Three topics are discussed in the review: 1) The non-random and specific chromosome changes in human and animal tumors, 2) prezygotic chromosomal mutations which specifically predispose to some human tumors, and 3) the role of cytogenetics in the discovery and study of a novel phenomenon for mammalian cells-gene amplification which was revealed in a number of tumors and in cell lines resistant to some anticancer drugs.

The aggregation of cancer in families, possible causes of tissue specificity of hereditary susceptibility to cancer, as well as various kinds of inherited enzyme disorders regarded as the basis of this susceptibility are discussed. Different aspects of the relationship between cell neoplastic transformation and differentiation are analysed. Special attention is given to the capacity of differentiation inducers to reverse in some instances the malignant phenotype of the tumor cell progeny. In addition, some data are cited that indicate instability of DNA molecule in neoplastic cell transformation, differentiation and hormone action.

The age of disease onset, sex, birth weight and stature were analysed in 150 children suffering from nephroblastoma. The material was compared with its own control group (92 normal children of the same age) and with the population data from literature. All nephroblastoma patients were divided into 2 groups by the age of disease onset: before 2 years old and after this. The proband birth weight and stature in the first group statistically differed from control and population exponents. Genetic heterogeneity of nephroblastoma is discussed.

During last three years, the mobile dispersed genetic elements (mdg) were isolated from the genome of Drosophila melanogaster, yeasts and mammals. According to a number of their properties, mdg elements are quite similar to endogenous pro-retroviruses. It is known that in many cases oncogeneity of retroviruses depends on the incorporation of the certain host genes (potential oncogenes) into the viral genome. We suggest that in some cases mdg elements could entrap the potential oncogenes in the course of transposition. As a result, oncogenes become uncontrollable by host regulatory systems and may induce cell transformation. Another possible mechanism underlying switch off of the gene responsible for differentiation control may be mdg transposition to a region in close vicinity of the gene. As transposition of mdg elements seems to occur rather often, they may be regarded as one of the most important factors of genome rearrangements leading to cell transformation.

Results of selection for the affinity for lung tissue in cells of three transplanted tumors of the rat are given. Tumor cell suspensions were injected intravenously-intraperitoneally or subcutaneously-intravenously (the clonal line -- clone circuit), or intravenously-intravenously (the clone-clone circuit). The efficiency of the method has been shown in the cases of the Worker carcinoma and of a 20-methylcholantren-induced rhabdosarcoma. A 10-fold recloning of cells of the ovary ascite tumor failed to increase their affinity for the lung tissue. It is suggested that a hereditary heterogeneity with the trait "the affinity for lung tissue" may be characteristic of tumor cell populations.

Cell diameter and cell value variations were studied in murine and rat rhabdomyosarcomas, both in clones obtained in lung tissue, and in subcutaneous tumors. Coefficients of heritability (h2) of these characters were calculated on the basis of their variances. They were equal to 0.15--0.31 for the diameters of cells, and 0.13--0.87 for the cell volumes. The problem of investigation of heritability of quantitative characters in somatic cell populations is discussed.

50 clones of murine rhabdomyosarcoma were grown in lungs, DNA contents of interphase nuclei of these clones being measured cytophotometrically. Significant differences in the mean DNA contents of clones obtained were observed, reflecting karyotypic differences of the initial clonogenic cells. The progenies of clonogenic cells had very high genome mutation rates (17.4 +/- 0.3.10(-2), and cells with increased numbers of chromosomes arose more frequently than hypoploid cells (12.5 +/- 0.3 and 2.9 +/- 0.2.10(-2), respectively). The mutability of tumor cells was non-equal in different clones, and positive correlations were observed between the mean DNA contents and mutability of the clones, whereas negative correlations were noticed between mutability and rates of cell proliferations.

Cell populations of eight experimental tumors (murine and rat rhabdomyosarcomas induced with 20-methylcholantrene, transplantable murine rhabdomyosarcoma A-7, and transplantable rat lymphosarcoma) have been selected for the affinity of their cells to lung tissue. The level of the affinity was measured as the number of lung nodules per 100 000 tumor cells injected intravenously. A 3-4-fold selection appeared to be non-effective, whereas 10-fold or more prolonged selections resulted in a gradual enhancement of the affinity of tumor cells to lung tissue. Thus, the transplantable murine and rat rhabdomyosarcomas were obtained with an increased capacity of their cells of yielding lung nodules. The affinity of rat rhabdomyosarcoma was 200-300 times higher after 40 steps of selection compared to the initial tumor affinity. With the rhabdomyosarcoma of CC57W mice, the affinity increased by 5 times after 20 steps of selection. Using our technique of selection (without an in vitro cultivation), the capacity of cells of persisting in lung tissue and yielding lung nodules looks likely as a quantitative character with a rather low heritability. It has been concluded that in cell populations of tumors examined there are only a few genetic population variations in cell capacity of making non-random metastases.