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Biomedical subjects

F L Kiselev

Publications and source records attributed to F L Kiselev.

At least 19 recordsLinked to original sources
PubMed2002

[Molecular markers of the cervical cancer].

The genome of human papilloma viruses from a high-risk group (HPV types 16 and 18) has been detected in 90% of cervical tumors and, in some cases, in the adjacent normal tissues. The presence of viral DNA is the main molecular marker of this neoplasia. HPV genome may persist in the tumors as episomal and integrative forms at early and late stages of tumor progression. The status of viral DNA and the pattern of its expression are similar in all cells of this tumor cell population and seem to be a marker of tumor cell monoclonality. Antibodies to the products of viral oncogenes E6 and E7 were found only in 35% of the patients with tumor where HPV genome is present. Thus, this criteria cannot be used for diagnostic and prognostic purposes. On chromosome 6 in the cervical tumors, the specific marker of heterozygocity on loci 6p21.3 was found. The marker appears at the precancer stage and may be regarded as a marker of tumor monoclonality. Heterozygocity loss in the specific locus in the region 6q16-21 correlates with tumor progression and suggests that there are potential tumor-suppressor genes in this region of chromosome 6. A group of HPV positive tumors with a hypermethylator phenotype is described. These tumors are characterized by the simultaneous methylation and inactivation of multiple genes, including tumor suppressor genes.

Female↗
PubMed1991

[The detection of the c-src protein gene product in human lung tumors].

Immunoblotting and immunochemistry were used to study the expression of a c-src gene-encoded protein in human lung tumors. The authors were the first to identify this otherwise rarely expressed protooncogene in as many as 60% of lung malignancies of various histogenesis. The expression of c-src protein was increased not only in neuroendocrine tumors (small-cell cancer and atypical carcinoid) but also in non-small-cell tumors such as adenocarcinoma, bronchoalveolar and squamous-cell lung cancer. A weak correlation between protein expression and degree of cell differentiation was established for squamous-cell tumors. The study failed to identify the oncoprotein in the normal tissue and benign lesions. Immunoblotting using Mab 327 monoclonal antibodies and the immunohistochemical method employing TBR polyclonal serum yielded similar data. To summarize, an increased expression of pp60c-src was observed in lung cancer of various histology.

Antibodies, Monoclonal↗
PubMed1990

[The immunohistochemistry of cellular oncogenes in precancer and cancer of the lung].

Operative material obtained from patients with lung cancer and precancer, carcinoids, secondary tuberculosis, chronic nonspecific diseases and pulmonary lymphosarcoma was examined immunohistochemically. Expression of the oncogenes was higher in lung carcinoma than in the foci of lung epithelium regeneration, metaplasia and dysplasia. All the oncogenes in precancer and cancer may be divided into two groups by the degree of their expression: oncogenes the activation of which occurs in the same way at certain stages of tumour progression regardless of the lung carcinoma histogenesis and oncogenes expressed at certain stages depending upon the carcinoma histogenesis. The majority of oncogenes studied may be included into the second group (C-myc, ras, sis, src) and only one c-fos into the first group. The oncogenes expression may occur at the precancerous stage and precede the morphological changes in cells and tissues. The expression of some oncogenes (C-myc, sis) takes place not only in the tumour parenchyma but in the cancer stroma as well thus making the immunohistochemical method most reliable that permits one to study a true expression of oncogenes by cancer cells.

Chronic Disease↗
PubMed1988

Interstrain restriction fragment length polymorphism of c-fos and c-src oncogene loci in spontaneously hypertensive and normotensive rats.

Interstrain restriction fragment length polymorphism was detected after Southern blot hybridization of spontaneously hypertensive (SHR) and control (WKY) rat DNA digested by Bam HI restrictase with a v-fos probe. The SHR genome was characterized by an additional minor band of 4.0 kb. Other restriction fragment length polymorphism was revealed in the c-src locus by Eco RI, Hind III and Pst I restrictases. The major characteristic bands were 1.6 kb (SHR) and 2.4 kb (WKY) after Eco RI restriction; 3.4 kb (SHR) and 4.1 kb (WKY) after Hind III restriction and 4.0 kb (SHR) and 4.6 kb (WKY) after Pst I restriction. This restriction fragment length polymorphism can be used as Mendelian traits in linkage studies on the distribution of blood pressure and other quantitative physiological traits in (SHR x WKY)F2 hybrids.

