An observation of multiple primary tumors of various histogenesis and a rare combination (uterine body carcinoma, mammary fibroadenoma, bronchial carcinoid, jejunum carcinoma) developing in a female patient at various periods of her life is described. The autosome-dominant type of the transfer proves the possibility of a genetic predisposition of the tumor development (the patient's mother and brother also had tumors). This observation demonstrates the variety of tumor combinations and tumor topography in cases of genetically predetermined blastomogenic process. This may represent a basis for distinguishing separate variants of Fraumeni syndrome.

Both c-myc and c-Ha-ras 1 oncogenes amplification and enhanced expression were revealed in some human mammary and thyroid carcinomas by the molecular genetic analysis. Amplification proves to be a second possible molecular mechanism of the ras family protooncogene activation besides a point mutation. The coexistence of c-myc and c-Ha-ras 1 in some human primary carcinomas suggests a multistep process of carcinogenesis.

The structure of DNA sequences homologous to the viral myc oncogene from ovarian tumours, intact tissues and the same patients peripheral blood leukocytes has been studied. The Southern blot analysis of malignant tumour DNA reveals amplification of c-myc protooncogene of 3 from 11 patients. Metastases DNAs of two from those patients also contain multiple copies of c-myc. No myc gene amplification has been detected in 6 examined benign ovarian tumours. The presence of extra copies of myc-related sequences has been shown in two from three DNA samples from peripheral blood leukocytes of patients with ovarian cancer.

The restriction analysis of BALB/c and AKR mice genome DNA was used to show the translocation and amplification of gene which is expressed with the Rauscher erythroleukemia as the 35S nuclear RNA. The homology of this RNA to 10 defined oncogenes was studied. It was found that the cDNA 35S RNA is efficiently hybridized only with v-sis oncogene. The clones homologous to the 35S RNA, v-sis oncogene and 3'-area of the Rauscher leukemia virus genome are isolated from the genes' library of mice erythroleukemic cells.

The role of bovine leukemia virus (BLV) expression was demonstrated in normal, BLV-infected and leukemic cattle. The studies established the changeable character of viremia on the basis of BLV p24 expression in blood plasma and native leukocyte lysates. The experiment revealed a marked regularity: a decrease of antibody titer in blood serum--the appearance of the virus in the body--lymphocytosis. The development of lympholeukemia shortly after experimental infection was detected in animals with an antigen regularly detectable in the plasma.

The complex morphocytochemical, immunological and cytogenetic investigation of the blast cells in acute lymphoblastic leukemia showed their considerable heterogeneity. There were several kinds of cells: typical blast cells, Ph'-positive blast cells expressing only Ia-like antigen and anaplastic blast cells with myeloid and erythroid differentiation.

Three syndromes of multiple endocrine neoplasia (MEN) have been identified to date: MEN--I, IIa and IIb. They involve various combinations of endocrine neoplasia and occur mostly in young patients. Predisposition transmission mechanism is autosomal-dominant with total penetration and variable expressiveness. Patients' families should undergo screening which involves identification of biochemical markers and cytogenetic examination. This would allow identification of subjects at high risk for cancer and improvement of early diagnosis.

The results of clinico-genealogic analysis of 46 patients with primary-multiple malignant neoplasms are given (among them 16 patients with primary-multiple malignant neoplasms of colon cancer and 30 patients with one or more neoplasms in combination with different malignant tumors of other organs). The values of segregation rates obtained for primary-multiple malignant neoplasms are lower than theoretically expected for simple monogeneous types of inheritance. The relation analysis of primary-multiple malignant neoplasms and colon cancer revealed that these tumors are likely to appear among relatives of probands under the influence of the same genetic system of determination. Risk of the colon cancer development for relatives of the patients with primary-multiple malignant neoplasms is higher than for relatives of the patients with colon cancer.

Linoleic acid hydroperoxides delivered to Ehrlich ascites tumor cells in vitro in a concentration reaching a threshold one (approximately 10(-5) M) sharply decrease their ionic permeability and the value of membrane capacity. With suprathreshold hydroperoxide concentrations (greater than 10(-5) M), the specific yield of chromosome aberrations and the share of aberrant cells increase while the mitotic index decreases. The correlation between general regularities and the equality of the threshold concentrations, with a reference to membrane and genetic effects of hydroperoxides, is thought to be an indication of a close relationship between membrane lesions caused by the development of induced lipid peroxidation and injury to genetic apparatus of the cell.

