A large number of hematological (blood cell) and solid tumors of various types show consistent chromosome abnormalities, and there is overwhelming evidence that the chromosome changes are essential for the malignant phenotype. Almost every chromosome band is involved, indicating the large number of genes that can play a role in oncogenesis (Mitelman et al., 1997). Many of these rearrangements lead to cancer by activating a cellular oncogene (protooncogene). Protooncogenes are normal genes present in all metazoan cells. Genes homologous to protooncogenes are found in the retroviruses known to cause cancer in various animal species. They transform cells, either by being inserted into the host genome or by being present in multiple copies in the host cell (Bishop, 1983). The retroviruses originally acquired these oncogenes from the metazoan cells they infected. The oncogene of the Rous sarcoma virus is called v-src, and its homologue in the normal human genome is c-SRC, or SRC. More than 80 human protooncogenes have been localized to a specific chromosome or chromosome band. A normal cell can be transformed by activating one or more oncogenes in it. This most often occurs through chromosomal mechanisms such as translocation or amplification. In leukemias and lymphomas, these are mostly balanced reciprocal translocations; in solid tumors, deletions and trisomies are also common (Cobaleda et al., 1998; Helm and Mitelman, 1995).
KeywordsLymphoma Tyrosine Leukemia Recombination Serine
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- Helm S, Mitelman F (1995) Cancer cytogenetics, 2nd ed, Wiley-Liss, New YorkGoogle Scholar
- Stec I, Wright TJ, Van Ommen G-JB, et al. (1998) WHSC1, a 90kb SET domain-containing gene, expressed in early development and homologous to a Drosophila dysmorphy gene maps in the Wolf-Hirschhorn syndrome critical region and is fused to IgH in t(4;14) multiple myeloma. Hum Mol Genet 7:1071–1082PubMedCrossRefGoogle Scholar