Animals↗
PubMed1988

[Model systems of carcinogenesis in vitro: the interaction of the ras oncogene with immortalized cells].

Gene transfer experiments have shown that ras effector functions are sufficient to transform cells from a variety of established lines (e. g., mouse NIH3T3 cells). In contrast, primary cells and early passage rodent cells can be transformed by ras oncogenes only at low frequencies, unless cotransfected with collaborating genes such as adenovirus early region IA (EIA) or myc retroviral oncogene homologue. Primary rat embryo fibroblasts (REF) were chosen as a model for the analysis of multistep cellular transformation. Transfection of REF, immortalized by early region of simian adenovirus SA7 with c-Ha-ras oncogene cannot induce their morphological transformation. This phenomenon is observed only after second transfection with the same oncogene. These different cell lines can be used for further analysis of the mechanisms of carcinogenesis.

Adenoviruses, Simian↗
PubMed1987

[Identification of virus-specific RNA in cells infected with the bovine leukemia virus by nucleic acid hybridization in situ].

Virus-specific RNA was detected in FLK cells producing bovine leukemia virus (BLV) by cDNA hybridization in situ. For calculation of the virus-specific RNA copy number in infected cells hybridization of 3H-cDNA BLV with the total cellular RNA in solution was used. FLK cells contain approximately 600 copies of virus-specific RNA per cell. Individual FLK cells producing BLV were identified by hybridization in situ. A successful identification of viral RNA in cells by hybridization in situ is possible if cells contain more than 100 copies of viral transcripts.

Animals↗
PubMed1987

[Synthesis and immunogenic properties of peptides corresponding to the 200-210 site of the oncoprotein p28sis].

Synthesis of peptides corresponding to the 201-210 and 200-206 sequences of p28sis oncoprotein is reported. This region of the oncoprotein was chosen as a probable epitope basing on the analysis of its secondary structure and hydrophilicity profile. The synthesis was carried out by classical method in solution using side-protecting groups of the benzyl type. Conjugates of the peptides with protein carriers and polyclonal antibodies to the peptides were obtained. Antiserum against the 201-210 peptide conjugate is shown to be specific to p28sis oncoprotein and its p56sis dimer.

Amino Acid Sequence↗
PubMed1986

[Production of a cell line of embryonic rat fibroblasts after transfection with the DNA from the early region of simian adenovirus SA7].

Transfection of plasmid DNA, containing coding sequences for the early region of simian adenovirus SA7, into primary cultures of the rat embryonic fibroblasts results in the establishment of a stable cell line REF-1. The cells have been passed more than 40 times (about 160 doublings) without reaching the critical stage. Their growth is substrate- and concentration-dependent.

Adenoviridae↗
PubMed1985

[Malignant cell transformation and oncogenes].

In genome of all transforming retroviruses special genes (oncogenes) have been identified which play a key role in malignant conversion of the cells, infected with these viruses. The homologues of these genes (protooncogenes) are persist in all normal cells. During transformation protooncogenes can be activated as a result of one of following processes: insertion of promotor-like elements, mutations, translocations, amplifications or rearrangements. Using transfection technique the transforming genes were isolated from different human tumors. The activation of one of the cellular oncogenes may switch on the other genes and malignant cell transformation may be characterized as a multifactor and multistage process.

Animals↗
PubMed1984

[A new HTLV retrovirus associated with human T-cell leukemia/lymphoma].

The data concerning retrovirus HTLV isolated from patients with T-cell leukemia/lymphoma are presented. The virus differs from the known C type viruses, possesses high tropism to T-lymphocytes. The virus is exogenous for human cells and its origin is still unknown. Virus specific nucleotide sequences are absent in a normal cell genome, but they are detected in blood cells and tissues of patients with this form of leukemia. HTLV-associated disease is rare and distributed mainly in two regions in the world: in the South-West of Japan and in the Caribbean islands. Mode of the virus transmission is probably horizontal.

Animals↗
PubMed1980

[Expression of virus-specific RNA in cells of mice infected with Mazurenko and Rauscher viruses].

Organs of mice with leukemia induced by Rauscher and Mazurenko viruses contain different amounts of virus-specific RNA. In Mazurenko virus-induced leukemia, virus-specific RNA content reached the maximum in the thymus and lymph nodes. Hybridization level of RLV 3H DNA transcript with RNA from mouse cells with RLV-induced leukemia amounted to 90% while in cells of mice with Mazurenko virus-induced leukemia it did not exceed 60%.

Animals↗