P01.42.B CHANGES OF MAJOR GENES RELATED TO CELLULAR SENESCENCE IN GLIOMA

Abstract BACKGROUND Cellular senescence is a process in which cells permanently cease to divide, playing a key role in controlling tumor growth and response to therapy. Increasing research indicates the significance of senescent glioma cells in shaping the clinical profile of glioma tumors. Gliomas are the most common primary tumors of the central nervous system, often with a poor prognosis due to aggressive clinical behavior and frequent recurrence after therapy. The aim of this study was to analyze the frequency and type of alterations in genes involved in cellular senescence in different types of gliomas. MATERIALS AND METHODS We analyzed 3425 glioma samples using data from the cBioPortal for Cancer Genomics. After querying 88 genes involved in senescence-associated secretory phenotype (SASP), we selected and studied in more detail the 10 most frequently altered ones: TP53, CDKN2A, EGFR, ATM, TNFRSF1A, IGFBP7, TNFRSF11B, TP53BP1, HGF and SERPINE1. Data analysis included determining the frequency of mutations, amplifications, deletions, and multiple alterations in each type of glioma. RESULTS The results showed that TP53, CDKN2A, and EGFR were the most frequently altered genes. CDKN2A, EGFR, ATM, IGFBP7, TP53BP1, and HGF had a higher percentage of alterations in high-grade gliomas (HGG), while TP53, TNFRSF1A, TNFRSF11B and SERPINE1 were more frequently altered in low-grade gliomas (LGG). A statistically significant difference in alterations between the HGG and LGG groups was found for TP53, CDKN2A, EGFR, IGFBP7 and TNFRSF11B. CONCLUSION We have shown that the studied genes are more frequently altered in high-grade gliomas. The results highlight the importance of specific gene changes in cellular senescence and their association to glioma grade. Further research is needed to better understand the mechanisms by which these genes influence senescence and the clinical course of gliomas.