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I F Seĭts

Publications and source records attributed to I F Seĭts.

At least 19 recordsLinked to original sources
PubMed1990

[The role of proto-oncogenes in fundamental manifestations of life].

Problems of the origin, structure and functions, in the cells and tissues, of the so-called proto-oncogenes (c-onc)--cell genes, homologues and oncogene foreparents (v-onc)--are considered in the review. Up-to-date data are given to show the participation of the main groups of proto-oncogenes in the processes of cell division, proliferation and differentiation. The role of c-onc genes is found to be important for fundamental manifestations of the cell life activity. Special attention is paid to the problem of interrelation of the proto-oncogenes with growth factors and their receptors.

Animals↗
PubMed1990

[Frequency and rearrangements of alleles of proto-oncogene c-Ha-ras-1 and their association with development of various malignant tumors in man].

The c-Ha-ras-1 locus in 84 cancer patients was examined for allelic restriction fragment length's polymorphism, as well as for distribution of four common c-Ha-ras-1 alleles (a1, a2, a3 and a4) in lung, ovarian and thyroid cancer patients. In approximately half (8 out of 15) lung and ovarian carcinomas possessing a4 allele, alterations in the Ha-ras locus (deletion, amplification and change in allele length) were detected, as compared to 2 cases of rearrangements out of 40 tumors lacking the a4 allele. An increased a4 allele frequency was found in individuals with lung and ovarian carcinomas, as compared to both controls--summarized literature data, and thyroid cancer patients. On the other hand, homozygosity for the a2 locus, resulting from deletion in another allele, and increased a2 allele frequency in thyroid cancer patients were observed. Thus, a4 and a2 alleles of the c-Ha-ras-1 may perhaps be viewed as genetic markers of predisposition to lung, ovarian and thyroid cancer, respectively, in combination with other clinical parameters.

Alleles↗
PubMed1989

[Can the presence of an RNA-lipoprotein complex in human blood serum give evidence of a cancerous disease?].

The fractional composition of serum lipoproteids in patients with malignant tumours and in noncancerous disorders as well as in healthy donors has been investigated to detect the cancer specificity of the appearance of the additional abnormal RNA-lipoprotein fraction. No distinct correlation is found between the presence of the additional serum lipoprotein fraction and human malignancy.

Blood Donors↗
PubMed1989

[Polymorphism of restriction fragments of the Ha-ras-1 protooncogene in patients with carcinoma and ulcers of the stomach].

Ha-ras restriction fragments' length polymorphism (RFLP) in white blood cells and stomach tissues from patients with carcinoma and ulcer of the stomach was examined. Genomic DNAs were digested with Xho I, Pvu II, Pst I, Msp I, Bcn I, Mva I, Bsp RI. No Ha-ras-1 polymorphic variants specifically associated with the cancer disease were detected. RFLP of the 3'-noncoding sequence of c-Ha-ras-1 gene had got features of the definite human population. The cells forming the tissue were examined and individual peculiarity of the methylated residues disposition seemed to influence RFLP of the 5'-noncoding sequence of c-Ha-ras-1.

DNA↗
PubMed1988

[Pepsinogen messenger RNA of human gastric mucosa and stomach cancer].

The cell-free translation method has shown that pepsinogen mRNA is a predominant fraction in the total poly(A)+ RNA from human gastric mucosa. The pepsinogen protein with the molecular weight of 45 kDa has been identified. The level of pepsinogen mRNA decreased in tumours as compared with normal mucosa but in most cases pepsinogen mRNA synthesis depression was not total.

Electrophoresis, Polyacrylamide Gel↗
PubMed1987

[Molecular-genetic aspects of drug therapy of malignant tumors].

State and prospects of the drug cancer therapy are examined in the light of achievements of modern molecular oncology. Special attention is paid to the molecular genetic analysis of the appearance of individual and multiple cellular drug resistance in connection with amplification of definite genes as well as oncogenes. The idea about the possible role of oncogene activation as a universal cell reaction in response to an injury of environmental factors is advanced. It concerns both oncogenesis and induction of cancer cell drug resistance.

