Prognostic implications of the proliferative potential of low-grade astrocytomas

Abstract

The proliferative potential of low-grade astrocytomas was estimated in 47 patients. Each patient received an intravenous infusion of bromodeoxyuridine (BUdR), 150 to 200 mg/sq m, at the time of craniotomy to label cells in deoxyribonucleic acid (DNA) synthesis; the percentage of S-phase cells, or BUdR labeling index (LI), of each tumor was determined immunohistochemically. In 29 patients (60%), the tumors had BUdR LI's of less than 1%, indicating a slow growth rate; only three (10%) of these patients died of recurrent tumor during a follow-up period of up to 3 1/2 years. In contrast, of the 18 patients (40%) whose tumors had BUdR LI's of 1% or more, 12 (67%) had a recurrence and nine died during the same follow-up period. These results show that the proliferative potential, as reflected by the BUdR LI, is an important prognostic factor that separates low-grade astrocytomas into two groups and provides a more scientific rationale for selecting treatment for individual patients.

Clinicopathological features, MIB-1 labeling index and apoptotic index in recurrent astrocytic tumors

“…4,10,11,12 Several studies have given a cut off value for MIB-labeling index beyond which prognosis was poor. Montine et al 21 reported that a MIB-LI >7.5% was associated with higher histological grade and poorer survival.…”

p53 protein in low-grade astrocytomas: a study with long-term follow-up

“…The fact that the trend is not apparent until 3-4 years follow-up could be interpreted as being a consequence of the time needed for the p53-positive subclone to outgrow the rest of the p53-negative neoplastic cell population. The long time needed for the p53-positive subclone to overgrow the other cells could be related to the low proliferative activity of low-grade astrocytomas (Giangaspero et al, 1987;Hoshino et al, 1988;Allegranza et al, 1991).…”

“…Among these parameters are the proliferative activity (Burger et al, 1986;Giangaspero et al, 1987;Hoshino et al, 1988;Allegranza et al, 1991;Jaros et al, 1992), DNA content (Nishizaki et al, 1989) and alterations of oncogenes and tumour-suppressor genes (BaugnetMahieu et al, 1990;Venter & Thomas, 1991;Orian et al, 1992;Jaros et al, 1992;Haapasalo et al, 1993).…”

The Cycling Pool of Cells within Human Brain Tumors:In SituCytokinetics Using the Monoclonal Antibody Ki-67

“…Infiltration, anaplasia, and recurrences of tumors are linked to There is increasing evidence that the LI carries clinical significance, the higher the LI the more ominous the prognosis. 6 -7 ' 39 The course of a brain tumor is influenced by multiple factors such as size, location, age, degree of edema, necrosis, 7 vascularity, 7 and invasiveness. 40 Nevertheless, the cellular proliferative potential, determined by Ki-67 immunohistochemistry, should be added to the armamentarium of the neuropathologist in the routine assessment of surgical material to provide dynamic cytokinetic data that will complement classical histopathologic diagnosis based upon morphology alone.…”

“…6 Early studies of brain tumor cytokinetics were performed with a pulse of 3 H-thymidine, a marker of the S-phase, given to the patient before surgical removal of the tumor. 2 -5 Modern immunohistochemical techniques using commercially available monoclonal antibodies to BUdR, a thymidine analogue, provide a rapid, reproducible method to perform cell kinetics in situ in human 7 -910 and experimental 8 brain tumors; the tumor labeling index is similar by either BUdR immunohistochemistry comparable to 3 H-thymidine autoradiography. 8 A recent advance in cytokinetic analysis of tumors is the introduction of a monoclonal antibody, Ki-67, that recognizes a nuclear antigen expressed in all phases of the cell cycle, but is absent in quiescent G 0 cells.…”