This is a review of the literature on the peripheral nerve sheath tumors with perineural differentiation. The authors provide an overview of the clinicopathological, immunohistochemical, ultrastructural, and genetic features of these neoplasms. Emphasis is laid on various morphological variants of perineurioma (intraneural, retifrm, sclerosing, plexiform, atypical, malignant, etc.) and so-called hybrid tumors (schwannoma-perineurioma, neurofibroma-perineurioma).

It has been recently shown that the HLA-A2 gene may be a negative predictor of ovarian cancer in Swedish patients with advanced tumor grades and stages (III and IV). We performed HLA-A2 typing in 69 ovarian cancer patients admitted to some St. Petersburg hospitals. HLA-A2 expression was determined by the PCR/sequence-specific oligonucleotide hybridization test (PCR/SSOP), by extracting DNA from the paraffin-embedded tissue specimens. The purified tissue was disrupted at 55(C in 10% SDS, proteinase K buffer twice. The amount and purity of DNA were measured by the Nano-Drop technology. HLA-A2 frequency from 2 832 healthy St. Petersburg bone marrow donors was used as a control. HLA-A2 was detected in 32.2% of the patients by PCR versus 51% in the healthy St. Petersburg population. Five year survival in our patient group was higher than that in ovarian cancer patients in St. Petersburg, which was 35.7% in general. The difference was statistically insignificant in 5-year survival between our ovarian cancer patients with stages III and IV according to the presence or absence of the HLA-A2 gene. In the cohort of the examinees, HLA-A2 expression does not correlate with prognosis. The selection of these patients for referral to our clinic is a possible explanation of the discrepancy of the rate of clinical stage and HLA-A2 phenotypes.

The authors present results of complex study concerning mutagenic and carcinogenic effects of work conditions in chemical-recovery industry. Oncologic morbidity and frequency of chromosomal aberrations in workers group is considerably higher than in controls. These effects appear to increase in males with longer length of service.

Lung cancer is one of the most frequent neoplasia in the Russia, the United States and Europe. This cancer is associated with functional activity changes of many genes. In the present study TIMP3, DAPK1 and AKR1B10 genes transcription analysis of squamous cell lung cancer specimens was carried out using reverse transcription-PCR. Substantial increasing of AKR1B10 transcription level is revealed in 80% tumor samples. TIMP3 and DAPK1 transcription level is considerably decreased in 76 and 72% tumor specimens, accordingly. These results may point out that all three genes are important for squamous cell lung cancer tumorogenesis while AKR1B10 is potential oncogene whereas TIMP3 and DAPK1 are potential tumor suppressor genes. We suggest that revealed substantial transcription level-changes of investigated genes may be used for oncodiagnostics.

Frequency of RET/PTC rearrangement and somatic BRAF mutation was investigated in patients with papillary thyroid cancer (PTC) vis-a-vis relevant demographic and clinico-pathological features. The study group included 76 patients with a female/male ratio of 4.8:1; mean age - 45.7 +/- 9.7 yrs. BRAF mutation was identified in 49 (65%) (V600E--47, KSRWS600--1 and E585K--1). RET rearrangement was detected in 9 (12%): RET/PTC1--5, RET/PTC3--2, unspecified RET/PTC--1 and delta RET/PTC--1. It was age at diagnosis alone that proved to be consistently associated with BRAF mutations (p = 0.017). Younger tumor patients were mostly prone to RET/PTC rearrangement (p = 0.08). No correlation between mutation and clinico-pathological features was established.

Gliomas are the most common tumors of the central nervous system (CNS). Malignant astrocytic gliomas account for 50% of all primary brain tumors. Cells of origin are unknown for the majority of brain tumors: CNS tumors have frequently in their content many histological forms and their classification will depend on what the parts of neoplasm that will be clearly identified at the material taking and further investigation. Current immunohistochemical studies may determine the antigenic structure of a tumor cell, compare it with the antigens expressed by a certain cell type and, thus, classify the tumor by its origin, but there are no antibodies which would correctly identify different types of tumors. The lecture reflects the current classifications of glial tumors: the typical three-leveled classification, the Kernokhan classification, the Duma-Duport classification. A part of the lecture deals with the specific features of genetics and molecular biology of gliomas: recent studies cast any doubt on the existing data on the sources of growth of these tumors.

