TITLE:
Cell Replication and Angiogenesis in Central Nervous System Tumors and Their Relationship with the Expression of Tissue Prolactin and Hyperprolactinemia
AUTHORS:
Denise M. D. Abech, Júlia F. S. Pereira-Lima, Carolina G. S. Leães, Rosalva T. Meurer, Lígia M. Barbosa-Coutinho, Nelson P. Ferreira, Miriam C. Oliveira
KEYWORDS:
Ki-67 Antigen; Mcm-2 Protein; Human; Endoglin Protein; Human; Prolactin; Central Nervous System Tumors
JOURNAL NAME:
Open Journal of Pathology,
Vol.2 No.3,
July
18,
2012
ABSTRACT: This study aimed to assess the effect of intracellular prolactin (ICPRL) and hyperprolactinemia on cell replication, using an immunohistochemical (IHC) technique for Ki-67 and Mcm-2, and angiogenesis, using IHC for endoglin CD-105, in central nervous system (CNS) tumors. This cross-sectional study included 79 cases of surgically excised primary CNS tumors of neuroepithelial origin (41.8% of all cases: 10.2% astrocytomas, 24% glioblastomas and 7.6% oligodendrogliomas) and meningeal origin (58.2% of all cases). Ki-67 and Mcm-2 indexes were calculated as a percentage of marked cells. The medians for Ki-67 and Mcm-2 indexes were significantly lower in meningiomas than in glioblastomas (p S = 0.60) replication markers. There were no significant differences in vascular density between the different histological types. Immunohistochemistry for ICPRL was positive in 45.6% of the tumors. Serum prolactin (PRL) was elevated in 30.6% of the cases. Multiple regression analysis revealed no important correlation of ICPRL and serum PRL on Ki-67 and Mcm-2 indexes or vascular density. The analysis of the combined impact of ICPRL and serum PRL variables revealed a trend towards an increase in microvessel density in tumor tissue and a significant increase in cell replication markers (p = 0.009 for Ki-67 and p = 0.05 for Mcm-2). PRL in tumor tissue may be one of the modulating factors of cell proliferation in the CNS.