Analysis of the chromatic dispersion effect on the subcarrier wave QKD system.

In this paper we investigate the chromatic dispersion impact on the quantum key distribution system based on multi-mode weak coherent phase-coded states. We provide an asymptotic secure key rate estimation, taking into account error detection probability due to chromatic dispersion. We demonstrate numerically and experimentally that the effect of chromatic dispersion in an optical fiber without any compensation hinders the secret key distribution at a distance more than 53 km.

[Cloning of alternative isoforms of the catalytic subunit of the human thelomerase (htert)].

Most human tumors, including cervical cancer, are characterized by telomerase activation (cell proliferation activation enzyme). Such activation is implemented in the elongation of the terminal segments (telomeres) of the telomerase chromosome. The gene of the enzyme is RNA-encoded, the RNA in tumors being observed in a few isoforms.

[MicroRNA and cancer].

Review is devoted to analysis of the role of microRNA in progression of human tumors. The following aspects of this problem are discussed: general characteristics of microRNA, expression pattern of these RNAs in human tumors and specificity of this expression, putative role of microRNAs as oncogenes and tumor suppressors for tumor growth, participation of microRNAs in induction of transformed phenotypes of tumor cells, possible role of microRNAs for early diagnosis of the disease and prognosis.

[Telomerase level versus spliced hTERT-specific RNA forms in cervical carcinoma].

An attempt was made to identify molecular markers of different clinical stages of cervical carcinoma caused by papilloma virus (HPV). Presence of viral genome, telomerase level and expression of a gene, which coded the catalytic activity of that enzyme (hTERT), were assayed in 89 patients. HPV (type 16) genome harboring tumors were detected in 73% which was in conformity with the literature and our own data.

The regulation of telomerase in oncogenesis.

The influence that the expression of the human (glial-derived neurotrophic factor (GDNF)) neurotrophic factor has on the morphology and proliferative activity of embryonic stem cells (SC) of a mouse with R1 lineage, as well as their ability to form embroid bodies (EB), has been studied. Before that, using a PCR (polymerase chain reaction) coupled with reverse transcription, it was shown that, in this very lineage of the embryonic SC, the expression of the receptors' genes is being fulfilled for the neurotropfic RET and GFRα1 glia factor. The mouse's embryonic SC lineage has been obtained, transfected by the human GDNF gene, and has been fused with the "green" fluorescent protein (GFP) gene.

[Genetic and epigenetic factors of cervical tumor progression].

Infection with high risk papilloma viruses (HPV types 16, 18, and relative ones) initiates the development and progression of uterine neck cancer. The viral genome is found in pre-tumorous lesions (stage I to III intraepithelial neoplasias--CIN) and carcinomas, persisting in cells in episomal or integrated state. In all tumors, there is the expression of two viral transforming genes, E6 and E7, the main function of which is the inactivation of genes that suppress tumoral growth, p53 and retinoblastoma gene.

[Tumor suppressor gene RBSP3 in cervical carcinoma: copy number and transcriptional level].

In this work for the first time copy number and expression changes of the tumor suppressor gene RBSP3 (3p21.3) were investigated. The study was performed on HPV-positive squamous cervical carcinoma (SCC) using real-time PCR.

[Loss of heterozygosity at chromosome 6 as a marker of early genetic alterations in cervical intraepithelial neoplasias and microinvasive carcinomas].

Oncogenic human papilloma viruses (mostly HPV types 16 and 18) are the major cause of cervical intraepithelial neoplasia (CIN) that progress into cervical cancer (CC). To reveal early genetic alterations at chromosome 6 important for CC progression we have analyzed loss of heterozygosity (LOH) in DNA from 45 CIN cases, 47 microcarcinomas and 19 invasive squamous cell carcinomas stage IB. LOH analysis of DNA samples prepared with microdissection from all CIN foci as well as from CC lesions and synchronous CIN has permitted the investigation of CIN and CC heterogeneity.

[Methylation of the putative tumor suppressor gene, RASSF1A, in primary cervical tumors].

The methylation level of 13 CpG-dinucleotides in the promoter region of the putative tumor suppressor gene RASSF1A (3p21.31) was analyzed in HPV-positive squamous cell carcinomas of cervix using methyl-sensitive restriction endonuclease analysis followed by PCR. The methylation from 3 to 13 CpG-dinucleotides was observed in 64% (25/39) tumors, 22% (2/9) morphologically normal tissues adjacent to tumors (P = 0.

