Clinical significance of molecular genetic changes in sporadic invasive pituitary adenomas.
- Author:
Do Hyun NAM
1
;
Sang Yong SONG
;
Kyoung Sook PARK
;
Mi Hyun KIM
;
Yeon Lim SUH
;
Jung Il LEE
;
Jong Soo KIM
;
Seung Chyul HONG
;
Hong Jin SHIN
;
Kwan PARK
;
Whan EOH
;
Jong Hyun KIM
Author Information
1. Department of Neurosurgery, Samsung Medical Center and Center for Clinical Research, Sungkyunkwan University School of Medicine, Sungkyunkwan University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
retinoblastoma;
p53;
multiple endocrine neoplasm type 1;
invasive pituitary adenoma
- MeSH:
Adenoma/*genetics/*pathology/physiopathology/radiography;
Adult;
Aged;
Aged, 80 and over;
Cell Cycle Proteins/genetics;
Cell Transformation, Neoplastic;
Chromosomes, Human, Pair 11;
Chromosomes, Human, Pair 13;
Female;
*Genes, Retinoblastoma;
Genes, Tumor Suppressor;
Genes, p53;
Human;
Loss of Heterozygosity;
Male;
Middle Age;
Mutation;
Neoplasm Invasiveness;
Neoplasm Proteins/*genetics;
Pituitary Neoplasms/*genetics/*pathology/physiopathology/radiography;
Polymorphism, Single-Stranded Conformational;
Protein p16/genetics;
Protein p53/genetics/metabolism
- From:Experimental & Molecular Medicine
2001;33(3):111-116
- CountryRepublic of Korea
- Language:English
-
Abstract:
Several molecular and genetic changes have been found in pituitary adenomas. We looked for correlations between these changes and the degree of invasiveness of the tumors. The invasiveness of 11 pituitary adenomas was graded by Hardy classification. We examined the retinoblastoma gene (RB1.20 on chromosome 13q) and the region around the MEN1 locus (chromosome 11q13.1-5) for loss of heterozygosity. Also examined are p53 mutations using single strain conformation polymorphism, p53 protein overexpression using immuno cytochemistry, homozygous deletions of p15 and p16 by polymerase chain reaction, and cellular proliferative activity using MIB-1 antibody. Six tumors (54.5%) had an LOH at either RB1.20 or the MEN1 locus. LOHs were found more frequently in Grade 4 and stage E tumors (72% and 67%) than in Grade 3 and stage D tumors (25% and 40%). However, no mutation or overexpression of p53 was found. No homozygous deletions of p15 or p16 were identified. The cell proliferative index ranged from 0 to 3%. LOH at 11q13 and 13q may be valuable in predicting the invasiveness of pituitary adenomas.
