[Astrocytic neoplasms and correlation with mutate p53 and Ki-67 proteins]. / Neoplasias astrocitárias e correlação com as proteínas p53 mutada e Ki-67.

The astrocytic neoplasms respond by 60% of the central nervous system tumors, being the study of the molecular biology an important step for the understanding of the genesis and biological behavior of these diseases. The Ki-67 proteins, which are markers of the cellular proliferation, and p53, which is the product of the tumor suppressor gene TP53, are both important tumoral markers. This study intends to identify and quantify the Ki-67 and p53 proteins in astrocytic tumors of different grades of malignancy, as well as to analyze their relations with age and gender. Ki-67 and p53 proteins in 47 patients with surgically resected astrocytic neoplasms were studied through immunohistochemistry. They have been previously classified and reviewed concerning their histological grade, as suggested by the World Health Organization. The immunomarked cellular nuclei were quantified by the program Imagelab-softium for the absolute parametric reason between the nuclei of the positive cells and the total amount of tumoral cells, being counted 1000 cells. The lineation used has been transversal not controlled. For the statistical analysis the variables were divided into groups. For the Ki-67 they were absent, <5% and >5% and for p53 they were absent (0), <25% (1+), between 25 and 50% (2+), between 50 and 75% (3+), and higher than 75% (4+). Ki-67 was present in 37 cases (78.72%) evidencing a correlation with a higher malignancy degree (p<0,001). p53 was present in 14 cases (35.13%) with a higher correlation with astrocytoma grade IV (p=0.59). There has not been a statistically significant correlation between p53 and Ki-67, as well as among these variables, age and gender. The hypotheses of a greater presence of Ki-67 and p53 in astrocytic neoplasms with a higher degree of malignancy, except for the correlation between grade III and p53, is corroborated by the results of this study.