Inbred albino mice and C57Bl/6 mice were exposed to nonthermal radiation of 37 GHz frequency in order to detect delayed effects caused by repeated irradiation. The detected pathomorphological changes and the dynamics of their formation suggest that these factors are responsible for delayed formation of immunodeficiency provoking mutagenic and carcinogenic effects.

Certain types of cancer are often correlate with certain chromosomal rearrangements. The chimaeric genes are formed as a result of this rearrangements, and the chimaeric proteins are the products of their expression. The breakpoints of such translocation are often clustered in the genome. Moreover, such breakpoint clusters often contain specific genomic elements like topoisomerase II consensus sites, nuclear matrix attachment regions and DNA sequences, which can make up secondary non-canonical structure. In this review we discuss whether breakpoints may be induced by chromatin structure. Furthermore, we bring up not touched upon literature question about the relation between the breakpoint clusters and the domain organization of corresponding proteins. We also consider possible mechanisms of chromosomal rearrangements.

The role of X-gene of hepatitis B virus (HBV), telomerase gene, structural HBV proteins is considered. Both factors of the virus and those of the host are involved in hepatocarcinogenesis. The duration of chronic B hepatitis may influence mitogenic and mutagenic conditions for accumulation of occasional genetic and chromosomal damage and result in hepatocarcinoma development.

It has been more than 15 years since the epidemiological studies revealed the interrelation between chronic pancreatitis (CP) and pancreatic cancer (PC). For the specified period of time pancreatology has advanced considerably. The genetic nature of mucoviscidosis and hereditary pancreatitis was revealed, and similar studies were carried out with respect to pancreatic cancer as well. As a result, several genetic processes were revealed, some of them promoting the development of a chronic inflammatory process in the pancreas, and others--malignant changes. It was established later that in some cases pancreatic cancer can have a precisely inherited nature being associated with other hereditary syndromes, yet the frequency of this form of pancreatic cancer does not exceed 3%, while some forms of chronic pancreatitis (hereditary and tropical) increase the risk of development of pancreatic cancer in 53-100 times.

Ten variants different from the canonical nucleotide sequence (GenBank, U14680) has been identified when studying the mutation spectrum in gene BRCA1. Six of them (5382insC, 2963del10, 3819de15, 3875del4, 2274insA, and R1203X) cause premature termination of protein synthesis, thus predisposing to breast cancer. A missense mutation E1250K is presumed to be a factor of predisposition to cancer. We classified three variants of nucleotide sequence found in some patients as DNA polymorphisms S694S, L771L, and E1038G. The 5382insC and 3819de15 mutations have been detected in four and two families, respectively. Five of the mutations detected have not been found in Russia before. However, all mutations except for 2963del10 have been found in other populations of the world, which indicates their long evolutionary history. Two mutations found in patients from St. Petersburg (5382insC and 3875de14) have also been found in oncological patients from other regions of the Russian Federation.

The article presents data on the association between the mutagenicity and carcinogenicity of chemical compounds. Genotoxic carcinogens, which universally act via interaction with DNA, are positive in tests for mutagenicity. The mechanisms of the carcinogenicity of non-genotoxic carcinogens include promotion, cytotoxicity and oxidative stress. As mutagenicity tests do not allow determination the carcinogenicity of chemical substances, long-term experiments on rodents should be considerred the only reliable method of carcinogenicity detection.

A rare case of aspergillesis sepsis in an one month old baby with inborn leukemia is reported. Of essential importance in the pathology is genetic deficiency of this child, decreased immunity and a grave intoxication due to leukemia chemotherapy.

The ploidometrical data on over 50,000 nuclei of intact and altered cells from cervical, endometrial, mammary, renal, pulmonary, thyroidal and cutaneous tissues at different stages of carcinogenesis showed theoretical and empirical evidence to match fully. That was interpreted as a mathematical support of the law of step-by-step development of the disease.

The Familial Cancer Register, Moscow, established in 1990, has a record of pedigrees of 6,000 cancer patients. The records on the probands and families have been studied since 1995. The paper presents the data of a repeat survey of the families conducted in 1990-1995. Only 794 out of 3,000 families, included in the first survey, responded. Relapse was reported in 135 probands and/or relatives from 108 families. The following subgroups were identified depending on the rates of cancer morbidity in familial histories (the criteria are presented): 1) no incidence; 2) few cases; (3) more cases, and (4) all family members have cancer. New tumors were detected in one-third of such families. A direct correlation was found between the morbidity rates and neoplasia incidence. In 12 families of group 3, originally, not all the members had tumors.

