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G M Volgareva

Publications and source records attributed to G M Volgareva.

32 records · Page 2Linked to original sources
PubMed1982

[Gene mutation induction by the antitumor preparation ftorafur].

The influence of antitumor drug ftorafur (Ft) on the frequency of gene mutations to 8-azaguanine resistance was investigated. Asynchronous and synchronized cultures of SV40 transformed Djungarian hamster cells were used. The 2 to 3,5 fold increase in the frequency of gene mutations over the control level was observed after the Ft treatment. The most pronounced effect was obtained in the experiments with synchronized cultures, when exposed to Ft in the S-phase of the cell cycle.

Animals↗
PubMed1981

Clastogenicity and sister chromatid exchange induction by ftorafur.

The main effect of Ftorafur at the chromosomal level is the induction of chromatid and chromosome breaks, which is some pronounced in neoplastic or transformed cells than in normal cells. Different cell lines used in the study exhibited both in vitro and in vivo varying sensitivity to Ftorafur. Ftorafur does not increase the frequency of SCE.

Animals↗
PubMed1979

[Effect of ftorafur and 5-fluorouracil on the chromosomes of human tumor cell cultures].

The effect of two antitumour drugs, ftorafur (Ft) and 5-fluorouracil (5-FU) on chromosomes of human tumour cells (strain CA-1) was studied in vitro. Since no data on the karyotype of this tumour strain had been published, the chromosome set of the model was investigated at first. Significant quantitative and structural divergence from the normal human male karyotype were observed. Steam line cells contained 47-49 chromosomes, including 9 permanent markers. No Y-chromosome was revealed. Ft and 5-FU hardly injured the chromosomes of CA-1 cells; the level of aberrant metaphases reached 94%. Chromatid deletions and gaps formed the major part of drug-induced cytogenetic abnormalities.

Cells, Cultured↗
PubMed1978

[Action of ftorafur on the chromosomes of normal and tumorous cells of the Djzungarian hamster in vitro].

The chromosome-breaking effect of antitumor agent ftorafur (0,1 mg/ml) was studied on cell cultures of normal and transformed Djungarian hamster's fibroblasts. After 24 hours of exposition with the drug 79% of aberrant malignant cells was registered, while the chromosomes of normal cells remained undamaged. After ftorafur's action for 2--12 hours and the following removal of the agent the level of aberrant metaphase among normal cells rose to 11--15%. Chromatid breaks were the predominant type of drug-induced aberrations. Thse results confirm the idea that ftorafur blocks the cell cycle of normal fibroblasts and that it's necessary to wash the drug off some period before fuxation in order to reveal its chromosome-breaking effect in metaphase cells. The striking distinctions in susceptibility of normal and malignant cells to the mutagenic effect of ftorafur is partly due to the distrubances of the cell cycle caused by this drug.

Animals↗
PubMed1977

[Mechanism of the chromosome damaging effect of ftorafur].

Chromosome damage induced by three antineoplastic drugs -- ftuorafur (Ft), 5-fluorouracil (5-FU) and 5-fluorodeoxyuridine (FUdR) hase been studied in Djungarian hamsters cell line after 24 hours exposition with these agents before the fixation. Ft at a dose of 10 micron/ml induced aberrations in 56.7% of metaphases. 60.0% of aberrant metaphases were obtained in experiments with 0.1 micron/ml of 5 FU. FUdr at the same dose induced 24.0% of aberrant metaphases. The high frequency of chromatid breaks and gaps was typical for the mutagenic action of these fluorinated pyrimidines. The addition of Ft or 5-FU to the cell cultures 1--12 hours before fixation did not produce any significant chrosome damage, while further exposition with the drugs for 15--24 hours caused breaks in more than 50% of metaphases. Thymidine at a concentration of 1.0 micron/ml suppressed the chromosome breaking effect of Ft and 5-FU. The results obtained are in accordance with the idea that fluorodeoxyruidinemonophosphate is the ultimate mutagen for both Ft and 5-FU and that the aberrations observed are due to the lack of thymidine nucelotides caused by the former agents while DNA replication.

Animals↗
PubMed1977

[Action of ftorafur and 5-fluorouracil on the chromosomes of normal and tumorous cells in vivo].

