An analysis of 422 Moscow hospital records of children suffering from acute leukemia during the period from 1959 and continuing through to 1979 showed that the proportion of those with morphologically "average" weight and body length values at birth, was significantly lower in the group with leukemia, than in the control group of healthy children. Genetic structure of leukemic and healthy children was found to be significantly different by phenotypic combinations of 2 loci (ABO and Rhesus). The distribution of children for their age at the beginning of the disease was studied. The results revealed that children with the low weight and body length values at birth, as well as those having ARh+ and BRh+ blood groups, develop leukemia earlier than those with "average" characteristics and blood groups other than ARh+ and BRh+. The anamnesis of children which developed leukemia demonstrated a higher infectious-inflammatory disease frequency, as compared with the control group. By comparison of some parental characteristics of two groups of children, it was found that parents of children which became ill, were on the average older at the moment of baby's birth than parents of healthy children. Babies of 2nd, 3rd and subsequent deliveries were registered more frequently in the group with leukemia than in that of healthy children. Evidence presented confirms the efficiency of the population-genetic approach to the problem of nonspecific resistance of human organism to diseases.

Morphological, caryological, cytoproliferative, and isoenzyme studies of Syrian hamster cells HTC-2 and HTC-1 transformed by herpes simplex virus type 2 and a HTCT line of tumor cells were carried out. The hamster origin of these cell lines was established by chromosomal analysis and electrophoretic mobility of lactate dehydrogenase and glucose-6-phosphate-dehydrogenase isoenzymes. The transformed and tumor cell lines differ from normal cells by altered morphology, an aneuploid chromosome set and increased proliferative activity. Electron microscopic examination of transformed cells revealed increased amounts of filamentous and tubular structures in the cytoplasm. No retroviruses were found.

Attempts have been made to find out 1/whether there is an interaction between normal killers (NK) and tumor cells transplanted in vivo and how both effectors' cytotoxicity against the third participant - NK-sensitive target cells, is affected by the hypothetical interaction; and 2/the implication of H2-complex in the interaction of both the effectors. Use was made of an experimental three-component model in vitro. It included the effector cells of two types. As NK use was made of splenocytes from C57BL/6; CBA; B10; SM; B10.D2; B10.A(3R); B10.A(5R); BALB/C; A/Sn; B10.D2(R107); B.10.D2(R101) mice. Tumor effectors were EL-4 MX-11 (H2b), L-1210 (H2b) and SA-1(H2b) cells transplanted on syngeneic mice. EL-4 cells adapted in culture in vitro were used as standard target cells. Two types of the effector interaction are described. The homology of NK and tumor effector cells in the D-end of H2-complex in the I-C subregion was found to lead to a marked mutual suppression of both the participants with reference to the third component - EL-4 target cells adapted in vitro. The absence of homology in the DC-end of H2-complex provided an opposite effect - summation of cytotoxicity of NK and tumor effector cells against EL-4 target cells. The authors discuss whether the cause of mutual suppression is repaired cytotoxicity (or membrane toxicity) of NK and tumor cells.

The synthesis of globin mRNA in cultured murine erythroleukemic cells transformed by the Rauscher leukemia virus and in the spleen of mice with Rauscher erythroleukemia was studied. The content of globin RNA sequence was estimated by cDNA hybridization with increasing amounts of cytoplasmic and poly (A)-containing RNA Globin RNA was found in the spleen of mice with Rauscher erythroleukemia, its content in cytoplasmic RNA and poly (A)-containing RNA being 0.02% and 0.4%, respectively. By contrast, no globin RNA sequences were found in transformed cultured murine erythroleukemic cells, which can be a cause of altered hemoglobin synthesis in these cells.

The viral theory of tumor origin has proved to be an important factor of accumulation of fresh evidence and working out new methods and approaches. The paper contains a summary of this evidence and discusses the problem of the indirect co-carcinogenic effect of tumor-inducing agents. Sometimes it is due to their activation of specific oncogenic viruses. In other cases, as the author suggests, it may be caused by the activation of potential oncogenes (protooncogenes) or normal cells. There are viral and non-viral tumors and human tumors are apparently chiefly non-viral. The author suggests that it is an endogenous disease (protooncogenes and their endogenous activators). The author considers his hypothesis (1962) on the cellular origin of oncogenes and the similarity of their transmission by viruses to microorganism transduction. A similar suggestion was made by P. Vogt and A. D. Altstein ten years later and it has been supported by some findings ever since. The viral theory cannot be regarded as the sole fundamental theory of carcinogenesis.

