The susceptibility of the ICR, DD/He and CC57/BR mice to urethane-induced lung tumors was analyzed in comparison with the A/He (highly susceptible) and AKR (resistant) lines of mice. Allelic variants of the K-Ras gene intron 2 in these lines have been determined. Susceptibility of the ICR mice was similar to that of the A mice, and intron 2 of the K-Ras ICR gene carried the 37-bp deletion analogous to that described in the A/He line. The DD mice intron 2 also contained the deletion, but despite the presence of the "susceptible" K-Ras allele, the DD/He mice were resistant to urethane induction of lung tumors. The CC57BR line carried the deletion and demonstrated relatively high susceptibility. Our findings indicate that the K-Ras gene may be important in the chemical induction of lung tumors.

Previous observations from our laboratory have demonstrated that the levels of immunoreactive inhibin (ir-inh) are elevated in almost all patients with granulosa cell tumors and in the majority of postmenopausal women with mucinous ovarian cancers. The present report confirms these findings in a larger group of post-menopausal women. Immunohistochemistry for the inhibin alpha. beta A and beta B sununits shows predominantly epithelial staining in granulosa cell tumors and in the majority of mucinous cancers. Serous cystadenocarcinomas also frequently show positive staining. Studies seeking to identify G alpha i-2 or FSH receptor mutations have provided negative results in contrast to other reports. Further studies of the roles of the inhibin-related family of peptides in ovarian cancer diagnosis and monitoring are clearly indicated.

Review of literature data and original experience with Richter's syndrome.

Evaluation of clinical effectiveness of two regimens of induction therapy of an early chronic stage of Ph'-positive chronic myeloid leukemia including interferon-alpha 2b (intron-A, "Schering Plough") in a cooperative randomised trial on the protocol CML MIG-97.

The comparative analysis of the frequencies of nucleotide exchanges in mutational spectra of gene p53 (5-8 exons) between germline cancer-prone families (Li-Fraumeni syndrome), between somatic mutations in the tumors of different histogenesis and cell lines, obtained from them, was carried out. The nucleotide positions with high level of mutation events (mutational "hot spots"), typical for germline mutational spectra, tissue-specific patterns of their disappearing and appearing of new ones in solid tumors in vivo, nearly complete absence of "hot spots" in lymphomas and cell lines in vitro were revealed. The obtained results allowed to suggest, that one of the leading factor controlling hot-spots distribution in 5-8 exons of gene p53 is the specificity of cell division conditions in vivo and in vitro.

Steady increase of the number of women that primary fell ill with uterus cancer has noted in Ukraine in 1980-1994. The clinic-genealogical analysis of the 262 families with uterus cancer patients of the Kiev region was made. Multifactorial type of heredity predominates. Share in general tendency to malignant tumors of the genetic component was 45.64 +/- 7.20 and of the environment factors was 54.36 +/- 7.20. Closest relatives of probands with the uterus cancer have to be subjected to systematic inspection.

The peculiarities of alternative CD44 mRNA splicing in thyroid cancer tissue of children from radiocontaminated areas was investigated. CD44 gene expression in thyroid cancer tissues of children exposed to radiation resembled that in spontaneously emerged cancers. It was concluded that CD44 gene expression is not the primary target of radioactive irradiation. Probably, the CD44 mRNA splicing deregulation is the consequence of cancer.

The report deals with a molecular-genetic study of human pepsinogen A (PGA) genetic locus. EcoRI, HindIII and BamH 1 restriction endonuclease technique were employed. The investigation involving 58 patients with stomach cancer (SC) and 18 healthy donors failed to identify any significant PGA genetic restructuring in the blood of healthy donors. However, DNA sampled from tumor tissue showed lower expression and deletion of PGA fragments as compared with those of unaltered gastric mucosa in the same patients. Such changes were identified in 27 SC patients.

1. Apparent expression of PCNA in different tumours should not be regarded as an unquestionable criterion of tumoral growth and progression but a negative result of an immunohistochemical assay for PCNA of certain human tumours is not to be taken as a proof that there is no tumoral growth whatever. 2. With results of the immunohistochemical study into the tumour for PCNA protein varying thus much, they are to be interpreted as different forms of manifestation of this protein gene abnormalities.

Segregation analysis of inheritance of adenomas, colorectal cancer (CRC), and multiple primary malignant tumors (MPMT) revealed their low penetrance: from 3.2 to 29% for homozygotes and from 2.0 to 14.4% for heterozygotes. This cast a doubt on the monogenic type of their inheritance, although it formally corresponded to the quasidominant type, i.e., only a fraction of heterozygotes was expressed. Therefore, the multifactorial model of inheritance was tested, which seemed more adequate because genetic heterogeneity of adenomas, CRC, and MPMT was suggested from the data on genetic correlations between various clinical forms. Predisposition to various clinical forms of adenomas, CRC, and MPMT was shown to be specific, i.e., the ratio between genetic and environmental predisposition-determining factors reflected pathogenetic differences between these diseases. However, analysis of variance which revealed genetic (pathogenetic) distinctions between adenomas, CRC, and MPMT is insufficient to confirm complete nosologic identity of each of these clinical forms.

A clinical/genealogical study of colorectal adenomas (CRA) and cancer (CRC), and multiple primary malignant tumors (MPMT) was performed. The CRA prevalence in the population was 4.7 +/- 1.4% (single CRA--6.3% and multiple CRA--3.0%). The frequencies of malignant adenomas, 0.7% CRC, and MPMT were 0.7, 0.17 +/- 0.07%, and 0.004 +/- 0.003%, respectively. The prevalence of cancer of the female reproductive organs was also estimated (cancer of uterine body, 0.2 +/- 0.1%; cancer of ovaries, 0.08 +/- 0.1%; cancer of uterine cervix, 0.55 +/- 0.1%; cancer of mammary gland 0.57 +/- 0.1%). The main parameters of the familial inheritance of adenomas, CRC, and MPMT were also studied in general and at various clinical variants of these pathologies. Among the first-degree relatives of patients with solitary and multiple adenomas, the adenoma frequencies were 5.9 +/- 0.6 and 3.7 +/- 0.5%, respectively. The CRC frequency among the first-degree relatives of patients with adenoma was 3.0 +/- 0.6% and the frequency of MPMT was 5.8 +/- 0.6%. On the basis of the data obtained on frequencies of malignant tumors in various groups of relatives, the following conclusions were made: (1) in families of each proband group, specific pathology was accumulated; (2) the familial frequency of malignant tumors increased with an increase in proliferative processes and the severity of a pathology in probands.