Aims and tasks of the investigation of the DNA contents in tumour cells are discussed. It is supposed that DNA aneuploidia is a specific sign of malignant cells. Such supposition permits solving the problem of quantitative identification of malignant cells in the complex cell populations and determination of their quantity. Certain conditions necessary for solving this problem are considered.

The dose and schedule dependent resistance occurred at the 17th (L1210/D1) and 27th (L1210/D2) generations during leukemia L1210 transplantation by the cells treated with suboptimal diazane doses. With growth of the resistance to diazane the selection of modal cell class with 39 chromosomes took place while in the parent leukemia line the modal cell class consists of the cells with 40 chromosomes. No reliable differences were observed in G-banded karyotypes between the resistant subline L1210/D1 and the parent line L1210. When the resistant sublines were transplanted without supporting the diazane doses no restoration of the leukemic cells sensitivity to the drug was observed (the time of observation for L1210/D1 was 92 transplantation generations and for L1210/D2-48 generations). The changed number chromosome characteristics remained the same in this case.

The relation was studied between the density of the electrical charge of the surface (DECS) and the karyological structure of the rat ovary tumour (OT) cells. For this purpose the sedimentation rate and electrical mobility of cells from two OT clones were measured. The OT1 and OT2 clones differed in their modal chromosome numbers (44 and 80-90, respectively). An increase in DECS by 4-5% on the average occurs in cells with the chromosome set close to the tetraploid one. The further increase in the chromosome number to the octaploid one does not change DECS. The results obtained show stability of DECS with significant changes in the structure of the OT cells karyotype.

Distribution of DNA in cells of 28 primary ethylnitrosourea-induced tumours of the rat nervous system was studied by the Feulgen cytophotometry method. Out of them 20 had paradiploid DNA quantity, 3 tumours--hypodiploid and 4--hyperdiploid content of DNA. A high heterogeneity of the DNA quantity and the absence of expressed modal class were found only in one case. No correlation is found between the DNA distribution in gliomas and the stage of their malignancy.

Data available in literature on clinical oncogenetics are reviewed. Pretumour and tumor processes with dominant, recessive and multifactorial inheritance are analyzed in particular. A possibility of application of cytogenetic indices to diagnose initial forms of tumour process and determine the level of anaplasia of developed malignant tumours is suggested. The role of Ukrainian oncologists in oncogenetic studies with the view of comprehending the nature of malignancy and expanding diagnostic possibilities in practical oncology is shown.

Since most cancers eventually become refractory to chemotherapy, the development of drug resistance within tumour populations remains a major concern in the cancer treatment. The development of drug resistance is often correlated with specific chromosomal modifications. Though chromosomal aberrations are generally much more frequent in cancer than in normal cells, there are no qualitative differences between the aberrations in cancer and in normal cells. At present the genetic basis of drug resistance may be induced by gene amplification, which can be alternatively associated with chromosomal homogeneously stained regions or with double microchromosomes. The both phenomena are essentially the same: they reflect the mechanism for the amplification of genes stimulating tumour viability under unfavourable conditions.

The properties and structure of Epstein-Barr virus (EBV) DNA are described. The restriction endonuclease maps of the viral genome are presented. Differences in the structure of DNAs from various subtypes of EBV and their influence on the phenotype status are discussed.

The structure and morphogenesis of the cattle leukemia virus, the main biochemical and immunological characteristics and its antigenic relationship with other members of the family Retroviridae are reviewed.

The data concerning retrovirus HTLV isolated from patients with T-cell leukemia/lymphoma are presented. The virus differs from the known C type viruses, possesses high tropism to T-lymphocytes. The virus is exogenous for human cells and its origin is still unknown. Virus specific nucleotide sequences are absent in a normal cell genome, but they are detected in blood cells and tissues of patients with this form of leukemia. HTLV-associated disease is rare and distributed mainly in two regions in the world: in the South-West of Japan and in the Caribbean islands. Mode of the virus transmission is probably horizontal.

The methods of hybridization in solution and blot hybridization have shown that the BALB/c mice spleen cells contain "silent" genes which can amplificate and change their structure following the infection by the Rauscher leukemia virus (RLV). The product of these gene activation is nuclear 35S RNA detectable by the comparative electrophoretic analysis of heterogeneous nuclear RNA of leukemic and normal cells. The expression of complete copies of 35S RNA was observed in nuclei of RLV-infected cells, while in cytoplasm this RNA is represented by incomplete copies. The expression of the sequences homologous to this 35 S RNA in normal mice spleen cells was not detected.

Tumorigenicity and anchorage independence in two types of the interspecies hybrids of the tumor and normal mammalian cells were studied. One hybrid type was derived from fusion of spontaneously transformed Chinese hamster and normal mouse cells; the second type was obtained by fusion of SV40-transformed Djungarian hamster and the same mouse cells. The tumorigenicity in the athymic nude mice was suppressed in the first type of hybrids. The hybrid clones derived from fusion of SV40-transformed and normal cells could form tumor in nude mice. Testing of hybrid clones for their ability to form colonies in soft agar showed that all hybrids grew well in the medium, similar to tumor parental cells. These data suggest that malignancy and anchorage independence are under separate genetic control. The influence of the origin of the tumor parental cells (spontaneous or SV40-virus transformation) on the expression of the malignancy in hybrids of the tumor and normal cells is discussed.

Four cell lines derived from tumors induced by adenovirus SA7, its DNA (intact and fragmented with restrictase Sal-1), as well as isolated C-Sal-1 fragment (19.5% of genome) containing oncogene were studied. All the cell lines had the phenotypic markers of tumor cells, similar tumorigenicity, and produced T- and S-antigens. The line derived from the tumor induced by intact DNA contained the smallest adenovirus SA7 genome region (12%) which suggests that the information required for the synthesis of T and S antigens of adenovirus SA7 lies within the limits of this genome region.

Some properties of four hybrids between continuous mouse cells Rag and human diploid embryonal fibroblasts were described. During initial four months after fusion, hybrid cells with the parental genome ratio 1 mouse (m) - 1 human (h) were displaced by cells with the ratio 2m - 1h and 3m - 1h. Further passages lead to selection of cells with 10-12 human chromosomes and two and three chromosome sets of Rag cells.

Malignancy and anchorage independence of Djungarian hamster tumor cell lines resistant to different doses (0.1-5.0 micrograms/ml) of colchicine were studied. The clones with low colchicine resistance (15-20-fold) did not differ in tumorigenicity from parental cells. The TD50 for highly colchicine-resistant cells (200-800-fold) was several orders of magnitude higher than that for wild-type cells. Colchicine resistance did not affect the expression of the cells anchorage independence. The cloning efficiency in a semi-solid medium was the same both for colchicine-resistant cell lines and wild-type cells.

Mouse mammary tumor virus (MMTV) is known to infect heterologous cells but it does not appear that it alters their growth or morphological characteristics. Djungarian hamster mammary tumor cells infected with MMTV were found to increase the ability of the above cells to grow in semi-solid media. This effect was demonstrable only in the presence of insulin and dexamethasone in cultural media. Meanwhile non-infected cells were discovered to show no responsiveness to hormones. The expression of non-viral antigen revealed by allogeneic anti-Thy 1.2 on the surface of infected cells was shown by the use of the cytotoxic test and immunofluorescence technique. However, the use of monoclonal anti-Thy 1.2 antibodies failed to prove that antigen in question was structural virion protein or Thy 1.2 antigen.