Tumor cells in lymphogranulomatosis include Hodgkin's cells, Berezovsky-Shternberg cells and variants thereof representing a single population characterized by aneuploidy, polyploidy, and marker chromosomes. All cells of this clone are capable of DNA synthesis and mitotic division. As the disease progresses, the number of tumor cells increases gradually. Their origin is still obscure. The hypotheses of their origin from B-lymphocytes because of the presence in them of cytoplasmic and surface immunoglobulins and also from macrophages because cells of tissue culture from tumor nodes were found to have nonspecific esterase, lysozyme, capacity for phagocytosis seem to be substantiated.

The object of the research was to examine whether tumor cell membranotoxicity as regards splenocytes depends on the protein synthesis in the latter ones and whether it depends on the similarity or differences in the subregions of H2-complex. As effectors the following tumor cells transplanted in syngeneic mice were used: EL-4 (H-2b), MX-II (H2b), L-1210 (H2d), SA-1 (H2a). As target cells, the splenocytes from the following mice were used: B10/Sn, C57BL/6, B10.A (3R), B10.A (5R), B10.D2, B10.SM, CBA, B10. D2 (R 101), B10.D2 (R 107). It was shown that noncoincidence of the effectors and targets as regards the genetic basis, K, IA, IB, IJ, IE and D-subregions does not lower the maximal membranotoxicity inherent in the entire syngeneic system. Noncoincidence of the effectors and targets as regards the D-terminal of H-2 complex reduces more than 2-fold the effect of tumor cells on splenocytes. Thus, the coincidence of the effectors and targets only as regards the IC-subregion of H-2 complex is enough for attainment of the maximal membranotoxicity of tumor cell as regards splenocytes. It is discussed whether the injury to the target membrane (membrane toxicity) recorded in the research under consideration should be considered as cytotoxic (the target death) or as cytostatic. It is suggested that the phenomenon studied may underlie the immunosuppression due to tumor cells.

Restriction analysis of hybrid plasmids from a number of clones allowed to screen out the plasmid p8-1. A detailed analysis of this plasmid and that of the inserted DNA was made using HhaII, AluI, Sau96I, Sau3A, MspI and BspI restriction endonucleases. The results demonstrated that the inserted DNA corresponds to the 3'-nontranslated region and to a portion of the C fragment of the light-chain immunoglobulin gene. Establishing the partial structure of the recombinant plasmid exhibited a complete coincidence of the inserted DNA 3'-terminus and the primary structure of the light-chain mRNA synthesized by MOPC-21 myeloma cells. This sequence corresponds to the amino acid sequence in the light-chain constant region (207-214 residues). The analysis of p8-1 plasmid showed that nucleotides of pBR322 plasmid at positions from 376 to 618 were deleted. The deletion might be predetermined by the plasmid property to be amplified more readily than all the other hybrid plasmids which were not deleted.

The copy-DNA was synthesized on the mRNA fraction which was isolated from MOPC 21 mice myeloma by reverse transcription. This copy was completed with another chain without adding the exogenous primer, with the aid of the Klenov fragment of DNA polymerase I. After treatment of the double-stranded pin DNA with endonuclease S1, the poly(dA) sequences were built up using terminal deoxynucleotidyl transferase. The building up of the poly(dT) sequences at the DNA 3'-termini of pBR322 plasmid previously treated with BamHI was performed in a similar way. The average length of connecting polynucleotide sequences was 50 nucleotides. After annealing and transformation of the cells with Escherichia coli hybrid plasmids, selection of clones was made for ApRTcS phenotype. Further, we applied a stepwise selection of clones by means of increasing the specificity: colony hybridization, quantitative hybridization of the excess of plasmid DNA with (32P)-cDNA and hybridization of plasmid DNAs with mRNA units which were transferred from electrophoregrams to the diazo-papers. As a result, bacterial clones were selected which contained gene fragments showing the ability to hybridize with the RNA fraction characterized by mRNA mobility of the light-chain immunoglobulin G.