The paper shows the role of tumor cell apoptosis induction in the mechanism of cancer cytoreductive therapy and the significance of the impaired cell death program for the pathogenesis of the phenotype of multidrug and radiation resistance resulted from the use of specific antitumor therapy and from the natural course of tumor progression.

Active specific immunotherapy with cancer vaccines is a new approach to treating cancer. After surgical tumor removal, vaccinotherapy has been ascertained to cause an increase in the duration of an asymptomatic period and to postpone the onset of recurrences. Moreover, vaccinotherapy leads to the regression or stabilization of growth of some types of tumors in patients with clinically determined metastases. The review outlines the principles of designing antitumor vaccines, the role of the immune system in the elimination of tumor cells, as well as tumor-associated antigens and presents the types of antitumor vaccines used in clinical practice.

It is suggested, on the basis of ploidic, to define more precisely the cytological analysis according to values of the mean ploidy of cell nuclei of epitheliocytes in neoplasms of the cervix of the uterus. Ploidiometry was found to ensure a more accurate differential diagnosis of 3 process stages, i.e. benign (low degree of intraepithelial neoplasia), marginal (high degree of intraepithelial neoplasia) and malignant stages of carcinogenesis (carcinoma) in the cervix of the uterus.

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 = 0.0306) and in 2 from 3 leucocytes of peripheral blood of patients. The methylation of these CpG-dinucleotides was absent in DNA of healthy donor leucocytes (0/10). Methylation level of the examined fragment of the RASSF1A promoter region was significantly higher in tumors of patients with lymph node metastases in comparison to tumors of patients without metastases (P = 8.5 x 10(-12)). The methylation frequency of RASSF1A gene was in two times higher than hemi- and homozygous deletion frequency at the region of location of this gene (chromosome 3p21.31), determined earlier. These data suggest that methylation of the RASSF1A gene is one of the main ways of this gene inactivation in HPV-positive cervical squamous cell carcinomas. The methylation of the RASSF1A gene is an early event in genesis of tumor and the level of methylation increased with tumor progression.

Multiplex methylation-sensitive PCR and methylation-specific PCR were employed in studying the methylation of CpG islands in the p16/CDKN2A and p14/ARF promoter and the first exon regions in non-small cell lung cancer (54 samples) and acute B-cell lymphoblastic leukemia (61 samples). Differences in methylation were detected between types of neoplasia as well as between CpG islands studied within the same types of tumors. High level of the p16/CDKN2A first exon CpC island methylation was revealed in non-small cell lung cancer (68%) and in acute B-cell lymphoblastic leukemia (55%) and the CpG island of p14/ARF first exon was nonmethylated in these types of tumors. The methylation of CpG-rich fragments of genes p16/CDKN2A and p14/ARF promoters was analysed. As was found out, CpG islands located in 5' areas of one and the same gene can differ in methylation frequencies. The comparison of sensitivity between methylation-specific PCR and methylation-sensitive PCR used in the methylations studies was carried out.

Female mice of CBA strain received diethylstilbestrol (DES) 1 g body weight intraperitoneally. High incidence of histiocytic uterine sarcoma was observed in parents (25%), first generation (F1), descendants (10.9%), and generation F2m (through F1 males mated with females in control) (17.8%). Morphologically, tumor cells examined through light and electron microscopy were referred to as histiocyte-like elements. Half of the animals had metastases in the liver, kidneys, lungs, spleen, pineal and adrenal glands and stomach. The development of tumors in generation F2m, which was not exposed to DES, might be accounted for by "transgeneration" carcinogenesis, i.e. passage of carcinogenic effect through a generation.

The data on tumor at presentation and 5-year follow-up after surgery for urinary bladder cancer were assessed retrospectively in 62 patients, with particular emphasis on nucleolar distribution revealed by silver staining. A close relationship was found between mean values and even distribution of argentaffine granules and nucleoli in tumor cells, on the one hand, and morphological features of carcinoma and clinical course, on the other. Also, correlations were established between distribution of nucleoli, nucleolar organizer regions and histological pattern (p=0.001), stage (p=0.013), grade (p=0.001), multiplicity (p=0.001), size (p<0.001), localization (p=0.005), frequency (p=0.014), period (p<0.001) and 5-year relapse-free survival (p=0.021). Grade and stage of disease appeared to be pivotal to tumor progression. Favorable course was reported when mean values of number of nucleoli and standard error of argentaffine granule distribution in tumor cells were less than 1.65 and 4.4. respectively. Relapse-free time was the shortest when coefficient of variation of distribution of argentaffine granules and nucleoli in tumor cells exceeded 42%.