Using ascite tumour cells (Ehrlich carcinoma, plasmacytoma MOPC-21, leukemia P-388, lympholeucosis NK/Ly) and bone marrow cells of intact rats, the possibility of regulation of transcription of a gene encoding 35S RNA via the alteration of the univalent cations Na+/K+ intracellular ratio was demonstrated. Gene 35S RNA was transcriptionally active within the range of 1 less than or equal to Na+/K+ less than 3 but was switched off at Na+/K+ less than 1. In synchronized Ehrlich carcinoma cells this gene was activated at the early steps of the mitotic cycle, when the cationic ratio was above 1. It was assumed that the so-called cationic mechanism of regulation of transcription predetermined the time and other of stimulation of certain genes in the course of the mitotic cycle and provided for the transcription of normally repressed genes as a result of malignant transformation.

A high increase in transcriptionally active DNA fraction (TA DNA) has been detected in the thymus of young AKR mice and in thymoma. Hybridization of TA DNA with [32P] cDNA synthesized on poly A+-mRNA of cortisol-induced animals has shown that TA DNA of young AKR mice contains 40 times as much cortisol-activated repeated sequences (RS) as that of thymoma. The decrease of cortisol-activated (RS) in AKR thymoma TA DNA was found to be the result of their transition into transcriptionally inactive (TI) DNA. It is concluded that chromatin conformation changes take place in cortisol-activated RS DNA region of AKR mouse thymus before transformation. Unstable conformation of RS DNA in the thymoma can possibly promote their transition into TI DNA.

High molecular weight DNA prepared from three undifferentiated human stomach carcinomas was assayed for transforming activity by transfection of mouse NIH 3T3 cells. One tumor DNA sample (stomach carcinoma CaVSt) induced (the transfection efficiency: 0.02 transformants/micrograms DNA X 10(-6) cells) transformation of NIH 3T3 recipient cells. Transforming gene of Ha-ras type was identified in transformants derived from this human carcinoma. The genetic lesion responsible for the activation of the CaVSt Ha-ras oncogene is not localized in the 12-th codon for p21c-Ha-ras protein.

The structure of subjection to different clinical forms of colon cancer and to the morbidity as a whole approximates better the quasi-continued phenotypical model within which the contribution of genetic factors reaches 68-84%, that of incidental medium factors being 16-32%. Genetic study of heterogeneity of colon cancer clinical forms revealed that their pathogenetic community was quite high. However, the origin of colon cancer depends strongly on genetic factors (83.7 +/- 7.3%), in comparison with rectal cancer (67.9 +/- 7.1%). The analysis of colon cancer interrelation with other malignant neoplasms (including specific ones for women--breast and uterus cancer) revealed that the development of another malignant neoplasms was the result of the influence of partially common genes (20-50%) which predetermined the development of colon cancer and other malignant neoplasms. According to the data obtained in this study, the tables of repeated risk have been worked out which may be used for medico-genetic consultation.

It was shown that gamma-irradiation of Zajdela hepatoma cells (10 Gy) induces inhibition of DNA synthesis initiation at a nuclear matrix and a change in its DNA-protein content. Irradiation of hepatoma cells with 10 and 50 Gy decreases incorporation of newly synthesized proteins in the firmly bound DNA-protein complexes of nuclear matrix. After 60-120 min postirradiation incubation of cells at 37 degrees C DNA-protein content of the nuclear matrix and its firmly bound DNA-protein complexes are restored. However the rate of DNA synthesis initiation being below the control level.

A study was made of the effect of poly(ADP-ribosylation) of proteins on the formation and repair of single-strand DNA breaks in gamma-irradiated (50 Gy) permeable Zajdela ascites hepatoma cells permeabilized by the treatment with 0.05% triton X-100. Incubation of gamma-irradiated permeable cells in conditions promoting DNA synthesis and providing ADP-ribosylation (in the presence of 1 mM NAD) did not cause any substantial changes in the formation of single-strand DNA breaks and did not influence their repair.

The analysis of 11 various oncogenes expression in different human tumors showed that each tumor is characterised by a specific functioning program of these genes. In 40-50% of tumors the oncogenes ras, fos and myc are expressed. All other oncogenes are either considered to be "silent" or are expressed only in few cases. The increased expression of sis and myb oncogenes is observed in metastases.

The data on clinico-genealogic studies of colon cancer are presented. 694 families were examined with 432 probands having rectal and 262 colonic carcinoma among them. Clear family accumulation of colon cancer (2.4 +/- 0.35%) as well as other malignant tumors (6.8 +/- 0.6%) (p less than 0.01) was shown among the relatives of the first degree of relation. The values of segregation rates obtained for clinical forms of colon cancer were lower than theoretically expected for simple monogenic types of inheritance. The analysis of incomplete penetration of genotypes showed that, though formally the inheritance of colon cancer and its clinico-anatomical forms may be described by quasi-dominant types of inheritance, the penetration values are very low: from 4.3 to 13.3% for homozygotes and from 2.1 to 6.6% for heterozygotes. It shows that the supposition about the monogenic types of the colon cancer inheritance is doubtful and suggests that the colon cancer is to be regarded on the basis of the multifactorial model.