Since breast cancer may emerge both before and after menopause onset, relevant forms of the disease show marked biological and clinical differences. Intrinsic properties of mammary fat located in the vicinity of tumor, which play a definitive role in stromal-epithelial interactions, are an important factor of development of such differences. The DNA damage promoting hormonal (leptin and adiponectin production, aromatase activity) and progenotoxic. The properties of mammary fat such as formation of tumor necrosis factor, interleukin-6, nitric oxide, malonic aldehyde, macrophage/histiocyte infiltration and estrogen 4-hydroxylase expression, were studied in mammary fat tissue of 95 patients with receptor-positive or receptor-negative breast tumors (reproductive--25, menopausal--70). It was found that progenotoxic properties might somewhat predominate, as far as differences in parameters and pathways are concerned, both in menopausal and still cycling patients. Hence, progenotoxic damage which represents mammary fat tissue status is perhaps modified by a number of genetic and mitochondrial factors. It may exert unfavorable effect on the course of the disease within a fairly wide period.

This review is devoted to genomic instability in the offspring of parents that were irradiated or treated with chemical mutagens. The evidence is presented, showing high frequency of cancer diseases and instability of the genome of somatic and germline cells in the offspring of radiation-exposed animals. Possible epigenetic mechanisms of these effects are considered, as well as their significance as components of genetic factors of radiation risk for humans.

The investigation of the cancer-associated structural and epigenetic changes in cell genome is a major approach for understanding mechanisms of cancerogenesis. To investigate these genome changes, novel technique of microarrays comprising NotI-linking genome clones was developed. Twenty eight samples from patients with cervical cancer were analyzed using NotI microarrays of human chromosome 3. Deletions, amplifications and methylation were detected for 109 out of 182 NotI clones with different frequency. Notably, 17 NotI-linking clones showed genomic changes in more than 35% of tumor samples investigated, which suggests involvement of genes associated with these clones in development of cervical cancer.

Changes in the intracellular signaling cascades underlay many human pathologies including oncological diseases. Modification of the Wnt-signaling pathway are often associated with development of tumor and may play a significant role in carcinogenesis. This gives rise to a significant interest to studies of regulators and components of the Wnt-signaling pathway and search for approaches to practical implementation of the properties of the regulators. The goal of this work was to review the properties of WIF1 (Wnt inhibitor factor-1), a regulator of Wnt-signaling pathway, as a possible diagnostic and prognostic marker of human tumors, as well as basis for development of novel antitumoral preparations.

RHOA protein, a member of small GTPases family, is implicated in cell morphogenesis, adhesion, and in cell cycle regulation. RHOA gene (3p21.31) exhibits cell transformation activity, and therefore gene is considered as a potential oncogene. The aim of this study was to investigate RHOA transcription and copy number changes in three epithelial tumors (breast, renal cell and epithelial ovarian carcinomas, 45 tumor/normal pairs altogether). EII, HhaI, AciI n Bsh1236I). Hypomethylation of the RHOA promoter region in tumor DNA was observed two times more frequently than increased methylation. Moreover, all (15) cancer cases with hypomethylation of the RHOA gene showed a 2-10 fold increased expression of RHOA. It was concluded that gene copy multiplication and demethylation of the RHOA promoter region can contribute to transcription activation of this gene in epithelial tumors.

The aim of the investigations was to study the efficiency of demedullation of both ovaries in the case of polycystic ovary syndrome (POS), determination of infertility structure in patients in case of ineffective operation of POS and determination of additional treatment tactics in these patients. In all 245 patients tests of functional diagnostics were carried out as well as the ultrasound investigation of pelvic organs and adrenal glands, X-ray of skull and sella turcica, hysterosalpingography were performed. In blood serum the basal levels of prolactin, LH, FSH, estradiol, progesterone and cortisol were investigated by RIA. In twenty four-hours urine 17 KS, DHA and 17 OKS levels were determined. In all patients laparoscopy, hysteroscopy, chromopertubation with diagnostic curettage of uterus cavity were performed. According to the data in operated patients without a positive effect the most frequent cause of infertility was anovulation. Therefore, even successful surgical intervention and recovery of ovarian function do not guarantee post operational adhesions, which can cause infertility of tuboperitoneal genesis. Treatment tactics of patients operated due to POS without effect can't be standard and depend on revealed pathology discovered in post operational period.

