The process of cell generalization of lymphatic leukemia transplanted clone of AKR mice was studied by the routine and differential methods of metaphase chromosome staining. In 99.5% cases, the cells have an additional small chromosome specific for this type of leukemia, the chromosome being comparable in size with 18-19 pairs of chromosomes of mouse karyotype. Generalization process within 7 days' experiment (from the moment of transplantation up to the moment of animals' death from lymphatic leukemia) appeared to be slower in thymus and bone marrow of AKR mice than in spleen, lymphatic nodes and liver of the same animals with nearly the same generalization rate. A change in the frequency of marked leukemic cells in various organs at different time intervals after transplantation of lymphatic leukemia correlated with intensive cell division of an undulating character in all organs. The data obtained show that hyperdiploid cells carrying the specific additional small chromosome are responsible for the generalization process, this chromosome being also present in spontaneous strain of AKR mice, from which this clone was obtained.

The library of genes was obtained from erythroleukemic AKR cells (C-1), that were maintained as suspension culture. Thirty four clones that had homology with 60-70S RNA of Rauscher Leukemia virus (RLV) were separated from this library. The restriction mapping was carried out with 14 clones, that contained most extensive proviral sequences. One clone (107) contains proviral sequences that are derived from one of the components of the RLV complex. The other 13 clones contain sequences of endogenous xenotropic viruses. The endogenous retroviral sequences obtained differ in restrictive maps from proviruses of ecotropic and xenotropic infectious endogenous MuLV and, apparently, might be attributed as non-inducible infectious xenotropic MuLV of class III. Some of the cloned retroviral sequences had symmetrical structure, that is typical for integrated proviruses, i. e. these sequences were separated from flanking cellular ones by long terminal repeats. All investigated retroviral sequences are deletion mutants of MuLV proviruses. It was shown that the inner regions of proviruses diverged more than the long terminal repeats. The expression of the main inner MuLV polypeptide (p30) was detected in NIH 3T3 cells, transfected with DNA of some clones.

In genome of all transforming retroviruses special genes (oncogenes) have been identified which play a key role in malignant conversion of the cells, infected with these viruses. The homologues of these genes (protooncogenes) are persist in all normal cells. During transformation protooncogenes can be activated as a result of one of following processes: insertion of promotor-like elements, mutations, translocations, amplifications or rearrangements. Using transfection technique the transforming genes were isolated from different human tumors. The activation of one of the cellular oncogenes may switch on the other genes and malignant cell transformation may be characterized as a multifactor and multistage process.

The spontaneous rate of occurrence of two characters of malignant transformation was studied in mouse embryo fibroblasts C3H10T1/2, clone 8. This cell line, though "immortal" in vitro, is characterized by a normal phenotype in respect to many other properties. The spontaneous rate of occurrence of anchorage-independence (aga+) and dense foci on cell monolayer varied in different experiments from 0.65 X 10(-6) to 1.2 X 10(-6) and from 1.2 X 10(-6) to 3.6 X 10(-6) per cell per generation, respectively. The fluctuation test has shown that both characters occur as random spontaneous events. The altered colony morphology proved to be stable in all 28 foci of independent origin tested. In most cases, the morphological transformants were anchorage-independent. It is suggested that the occurrence of the characters studied is due to mutation in a gene with pleiotropic effect.

The paper presents cytogenetic data available in literature concerning results of the study of malignant somatic cells at chromosomal and genetic levels in the pretumour period and in advanced tumours.

Provirus from a component of Rauscher leukaemia virus (RLV) has been cloned. The provirus (the size of 5000 b. p.) contains two LTR sequences and shares expressed sequence homology with Mo-MuLV. Restriction analysis and determination of the LTR nucleotide sequence and of the site from 3'-end of proviral genome have shown the cloned provirus to be the SFEV component of RLV. LTR from this cloned provirus contains all sites necessary for transcription: CAAT and TATA sequences, "cap" site and polyadenylation signal. The LTR of the cloned provirus from SFEV component of RLV has been shown to function as a promoter in E. coli cells.

It was shown on Ehrlich ascites tumor cells that for realization of the radioprotective effect of anoxia and beta-mercaptoethylamine normal content of glutathione is necessary not only at the time of irradiation but in the postirradiation period as well while glutathione content should be normal only after irradiation for realization of the radiotherapeutic effect of serotonin.

Linear differences were discovered in the quantitative ratio and proliferative activity of the cells of the epithelium and mesenchyma of organ cultures of the normal embryonal pulmonary tissue of mice resistant (C57BL) and predisposed (A) to lung blastomogenesis. In A mouse embryos, the index of the cell labels of the bronchiolar epithelium and fibroblast-like cells of the mesenchyma which migrate on the surface of the membrane filter was several times higher than that in C57BL mice. The number of the mesenchymal cells capable of migration in A mouse explants was essentially greater, that of the mesenchymal cells being in a direct contact with the epithelium of alveoloid and bronchiolar structures was, on the contrary, lower than in C57BL mouse explants. It is suggested that the differences described, particularly epithelial-mesenchymal interactions, are of importance for realization of the genetically determined sensitivity of these mice to spontaneous and induced lung blastomogenesis, which manifests as early as during prenatal ontogenesis.

The paper reports reasons for a possibility of tumour regression due to selection of low-malignant and differentiating clones. Experimental evidence is provided supporting this view.

A comparison of the expression of two mobile genetic elements A1 and B2 was studied in normal and tumor tissues. The A1 element is a chromosomal homolog of IAP genes, and B2 is a short ubiquitous repetitive sequences of the mouse genome. These sequences were earlier cloned in our laboratory and in this study were used as probes in hybridization experiments with RNA isolated from different mouse tumor and normal tissues. Both elements were efficiently transcribed in tumor cells. The level of expression of A1 sequences in tumors was 100-200 times higher than in normal tissues. The amount of B2 small cytoplasmic RNA significantly varied in different normal tissues. The content of this RNA was much higher in tumors. Closed circular DNA molecules containing IAP sequences were found in Ehrlich carcinoma cells. These DNA molecules are considered as intermediate forms of the mobile elements. The role of these mobile elements in the regulation of RNA expression and tumor progression is discussed.

Northern blot hybridization of nuclear, cytoplasmic and polysomal poly(A)+RNAs from different normal and tumor mouse cells was carried out with labelled separated DNA strands of the cloned cDNA fragment containing repetitive B2-element. Several important results were obtained in these experiments: (i) while nuclear RNAs contain copies from both strands of B2 element, only one strand ("canonical" orientation) of B2 can be detected in the mature cytoplasmic poly(A)+RNAs of all mouse tissues studied, (ii) the abundant 2 kb B2+mRNAx is tissue-specific for mouse liver and kidney cells, its transcription is greatly increased in regenerating liver and completely abolished in hepatoma, (iii) an elevated level of small B2+RNAs and 1.6 kb B2+RNA in some tumor cells is observed, (iv) differential transcription of the major classes of B2+RNAs in different mouse tissues suggests the non-coordinated regulation of their expression.

Cytogenetic analysis of 15 retinoblastomas developed in children having no constitutional chromosome 13 deletion has been carried out. In tumor cells, no deletion or loss of chromosome 13 was revealed. The specific marker chromosome i(6p) described in our previous publications has been found in 9 tumors. Besides, in two cases, trisomy of short arm of chromosome 6 was present. Other non-random changes (trisomy 1q, monosomy 16 and loss of one of the sex chromosomes) were not specific for retinoblastomas, because they were described in literature for some other tumors as well. The possible significance for genesis of retinoblastomas of dose multiplication of the genes located in the 6p is discussed.