No chromosome aberrations were found in the bone marrow cells and Djungarian hamster tumor cells and bone-marrow cells of thymectomized mice receiving different doses of fluorafur and 5-fluoruracil in vivo. The time of exposure to these antitumor drugs varied from 2 to 72 hours. 12% of aberrant metaphases under 400 mg/Kg of fluorafur and 38%--under 200 mg/Kg of 5-fluoruracil were found in cells of human colonic tumor trasplanted into thymectomized mice.

Animals↗
PubMedDate not supplied

[Search for biological remedies for fungi of the Candida genus].

51 bacterial strains were studied with a view to find out anticandidial activity; of these, 15 strains were found to have activity, more on less expressed with respect to fungi of the genus Candida. In most cases the anticandidial activity of an antagonist strain was manifested to a similar degree against several Candida strains. The preliminary analysis of antifungal substances produced by microbial strains makes it possible to suggest their antibiotic nature.

Bacteria↗
PubMedDate not supplied

[Expression of the protein marker p16INK4a in the cervix uteri cancer].

Immunohistochemical study was carried out of 18 cervical carcinomas (13 squamous and 5 adenomatous) and of 3 cases of cervical intraepithelial dysplasia. Formalin-fixed paraffin-embedded tissue samples from biopsies as well as from surgical material were used. Staining was performed with monoclonal antibodies to protein p16INK4a. Cytologic smears of epithelial cervical cells from 7 healthy women were taken as a negative control. The reference group consisted of 5 cancer patients with other tumors (breast cancer, B-cell lymphoma). Overexpression of p16INK4a was registered in cervical cancer.

Adenocarcinoma↗
PubMedDate not supplied

[Interaction of viral and cellular genes in cervical tumors].

The results obtained in the Laboratory of Molecular Biology of Viruses, CRC carried out in the framework of the Human Genome program and devoted to the study of the activity of cell and viral genes in cervical cancer are summarized. DNA of human papillomaviruses persists in tumors both in episomal and integrative forms. Integration may occur in different regions of chromosomes. Viral transforming genes E6 and E7 are always present in tumor cells, while antibodies to these proteins are detected only in approximately 30% of patients. Loss of heterozygosity is detected on long and short arms of chromosome 6; some such cases are manifest already at the early stages of tumor progression, while others are typical of the late stages. Several genes that are potentially involved in tumorigenesis and are subject to hypermethylation in CpG islands were identified. Methylation of several genes is observed in approximately 30% of tumors. Tumor progression is associated with increased expression of p16ink4a, an inhibitor of cyclin-dependent kinases.

DNA Methylation↗
PubMedDate not supplied

[Expression of p16INK4a in various cancer cells].

The p16INK4a protein was detected by means of monoclonal antibodies to this protein in the cells of some carcinomas: that of the lungs (17 samples), urinary bladder (6 samples) and mammary gland (4 samples) as well as in the cells of three cell lines from of human uterine cervix carcinoma: SiHa (containing high risk HPV genome), C33A and HT3 (both HPV-negative but have RB mutations in RB gene). Lung carcinoma samples were very heterogenous by the part of cells expressing p16INK4a. High content of this protein was found in all 6 samples of transient cell urinary bladder carcinoma and in 1 sample of mammary gland ductal carcinoma. Cells of all three cell lines also contained p16INK4a. Thus, hyperexpression of this protein is not specific for only HPV-positive cancer of the uterine cervix. The protein presence in cancer cells seems to be an indicator of gene RB mutation or other disturbances of RB pathway.

Biomarkers, Tumor↗
PubMedDate not supplied

[Synaptonemal complexes in vaccinated mice].

Synaptonemal complexes of spermatocytes I obtained from C57BL/6j male mice treated with inactivated bacterial vaccines were spread over the hypotonic phase and then were investigated using light microscope. The slides of synaptonemal complexes of mice treated with cyclophosphamide were used as positive control. It is shown possible in principle to reveal synaptonemal complex abnormalities by means of light microscopy. These abnormalities were not more frequent in vaccinated animals than in intact ones. Cyclophosphamide at doses of 100-200 mg/kg induced synaptonemal complex damage practically in 100% of cells 96 hours after the injection.

Animals↗
PubMedDate not supplied

[General problems in the study of the mutagenic properties of drugs].

The article deals with the results characterizing the state of Russian and foreign elaborations in the study of genotoxic effects of drugs and immunobiological agents. Particular attention is placed on general problems of strategy and tactics in the study of mutagenicity of drugs the solution of which is insufficiently substantiated or insufficiently discussed in the literature. The perspective problems of research into the field of genotoxicity of drugs are discussed.

Animals↗