Elevated β-catenin and C-myc promote malignancy, relapse, and indicate poor prognosis in patients with relapsed glioma

J Cancer Res Ther. 2022 Apr;18(2):553-559. doi: 10.4103/jcrt.jcrt_246_22.

Abstract

Context: Extensive studies have shown that β-catenin and C-myc have been linked to a number of human cancers. However, the role of β-catenin and C-myc in relapse glioma remains unclear.

Aims: The aims of this study were to investigate the role of β-catenin and C-myc in relapsed glioma patients and to explore the possible impact of malignancy, relapse, and prognosis.

Materials and methods: We collected surgical samples of 100 patients with primary and relapsed glioma treated at our institution. Immunohistochemistry (IHC) staining was used to evaluate the expressions of β-catenin and C-myc. The impact of the differences on disease-free interval (DFI), initial overall survival (iOS), and overall survival from the time of glioma relapse (rOS) of the patients was analyzed. Kaplan-Meier survival functions were used to plot survival time, and a log-rank test was used for analyzing statistical significance. Cox multivariate regression analysis was used to determine independent prognostic parameters.

Results: Compared to primary tumors, relapsed gliomas had higher expressions of β-catenin and C-myc (P < 0.05). Furthermore, the expressions of β-catenin and C-myc were significantly correlated with glioma grade (P < 0.05). These changes in expression at the time of relapse were independent of radiotherapy use. In multivariate Cox analysis, we found that β-catenin and C-myc were independent prognostic factors for rOS (P < 0.05).

Conclusions: Elevated β-catenin and C-myc promote malignancy, relapse, and indicate poor prognosis in patients with relapsed glioma. The elevated levels of β-catenin and c-myc in relapsed glioma were not affected by radiation therapy. The results of this study may provide a new therapeutic target for patients with relapsed glioma.

Keywords: C-myc; glioma; malignancy; prognosis; relapse; β-catenin.

MeSH terms

  • Glioma* / genetics
  • Glioma* / metabolism
  • Glioma* / therapy
  • Humans
  • Prognosis
  • Proto-Oncogene Proteins c-myc* / genetics
  • Proto-Oncogene Proteins c-myc* / metabolism
  • Reactive Oxygen Species
  • Recurrence
  • beta Catenin* / genetics
  • beta Catenin* / metabolism

Substances

  • CTNNB1 protein, human
  • MYC protein, human
  • Proto-Oncogene Proteins c-myc
  • Reactive Oxygen Species
  • beta Catenin