Animals↗
PubMed1986

[Changes in the content of pepsinogen messenger RNA in the gastric mucosa of rats during N-methyl-N'-nitro-N-nitrosoguanidine-induced carcinogenesis].

Pepsinogen mRNA is shown to be the major fraction of rat poly (A)+RNA. It codes polypeptide with molecular weight of about 45 kD. Changes in the pepsinogen mRNA content at the early stage of carcinogenesis are nonspecific and are due to the toxic effect of MNNG. Steady shifts in the quantity of pepsinogen mRNA are found between the 1st and 3d months. Pepsinogen mRNA content decreases down to the half of the normal one between the 3d and 6th months. A quantity of RNA capable to be a template for pepsinogen synthesis is reduced by more than 90% in the MNNG induced tumour. The pepsinogen production defect in gastric mucosa neoplasia is mainly due to pepsinogen mRNA synthesis damage.

Animals↗
PubMed1986

[Virus-specific proteins in cells transformed by the chicken sarcoma virus D6].

The structural proteins and the oncogene product of the avian sarcoma virus (ASV) D6 were analyzed by the radioimmunoprecipitation. ADV D6 was obtained from the chemically induced tumour. ASV D6 contains all the structural proteins found in RSV, but some of them (p19, gp 85) differ from those of RSV. The product of ASV D6 oncogene is pp65src. The protein kinase activity of this src protein is identical to that of wt pp60src. The nature of some other proteins, which can be phosphorylated in this reaction, is discussed.

Animals↗
PubMed1986

[Molecular mechanisms of the transformation of protooncogenes into oncogenes].

The problem of cellular protooncogene activation is considered. This stage during carcinogenesis is evaluated as critical in the whole process of neoplasia development. Four possible principal pathways of protooncogene activation are discussed: oncogene amplification; chromosomal translocations; insertions and transpositions of genetic material; point mutations. Two ideas in carcinogenesis based on the oncogene conception have attracted special attention: the "dose hypothesis" emphasizing the importance of the quantitative changes of oncoproteins and the idea of the qualitative alterations of protooncogenes.

Humans↗
PubMed1986

[Changes in the supramolecular structure of chromatin and pepsinogen synthesis in the gastric mucosa of rats undergoing N-methyl-N'-nitro-N-nitrosoguanidine-induced carcinogenesis].

A model of gastric tumour induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in rats made it possible to detect essential alterations of chromatin-DNA-protein complexes, that is a weakening of the DNA-protein linkage. The changes appear at early stages of carcinogenesis and persist in induced adenocarcinomas of the stomach. Simultaneously an inhibition was established in pepsinogen synthesis during MNNG carcinogenesis, which reflects a damage in expression of functionally important genetic information. This fact shows a molecular-genetic connection between the process of the gastric mucosa malignization and a disturbance of physiologically important tissue-specific gene functions.

Adenocarcinoma↗
PubMed1985

[Use of nucleic acid preparative electrophoresis in molecular oncological research].

Application of preparative electrophoresis in agarose gel for isolation of chromosomal and extrachromosomal genetic elements is described. The above-mentioned method is used for fractionation of chromosomal DNA according to the molecular weight; for isolation of the plasmid containing the insertion of the viral oncogene myc and for separation of the viral oncogene myc insertion from the vector (a linear form of plasmid pBR 322). The method can be successfully applied in molecular biology, microbiology and medicine.

Chromosomes, Human↗
PubMed1985

[Changes in the pepsin activity of the gastric mucosa of rats in the early stages of carcinogenesis].

The paper discusses changes occurring in the enzymatic activity of pepsin in rat's gastric mucosa at early stages of carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine treatment with drinking water. All doses (5, 15, 45, 75 and 150 mg/l) proved to be effective and inhibited pepsinogen biosynthesis considerably. Particularly sharp drops in the enzyme activity were observed with the concentrations of 45, 75 and 150 mg/l. The effect was reversible at early stages, particularly, at low concentrations of the agent. It is suggested that the critical point reached by pepsinogen synthesis in gastric mucosa carcinogenesis, which is manifested by the enzyme synthesis resumption on treatment being suspended, may be regarded as the check point in the course of neoplastic development.

Animals↗