[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.

[Cervical carcinoma progression-associated genetic alterations on chromosome 6].

To identify the loci associated with progression of cervical carcinoma, chromosome 6 regions were tested for loss of heterozygosity. Detailed analysis with 28 microsatellite markers revealed a high frequency of allelic deletions for several loci of the short (6p25, 6p22, 6p21.3) and long (6q14, 6q16-21, 6q23-24, 6q25, 6q27) arms of chromosome 6.

[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.

[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.

[Status of the human DNA papillomavirus in cervical tumors].

Cervical carcinoma is etiologically associated with the human papilloma virus (HPV), HPV 16 and HPV 18 being the most common. Viral DNA is thought to persist mostly in the episomal form in early tumor development, and in the integrated form in carcinomas. This assumption was checked with a new method that discriminated between RNAs transcribed from episomal and integrated HPV DNAs.

[Cloning transforming genes from human papillomavirus type 18].

Nucleotide sequences of type 18 human papilloma virus genes E6 and E7 inserted in human DNA cloned from cervical tumor are determined. The resultant sequences are compared to the prototype variant. Five point mutations not leading to replacement of amino acid residues in polypeptide chain and 1 substituting the amino acid in codon 129 are detected in gene E6 sequence.

[Cathepsins L and B and their endogenous inhibitors in embryonal fibroblasts transformed by different genes].

Expression of cysteine proteinases, cathepsins L and B, and their inhibitors was studied out in three model systems of rat embryo fibroblasts, sequentially immortalized and transformed by different genes. In Model I rat embryo fibroblasts were immortalized with DNA of early region of simian adenovirus SA7 (clone REF-1) and then transformed by c-Ha-ras oncogene (REF-2EJ; malignant transformation). In Model II and III, the immortalized fibroblasts (clone IE5) were obtained by transfection with the polyoma virus LT gene and the clone IE5 used lost this gene; the malignant transformation was achieved by transfection with the E7 gene (clone trF8; Model II) and E6/E7 genes ¿clone A5E5(pC7-1); Model III]¿ of human papilloma virus types 16 and 18 respectively.

[Nuclear oncoprotein expression in lung precancer and cancer at various stages of tumor progression studies at the level of light- and electron-immunohistochemistry].

68 cases of lung carcinoma, 3 carcinoids and 15 fibrosing alveolitis with foci of adenomatosis and bronchiolo-alveolar carcinoma were studied. Oncoproteins c-fos, c-jun, c-ets-1, c-myc L and L-myc were identified in the tumour and surrounding tissue. Expression of c-fos was revealed in 79 of 138(59.

[Cell oncogene expression in normal, metaplastic, dysplastic epithelium and squamous cell carcinoma of the uterine cervix].

Immunohistochemical analysis of the protein expression c-myc, ets 1, ets 2, TPR-met, c-fos, c-jun, c-ras-pan, p53, yes, src in 79 samples of normal, metaplastic squamous epithelium, intraepithelial and invasive squamous cell carcinoma of uterine cervix was performed using polyclonal rabbit antibodies to the synthetic peptides homologous active areas of corresponding oncoproteins. Higher content of myc, fos, ets2, p53, ras is noted in metaplasia, dysplasia and in tumours as compared to the normal tissues. Protein myc is revealed in the cytoplasm at a grave dysplasia and in the nucleus in the intraepithelial carcinoma: this may serve as a criterion at a differential diagnosis of these conditions.

[In vivo identification of YB-1 protein, interacting with the enhancer of human papillomavirus (HPV) type 18, using antibodies to a synthetic peptide].

Enhancer sequences of human papilloma virus (HPV) type 18 were used for screening of HeLa cells cDNA library in lambda gt11 using the protein binding method. Clones with YB I gene homology sequences were isolated. This gene is coding the protein which binds the regulatory region of Y gene of main histocompatibility complex (HLA 11).

[A new recipient cell line for transfection of biologically active oncogenes].

The properties of the new immortalized rat cell line (REF-1) were analyzed. These cells can be used as recipient ones in transfection assays. REF-1 cells never convert spontaneously to transformed phenotype during long-term passages in vitro unlike NIH3T3 cells.

[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.