Transition progression with transformation of Astrocytoma to Glioblastoma multiforme
coincides with the acquisition of decontrolled cell cycling activity of the tumor cells as clonal
expansions of a single common cell of origin for the neoplasm. One would operatively consider
dysfunctional pathways of mutant p53 and pRb components in the light of amplification of mutant
Epidermal Growth Factor Receptors and of immortalization arising from reactivation of telomerase
activity. Glioblastoma as a highly heterogeneous group of lesions would implicate biologic and
histologic diversity in the further development of decontrolled cell cycling due to both complete and
partial deletion of genes and of splicing of coding sequences. Both loss of expression of protein
products such as Glial Fibrillary Acidic Protein and the acquisition of new forms of expression such as
nestin immunoreactivity might account for a transition phenomenon centrally deregulating cell
division mechanics in terms of both initiation and progression of the glioma. Early stages of
gliomagenesis would faithfully predict a transition mechanics aimed at reproduction of phenotypic
traits indicative of transformation of both Grade and dynamics of cell cycling in the first instance.
Keywords: transformation, astrocytoma, growth factors, receptors.
