LAUSR

The diversity of expansion and resistance within the group of diffuse and anaplastic gliomas might be possible due to variations in the cell-to-cell communication, determined by the Cx43- junctional activity and microtubules-defined networking with GAP43 as the main structural component. The aim of our trial was to assess the expression of these crucial proteins in samples of patients. Tissue of adult patients with WHO°II and III gliomas, who underwent surgery 2014 to 2018, were selected from institutional biobank. The expression was analyzed using immunohistochemistry and routine findings gained from patient charts. 43 (57%) males and 33 (43%) females with a median age of 47 years (IqR: 35–61) were analyzed. In 15 (20%) patients a diffuse glioma (WHO°II) and in 46 (60%) an anaplastic glioma (WHO°III) was diagnosed. Further 15 patients (20%) were diagnosed with a diffuse glioma showing focal anaplasia. The IDH1 wildtype tumors demonstrated higher Cx43 expression in patients with longer intervals between imaging-based diagnosis and biopsy (p=0.032), whereas this association was absent in IDH1 mutated gliomas (p=0.549). The IDH1 wildtype tumors showed a higher expression of Cx43 (p=0.003) and a trend towards higher expression of GAP43 (p=0.075). Advanced Cx43 expression correlated with lower Ki67 nuclear expression in both IDH1 wildtype (p=0.003) and mutated gliomas (p=0.019). The IDH1 wildtype gliomas showed advanced expression of Cx43 and GAP43 as well as longitudinal increase of Cx43. In the same time, tumors with lower mitosis rate produced more communication proteins, probably due to longer interphase. It can be interpreted as the intercellular networking provides acquired pathogenicity in the tumors with lower, e.g. “favorable”, proliferation rate. Moreover, IDH1 wildtype gliomas showed here advanced results, matching their aggressive behavior and poor outcome. Thus, diffuse and anaplastic gliomas are not homogenic and need to be evaluated considering their genetic profile.