Solid tumor cytogenetics. Progress since 1979.
Some of the advances in the past decade in the field of solid tumor cytogenetics are described, with particular reference to nonrandom structural chromosome changes. Although it had been known for many years that meningiomas and salivary gland tumors were associated with changes involving particular chromosomes, it has only quite recently become clear, following the application of suitable culture techniques, that other benign tumors such as lipomas and leiomyomas may also be characterized by specific changes, particularly reciprocal translocations. Reciprocal translocations may also be found in malignant soft-tissue tumors such as liposarcomas (involving 12q as in lipomas) and Ewing's sarcoma. In contrast, the common forms of carcinoma present a more variable picture, although certain chromosomes may undergo nonrandom changes of various types, including translocations, which, however, are generally nonreciprocal. Some of these chromosomes may be quite specific (e.g., chromosome 10 in prostatic and #18 in colorectal cancer), while others appear to be common to many or all types of carcinoma, such as chromosomes 1, 3, 11, and 17, and a small metacentric that may be an i(5p). In carcinoma of the bladder, different chromosome changes may characterize subsets of the tumors. In carcinoma of the cervix, however, the commonly involved chromosomes, 1, 3, ?5, 11, and 17, appear in markers in any combination and are thus not mutually exclusive. Although further study of the chromosome changes in carcinomas is essential to an understanding of their relationship to the molecular changes that are associated with malignant transformation, it can be hypothesized that, while some of the changes result in the duplication of particular genes, e.g., on chromosome 1q, a more important role may be to bring about the loss of chromosomal segments containing tumor-suppressor genes. Evidence from molecular studies that has recently been accumulating for the loss of alleles on, for instance, 3p, 11p, and 17p, which could in part be due to gross chromosomal rearrangements, also strongly suggests the importance of genic loss in malignant transformation. In carcinomas, at least, the changes probably involve a number of genes, each change representing one of the several steps necessary for tumorigenesis.
Atkin
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NB
Department of Cancer Research, Mount Vernon Hospital, Northwood, Middlesex, U.K.
D002869:Chromosome Aberrations; D005819:Genetic Markers; D006801:Humans; D009369:Neoplasms / Q000235:genetics*
D005819:Genetic Markers