Rare glial astrocytic tumours like PXA and GCGB typically affect children’s and young adults’ superficial cerebral hemispheres [1]. Histopathological characteristics and reticulin stains mostly successfully address the differential diagnosis of PXA and GCGB. However, some instances are still unclear because of their small sample size, unusual histologic patterns, and expression of immunohistochemical markers [1], necessitating further diagnostic testing to reach the right diagnosis. Reticulin fibre depositions and CD34 expression, which are frequently used in PXA and GCGB, were found to be particularly useful as diagnostic markers in PXA. However, Lohkamp and colleagues [12] cautioned that these markers should not be used carelessly for the purpose of differentiating between the two entities, since dense reticulin fibre networks and CD34 expression were also found in over 25% of GCGB.

The term “gliomas” refers to a fairly broad category of intrinsic brain tumours that are often categorized based on microscopic similarities with potential source cells that belong to glial precursor cell lineages [15]. Our findings corroborate a number of other investigations that found elevated levels of GFAP and neural markers like synaptophysin in various tumour forms [10, 12, 16]. Because of PXA's high, diffuse GFAP staining, it was first thought to be glial in lineage [1].

Studies using immunohistochemistry and ultrastructural analysis have also revealed the presence of neuron-like fine features and neuronal immunophenotype [17, 18]. Consequently, our research lends credence to the theory that these tumour entities belong to the glioneuronal lineage.

All forms of cancer have TP53 mutations, which are genetic events that are assumed to be inactivated early in the carcinogenesis process [19]. Furthermore, p53 contributes to genomic stability through its roles in cell-cycle arrest and centrosome duplication [18, 20].To identify underlying TP53 gene alterations, p53 protein immunostaining is a trustworthy proxy method [21].

In contrast to low expression in PXA, the current investigation found strong P35 expression in GCGB and APXA. Our results more closely resemble the two comparative studies by Martinez-Diaz and colleagues [1], who found that p53 staining was found in many tumour cells in 5 out of 8 GCGB tested, while this antigen staining was negative or focally positive in 6 out of 8 PXAs, and Lohkamp and colleagues. [12], who found that nuclear p53 positivity was found in 74% of GCGB and that p53 positivity was less common in PXA cases (30%). Hirose and colleagues. (2008) reported, in contrast to our observations, that all tumour samples (12 PXA cases: six with conventional features and six with anaplastic features) showed evidence of p53 immunoreactivity. These differences could have to do with methodological evaluation and sample size. The results support the theory introduced recently by Cantero and colleagues [9] that the high rate of TP53 change in GCGB indicates that this gene is involved in these tumours and may be one of the first events in the gliomagenesis of GCGBs. The P53 protein is not involved in the pathophysiology of PXA, despite being well-known to exist in diffusely invading astrocytic gliomas, such as glioblastomas and anaplastic astrocytomas. These genetic variations appear to be the cause of PXA's unique biological characteristics.

Hematopoietic stem cells (HSCs) and hematopoietic progenitor cells were initially thought to be identified by CD34 [18]. Our findings showed that while CD34 was not expressed in GCGB or APXA, it was highly expressed in PXA. Our findings are consistent with the earlier reports by Hirose and colleagues [10] and Reifenberger and colleagues [11], which reported that tumour cells expressing CD34 were more frequently found in WHO grade II PXAs than in PXAs exhibiting anaplastic features. As far as we are aware, CD34 expression has not yet been investigated in relation to GCGB. Strong, widely distributed positivity was observed in giant cell glioblastomas (55%), according to Galloway and colleagues [22]. Our results are consistent with the findings of Lohkamp and colleagues [12], who observed low CD34 expression in GCGB (27%), in large series.

Relatively little is yet understood regarding CD34's role. Hematopoietic cell studies point to functions in cytoadhesion and the control of cell proliferation and differentiation [18, 23]. Hence, despite APXA and GCGB having less frequent and weaker CD34 immunoreactivity, PXAs had higher expression of CD34, which may help explain why these tumours' growth is more restricted. Moreover, could be a sign of dedifferentiation and suggest a function for decreased or lost CD34 expression in the development of tumours [11].

In many tumours, the proliferative activity, also known as the Ki67 proliferation/labelling index, is a significant prognostic indicator. High-grade gliomas and other high-grade tumours have high Ki67 indices [24].

We discovered comparatively high Ki67 labelling indices in GCGB and APXA, but not in PXA, as other researchers have [25,26,27]. When combined with other research findings, our findings bring up a number of ideas. High-grade gliomas can be diagnosed with the help of the Ki67 labelling index. It can assist in identifying the anaplastic transition in PXA and has a significant prognostic function.

According to published research, between 9 and 20% of PXAs may develop a malignant transformation upon recurrence or may exhibit it at the time of first presentation [11]. Two secondary APXA cases were shown in this investigation; one patient experienced a tumour recurrence after a year, and the other after a year and a half. The intriguing immunohistochemistry results showed that CD34 expression had decreased and p53 expression had increased in both of the recurrent PXA patients. As a result, APXA showed an immunological profile (negative CD34 and positive P53) that is comparable to GCGB, with positive synaptophysin and GFAP in both tumours.

Certain immunohistochemical patterns (positive p53 and negative CD34) for these neoplasms were observed in a number of published case reports of PXA transforming into APXA or GB [18, 25, 28]. The idea that p53’s positive expression and CD34’s negative expression are distinctive features of GB and APXA is further supported by our data. Another theory is that PXA carcinogenesis may not be initiated by a mutation in the p53 gene, but rather may be accelerated by it. Loss of CD34 expression concurrently could be a sign of dedifferentiation.

However, the precise biological processes behind the accumulation of p53 proteins in PXA as well as their predictive significance are yet unknown. The information supports the theory that APXAs are thought to display the interphase between PXA and lipidized GCGB [18].