PubMed Health⌕ Search

PubMed · 8752732

[Chromosome analysis and FISH method].

Abstract

In hematologic malignancies activation of oncogenes or inactivation of tumor suppressor genes are thought to be responsible for its carcinogenesis, just like other solid tumors. As these genetic changes are detected as chromosome abnormalities, cytogenetic analysis has been used as a tool for diagnosis and follow up after therapy. The fluorescence in situ hybridization (FISH) method is a new technic which enables us to detect genetic changes both in mitotic and interphase cells. It is a useful method in the clinical field which covers the disadvantages in cytogenetic analysis, RT-PCR and Southern blotting. We practically used the FISH method in diagnosis and follow-up observation of minimal residual disease in several kinds of hematologic malignancies. By the morphology-FISH method, the relationship between cell morphology and genetic changes could be analyzed simultaneously. The FISH method was also applied to probe mapping to identify a novel breakpoint cluster region in the 11q23 area in adult hematological disease. FISH method is a rapid and powerful tool both in clinical and basic study in hematologic disorders.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Eguchi, K Tanaka. 1996. [Chromosome analysis and FISH method].. https://pubmed.ncbi.nlm.nih.gov/8752732/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Correlation of histologic subtypes and replication error phenotype with comparative genomic hybridization in gastric cancer.

To characterize phenotypic and genotypic changes in gastric cancer (GC), DNA copy number aberrations (CNAs) were assessed in 53 tumors using comparative genomic hybridization (CGH) and correlated with clinicopathologic characteristics and status of TP53 and replication error (RER). The number of CNAs per tumor was 6.8 (gain 5.3, loss 1.5), and the number of changes was significantly higher in tumors with advanced stage, TP53 mutation, and without RER than in those with early stage (7.7 vs. 3.0), no TP53 mutations (12.4 vs. 4.8) or RER phenotype (8.2 vs. 2.6). Frequent abnormalities included gains on chromosomal arms 8q (43%), 6q (26%), 11q (26%), 13q (24%), 7p (23%), 17q (23%), and 20q (23%), and losses on chromosomal arms 16q (26%), 19p (23%), 5q (19%), 3p (15%), 4q(15%), and 1p (15%). Advanced GC demonstrated a higher prevalence of gains of 8q (51% vs. 10%, P < 0.05) and loss of 16q (33% vs. 0%, P < 0.05) than early GC. Gains on 8q (64% vs. 20%, P < 0.05), 17q (39% vs. 4%, P < 0.05) and losses on 3p (25% vs. 4%, P = 0.05) and 5q (32% vs. 4%, P < 0.05) were higher in intestinal GC than in diffuse GC. On the other hand, gains on 13q were more common in the diffuse type (40% vs. 11%, P < 0.05). As compared with noncardia cancer, cardia cancer showed more gains on 7p (58% vs. 12%, P < 0.05) and 20q (58% vs. 12%, P < 0.05) and more losses on 4q (50% vs. 5%, P < 0.05). The finding of histology-related aberrations and the combination of CGH and molecular data thus provide additional evidence suggesting genetic heterogeneity of GC.

Chromosome Aberrations↗

Molecular cytogenetics of prostate cancer.

Prostate cancer is the most common malignancy among men in Western industrialized countries. The molecular pathogenesis of the disease is poorly known. Over the past 10 years, chromosomal aberrations in prostate cancer have been studied with several techniques, such as loss of heterozygosity (LOH), classical cytogenetics, and molecular cytogenetics, namely with fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH). These analyses, especially those performed by CGH, have enabled the distinction of the predominant chromosomal regions of involvement in prostate cancer. Studies have shown that the most common chromosomal alterations in prostate cancer are losses at 1p, 6q, 8p, 10q, 13q, 16q, and 18q and gains at 1q, 2p, 7, 8q, 18q, and Xq. Fluorescence in situ hybridization (FISH) has been used to identify the target genes for some of these chromosomal alterations. For example, amplifications of AR (at Xq12), MYC (8q24), and EIF3S3 (8q23) have been found in a large fraction of hormone-refractory prostate cancer by FISH. However, many of the critical oncogenes and tumor suppressor genes located in the altered chromosomal regions have not yet been identified.

Chromosome Aberrations↗