The hybrid clones derived from the fusion of tumour and normal cells of Djungarian hamster were tested for their ability to grow progressively in vivo and to form colonies in semisolid medium. In all cases the hybrids were able to produce tumours in animals, but tumorigenicity of different clones varied. Some clones had high take incidence of tumours comparable to that of malignant partner, others had a very low one. The hybrid clones differed in their ability to form colonies in soft agar. No correlation was found between the malignancy of the hybrid clones in vivo and their ability to grow in semisolid medium. Chromosome analysis of 23 hybrid tumours arising from the injections of the hybrid cells showed that in 18 tumours the drastic reduction of chromosomes from tetraploid to near-diploid level, comparable to that of malignant parent, took place. As a rule, morphologically unchanged chromosomes were preferentially lost from the hybrid tumour cells, the markers of the malignant partner being retained. Some hybrid tumours showed insignificant chromosome elimination of all pairs, except chromosomes of the IV and VIII pairs, their number always being reduced.

Normal Djungarian hamster lymphoid cells were fused with SV40 transformed malignant fibroblasts. The resulting 11 hybrid clones were subjected to the chromosome analysis. The karyotype of hybrids proved to be unstable. In some cases the total tetraploid number of chromosomes in hybrids drastically decreased up to the near-diploid level close to that of the malignant parent cells. The G-band chromosome analysis showed that as a rule morphologically unchanged chromosomes were preferentially lost from the hybrid cells, the markers of the malignant partner being retained. On the basis of these data it is assumed than the hybrids between normal and tumour cells of Djungarian hamster preferentially lose the chromosomes of the normal parent cells during cultivation in vitro.

By C-method of chromosome staining three transplantable murine tumor lines passaged in vivo were studied. Marker chromosomes were discovered in all cell lines under observation. The previously described marker chromosomes B and C were found in transplantable Ehrlich ascites carcinoma cells, acrocentric chromosome with additional C-band --in cells of line C-37, acrocentric chromosome with double quantity of subcentrometric heterochromatin in cells of line TG-180. The data obtained make it possible to distinguish the lines under study by C-method of chromosome staining.

A study has been made of 7 transplatable lines of mice rhabdomyosarcomas and one line of rat rhabdomyosarcoma during their transplantation into the eye anterior chamber subcutaneous tissue. In all, 10 subcutaneous transplants and 15 transplants into the eye anterior chamber (EAC) were examined. Etanol fixed print smears were subjected to the Feulgen reaction to measure the DNA content using a cytophotometer MCPhU-1; 100 cells being measured in each transplant. In the majority of the EAC transplants, a statistically significant decrease of the karyotypic variability was found in additionto the augmentation to the diploid cell ratio as compared to subcutaneously proliferating populations of the same tumour lines. In some cases EAC transplants displayed exclusively diploid (periploid) populations of tumour myoblasts. Shifts in the karyotypic structure of populations towards diploidy, revealed during the cultivation of transplantable rhabdomyosarcomas, may be regarded as a phenomenon of the "karyotypical normalization" of tumour cells. The disappearance or sharp decrease of tetraploid or hypertetraploid classes of cells in EAC transplants may be due to the increase of their selective value in condition of immunological privilege of diploid, karyotypically normal cells, and of reduction of the genome mutation frequency in a diploid fraction of tumor myoblast populations.

Spontaneous leucosis was cytogenetically studied in subsequent generations (from 1 to 150) of AKR mice. By means of the differential staining technique of chromosomes, large variations in chromosome numbers were found in the karyotypes of leucotic cells of different generations, and the formation of cell clones containing different marker chromosomes as well as the dominance of a hyperdiploid clone with 41-42 chromosomes was revealed. Chromosome analysis of such hyperdiploid cells of the 150th generation has indicated that the supernumerary chromosomes (in 88.0% of cases examined) belong to the smallest chromosomes of the mouse karyogramm (to the 18-19th chromosome pairs or to chromosomes smaller than those of 19th pair). Similar trisomy was also observed in hypodiploid and pseudodiploid leucosis cells. It is suggested that the cell clone with trisomy for the smallest chromosomes is specific to the spontaneous lympholeucosis in AKR mice as well as to the leucosis transplanted to isogenic mice for a number of subsequent generations. Increased rate of hyperdiploid cells was associated with a generalization of leucosis. It was concluded that the development rate and the severity of transplanted lympholeucosis in AKR mice was determined by the domination of the cell clone with trisomy for the 18-19th chromosome pairs in the population of leucotic cells.

An ascite variant of spontaneous mammary gland tumor of C3H/Sn mice was transplanted subcutaneously into syngenic mice. During the tumor growth (150 days) some alterations occur in the genetical structure of the tumor population: a change in the stem line, the increase and a further decrease of nearoctaploid cells.

A study was made of the action of glucose or sodium succinate on subpopulations of the Ehrlich-I.Ch.Ph. ascite strain characterised by markers "A1" and "A", resp. After i.p. injection of glucose the amount of "A1"-cell reached 50 and almost 100% on the 5th and 7th day of tumor growth. After the transplantation of "A1"-cells into intact animals, a homogenous cytogenetic feature of subpopulation persisted during 2 passages only. Kinetics studies of a subvariance of the Ehrlich-I.Ch.Ph. tumor containing "A1"-cells show that the tumor growth rate and grade of malignancy slightly differ from those seen in the controls.