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The computer‐assisted microscopic analysis of Feulgen‐stained nuclei enabled us to identify two subgroups of astrocytomas (WHO grade II) and two subgroups of anaplastic astrocytomas (WHO grade III) with significantly distinct clinical outcomes (Decaestecker et’al. Brain Pathol 1998; 8: 29–38). The astrocytomas labelled in the present study as typical (TYP‐ASTs) behaved clinically like real astrocytomas while atypical astrocytomas (ATYP‐ASTs) behaved similarly to anaplastic astrocytomas. The anaplastic astrocytomas that we labelled as typical (TYP‐ANAs) behaved clinically like anaplastic astrocytomas while atypical ones (ATYP‐ANAs) behaved like glioblastomas. In the present study, we investigate whether some biological characteristics could be evidenced across these four groups of TYP‐ and ATYP‐ASTs and TYP‐ and ATYP‐ANAs. The data show that the levels of expression (immunohistochemically assayed and quantitatively determined by means of computer‐assisted microscopy) of vimentin, the glial fibrillary acidic protein and the platelet‐derived growth factor‐α did not differ significantly across these four groups of astrocytic tumours. The level of cell proliferation (determined by means of both the anti‐proliferating cell nuclear antigen and the anti‐MIB‐1 antibodies; P < 0.001 to P < 0.0001) differed very significantly between the astrocytomas and anaplastic astrocytomas, but not between the typical and atypical variants identified in each group. In sharp contrast, the levels of expression of the S100A3 and S100A5 proteins differed markedly in the solid tumour tissue in relation to the astrocytic tumour types and grades. In addition, while the levels of expression of S100A6 did not change in the astrocytic tumour tissue in relation to histopathological grade, the levels of expression of this S100 protein (but not those of S100A3 and S100A5) differed markedly in the blood vessel walls according to whether these vessels originated from low‐ or high‐grade astrocytic tumours. [ABSTRACT FROM AUTHOR]