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Title: Genomic alterations in cervical carcinoma: Losses of chromosome heterozygosity (LOH) correlated with cytogenetic, HPV, and p53 evaluations

Abstract

This study was undertaken to obtain indications of chromosomes likely to carry tumorigenicity suppressor genes the loss of function of which play a role in the origin or progression of cervical carcinomas. PCR and electrophoresis with primers for 73 highly polymorphic microsatellite chromosome markers were used to determine the incidence of LOH of all of the autosomes in 38 cervical carcinomas. According to these criteria 14 of the autosomes are involved in LOH in 24% to 42% of the tumors. This involves chromosomes 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 13, 16, 18 and 19. Most frequently involved are chromosomes 3 and 6 with LOH in 42% of the tumors. The chromosomes next most frequently involved are 4, 7, 11 and 18, with LOH in 31-32% of cases. Chromosomes 1, 2, 5, 8 and 16 each had LOH in 29% of the tumors; 9 and 13 each in 26%; and 19 in 24% of the tumors. All other autosomes had LOH in 18% or fewer of the tumors. Cytogenetic analyses performed on direct preparations from many of the same tumors agreed well with the molecular LOH assays. Correlation of the information obtained with both of these methodsmore » provides considerable insight into the mechanisms involved in the occurrence of these chromosome alterations. Chromosome 3 is the third most frequent chromosome involved in LOH in all types of cancer. In cervical carcinomas the region most frequently involved is 3p13-p25, which is a segment within which suppressors have been implicated in several other types of malignancies. Chromosome 6 on the other hand is rarely involved in other neoplasias and this appears to be unique to cervical carcinomas. Of interest was the finding that many of the HPV-negative tumors had LOH of chromosome 17 and many of these expressed mutant p53. The latter tumors occur in older women and are on the average much more aggressive than the HPV-positive tumors.« less

Authors:
; ;  [1]
  1. Albert Einstein College of Medicine, Bronx, NY (United States); and others
Publication Date:
OSTI Identifier:
133529
Report Number(s):
CONF-941009-
Journal ID: AJHGAG; ISSN 0002-9297; TRN: 95:005313-0257
Resource Type:
Journal Article
Journal Name:
American Journal of Human Genetics
Additional Journal Information:
Journal Volume: 55; Journal Issue: Suppl.3; Conference: 44. annual meeting of the American Society of Human Genetics, Montreal (Canada), 18-22 Oct 1994; Other Information: PBD: Sep 1994
Country of Publication:
United States
Language:
English
Subject:
55 BIOLOGY AND MEDICINE, BASIC STUDIES; GENES; GENE MUTATIONS; HUMAN CHROMOSOMES; GENETIC MAPPING; CHROMOSOMAL ABERRATIONS; STRUCTURE-ACTIVITY RELATIONSHIPS; PATIENTS; CARCINOMAS; UROGENITAL SYSTEM DISEASES; BIOLOGICAL MARKERS; POLYMERASE CHAIN REACTION; ELECTROPHORESIS

Citation Formats

Klinger, H P, Mullokandov, M, and Khollodilov, N G. Genomic alterations in cervical carcinoma: Losses of chromosome heterozygosity (LOH) correlated with cytogenetic, HPV, and p53 evaluations. United States: N. p., 1994. Web.
Klinger, H P, Mullokandov, M, & Khollodilov, N G. Genomic alterations in cervical carcinoma: Losses of chromosome heterozygosity (LOH) correlated with cytogenetic, HPV, and p53 evaluations. United States.
Klinger, H P, Mullokandov, M, and Khollodilov, N G. 1994. "Genomic alterations in cervical carcinoma: Losses of chromosome heterozygosity (LOH) correlated with cytogenetic, HPV, and p53 evaluations". United States.
@article{osti_133529,
title = {Genomic alterations in cervical carcinoma: Losses of chromosome heterozygosity (LOH) correlated with cytogenetic, HPV, and p53 evaluations},
author = {Klinger, H P and Mullokandov, M and Khollodilov, N G},
abstractNote = {This study was undertaken to obtain indications of chromosomes likely to carry tumorigenicity suppressor genes the loss of function of which play a role in the origin or progression of cervical carcinomas. PCR and electrophoresis with primers for 73 highly polymorphic microsatellite chromosome markers were used to determine the incidence of LOH of all of the autosomes in 38 cervical carcinomas. According to these criteria 14 of the autosomes are involved in LOH in 24% to 42% of the tumors. This involves chromosomes 1, 2, 3, 4, 5, 6, 7, 8, 9, 11, 13, 16, 18 and 19. Most frequently involved are chromosomes 3 and 6 with LOH in 42% of the tumors. The chromosomes next most frequently involved are 4, 7, 11 and 18, with LOH in 31-32% of cases. Chromosomes 1, 2, 5, 8 and 16 each had LOH in 29% of the tumors; 9 and 13 each in 26%; and 19 in 24% of the tumors. All other autosomes had LOH in 18% or fewer of the tumors. Cytogenetic analyses performed on direct preparations from many of the same tumors agreed well with the molecular LOH assays. Correlation of the information obtained with both of these methods provides considerable insight into the mechanisms involved in the occurrence of these chromosome alterations. Chromosome 3 is the third most frequent chromosome involved in LOH in all types of cancer. In cervical carcinomas the region most frequently involved is 3p13-p25, which is a segment within which suppressors have been implicated in several other types of malignancies. Chromosome 6 on the other hand is rarely involved in other neoplasias and this appears to be unique to cervical carcinomas. Of interest was the finding that many of the HPV-negative tumors had LOH of chromosome 17 and many of these expressed mutant p53. The latter tumors occur in older women and are on the average much more aggressive than the HPV-positive tumors.},
doi = {},
url = {https://www.osti.gov/biblio/133529}, journal = {American Journal of Human Genetics},
number = Suppl.3,
volume = 55,
place = {United States},
year = {Thu Sep 01 00:00:00 EDT 1994},
month = {Thu Sep 01 00:00:00 EDT 1994}
}