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Genome-wide profiling of gene amplification and deletion in cancer
1Department of Biochemistry and Molecular Oncology, Institute of Basic Medical Sciences, University of Tsukuba.
Abstract:
Accumulations of genetic changes in somatic cells induce phenotypic transformations leading to cancer. Among these genetic changes, gene amplification and deletion are most frequently observed in several kinds of cancers. Amplification of oncogene and/or deletion of tumor suppressor gene, together with dysfunction of the gene by point mutation, are the main causes of cancer. Genome-wide analysis of amplification and deletion of genes in cancers is basic to resolving the mechanisms of carcinogenesis. Comparative genomic hybridization (CGH) developed in 1992 has been utilized to identify DNA copy number abnormalities in various kind of cancers and several reports have shown its usefulness in screening of the genes involved in carcinogenesis, and also in the identification of prognostic factors in cancer. We have shown that 1q23 gain is associated with neuroblastomas that are resistant to aggressive treatment, and have poor prognosis, and 1q and 13q gains are possibly related to drug resistance in ovarian cancers. Recently, the "rough draft" of the human genome was reported and we are ready to utilize the vast information on genomic sequences in cancer research. Moreover, microarray technology enables us to analyze more than ten thousand genes at a time and revealed genetic abnormalities in cancers at a genome-wide level. By combination of microarray and CGH, a powerful screening method for oncogenes and tumor suppressor genes in cancers, called array-CGH, has been developed by several groups. In this article, we overview these genome-wide analytical methods, CGH and array-CGH, and discuss their potential in molecular characterization of cancers.
Insights
Genome-wide analysis using comparative genomic hybridization (CGH) and array-CGH identifies gene amplifications and deletions. These genetic changes are crucial for understanding cancer development and identifying prognostic factors.
Area of Science:
- Genomics
- Cancer Biology
- Molecular Oncology
Background:
- Somatic genetic alterations, including gene amplification and deletion, drive cancer development.
- These alterations, alongside point mutations, are key contributors to oncogenesis.
- Genome-wide analysis is fundamental to understanding cancer mechanisms.
Purpose of the Study:
- To overview genome-wide analytical methods for identifying genetic changes in cancer.
- To discuss the potential of CGH and array-CGH in the molecular characterization of cancers.
- To highlight the role of gene copy number abnormalities in carcinogenesis and prognosis.
Main Methods:
- Comparative Genomic Hybridization (CGH) for identifying DNA copy number abnormalities.
- Microarray technology for high-throughput gene analysis.
- Array-CGH, combining microarray and CGH, for genome-wide screening of oncogenes and tumor suppressor genes.
Main Results:
- CGH has proven useful in screening cancer-related genes and identifying prognostic factors.
- Specific findings include 1q23 gain associated with poor prognosis in neuroblastomas.
- 1q and 13q gains may relate to drug resistance in ovarian cancers.
Conclusions:
- Genome-wide analytical methods like CGH and array-CGH are powerful tools in cancer research.
- These techniques facilitate the molecular characterization of cancers.
- Understanding gene copy number abnormalities is essential for advancing cancer diagnosis and treatment.