusion, H3K36me2 may be considered as a potential biomarker for glioma diagnosis, grading, and prognosis, but the overall clinical value of H3K36me2 determination deserves further investigation. These results may have important implications for accurate diagnosis and future precision treatment of gliomas.

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Source
http://dx.doi.org/10.1093/jnen/nlad016DOI Listing

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