A link between HLA allelic variants and long-term results of surgery for gastric tumors was established on the basis of a 10-years follow-up of 112 cancer patients (stage I-II--37.9, III-IV--62.1%; radical surgery--44.6%). HLA class I was studied in a lymphocytotoxic test; HLA class II--gene DRBI specificity using polymerase chain reaction of peripheral blood cell DNA. The control group included healthy subjects living in the city of Novosibirsk (n = 341). High frequency of antigens HLA-B41, -DR1, -DR7 (p < 0.01) co-occurred with HLA-A2, -B12, -B13 and -B18 presence (p < 0.05) in breast cancer patients. Clinical manifestations of cancer were shown to develop in HLA-A1, -B8, -B15, -DR3 and -DR5 carriers at early stages. Tumor development at later stages (III-IV) was associated with HLA-A2, -B12, -B17, -B35, -B41 and -DR7. A link was registered between lethality rate, on the one hand, and HLA-A3, -B22, and, in particular, DR4, on the other, while remission of more than 7-years--with HLA-A11, -B13, -B21 and -DR5. HLA-B22/DR3 phenotype involved worse prognosis in radically-treated patients whereas that of HLA-B8/DR3--a better one.

Changes in mitochondrial DNA (mtDNA) copy number were compared versus the nuclear beta-globulin gene (internal standard), as well as occurrence of large mtDNA deletions in peripheral blood samples from 21 breast cancer patients following chemoradiotherapy. The study used polymerase chain reaction. Distinct variations were identified both in mtDNA copy number versus nuclear DNA and large mtDNA deletions occurrence in blood cells in response to genotoxic influence of chemoradiotherapy. Some mtDNA copies in breast cancer patients blood cells revealed large deletions whose frequency increased after chemoradiotherapy. Mitochondrial DNA lesions would induce synthesis of mtDNA copies in the course of chemoradiotherapy, which pointed to a compensatory reaction in peripheral blood cells as a consequence of a disturbed energy biogenesis.

The paper presents a clinicoanatomic case of the polycystic ovary in a 3-month-old girl who died from intestinal infection. It shows the pathomorphological changes of ovaries, the structure of cysts, primary ovocytes, with defects of their structural and spatial pattern. It is suggested that there is a dynamic imbalance of the biological program of folliculogenesis and follicular atresia, which leads to the cystic transformation of ovaries and the persistence of biologically defective primary ovocytes.

Results of clinical and instrumental-laboratory study of 17 cases are presented. According to the rapid urease test (CLO) and histological studies, the helicobacter infection was found in 12 (70.6%) cases out of the group of 17 suffering from chronic atrophic gastritis, gastric ulcer adenomatous polyposis. Analyses of Helicobacter pylori dissemination over the gastric mucosa manifested the I (weak) degree (up to 20 microbes within field of vision) prevailing in 8 (66.7%) of 12 cases, while the II (medium) degree (up to 50 microbes within field of vision) and III (high) degree (over 50 microbes within field of vision) occurred only in 4 cases (33.3%). By comparative cytogenetic research of the peripheral blood lymphocytes we found the immunogenetic markers and characteristic features of cytogenetic disturbances in the immunocompetent cells in cases of pre-cancer Helicobacter pylori-associated diseases (chronic atrophic gastritis, gastric ulcer, adenomatous polyposis). Statistical data confirmed an increase in the percentage of cells with chromosomal aberrations, which amounted to 4.25+/-0.51 in the chronic atrophic gastritis cases, 3.5+/-0.46 in the gastric ulcer cases, 5.75+/-0.60 in the adenomatous polyposis cases for 100 analyzed metaphases. Considering the questionable role of Helicobacter pylori as a direct initiator of mutagenesis, the immune disturbances may be caused by the damage of DNA of lymphocytes resulting from the genotoxic effect of some intermediates of inflammation.

To study a relationship between cytogenetic disorders, clinicobiological characteristics and prognosis in chronic B-cell lymphoid leukemia (B-CLL).