Metabolic disorders occurring in menopause, including dyslipidemia, disorders of carbohydrate metabolism (impaired glucose tolerance – IGT, type 2 diabetes mellitus – T2DM) or components of metabolic syndrome, constitute risk factors for cardiovascular disease in women. A key role could be played here by hyperinsulinemia, insulin resistance and visceral obesity, all contributing to dyslipidemia, oxidative stress, inflammation, alter coagulation and atherosclerosis observed during the menopausal period. Undiagnosed and untreated, metabolic disorders may adversely affect the length and quality of women's life. Prevention and treatment preceded by early diagnosis should be the main goal for the physicians involved in menopausal care. This article represents a short review of the current knowledge concerning metabolic disorders (e.g. obesity, polycystic ovary syndrome or thyroid diseases) in menopause, including the role of a tailored menopausal hormone therapy (HT). According to current data, HT is not recommend as a preventive strategy for metabolic disorders in menopause. Nevertheless, as part of a comprehensive strategy to prevent chronic diseases after menopause, menopausal hormone therapy, particularly estrogen therapy may be considered (after balancing benefits/risks and excluding women with absolute contraindications to this therapy). Life-style modifications, with moderate physical activity and healthy diet at the forefront, should be still the first choice recommendation for all patients with menopausal metabolic abnormalities.

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The prognostic value of the MDM2 gene amplification/expression in many types of cancer remains unclear. Polymorphisms in the promoter region of the MDM2 gene have been shown to alter the protein expression and thus, may play a role in carcinogenesis. The aim of the present study was to evaluate the association between the risk of endometrial cancer and SNP309 polymorphisms in the MDM2 gene. The genotype analysis of SNP309 MDM2 gene polymorphisms in 152 endometrial cancer patients and 100 controls of cancer-free subjects, in the Polish population, was performed using the PCR-based restriction fragment length polymorphism (PCR-RFLP). In the presented study, an association between MDM2 SNP309 polymorphisms and the incidence of endometrial cancer was identified. Our results obtained for the SNP309 polymorphisms of the MDM2 gene indicated that both the G/G genotype and the G allele are strongly associated with endometrial cancer. We did not observe any relationship between gene polymorphism and endometrial cancer progression assessed by FIGO grade. This is the first study linking single nucleotide polymorphisms of the MDM2 gene with endometrial cancer incidence in the population of Polish women. The results support the hypothesis that the SNP309 polymorphism of the MDM2 gene may be associated with the incidence of endometrial cancer in the female population.

Telomerase activation can be considered as a critical step in cell immortalization. The enzyme elongates or maintains telomere length by adding to its end tandem TTAGGG repeats by using its endogenous RNA template. Telomerase is not detectable in most somatic cells but is upregulated in germ line cells and in 85-90% of human cancers, which suggests important role of telomerase in neoplastic transformation. Consequently, telomerase has been proposed as a potentially highly selective target for the development of antiproliferative agents. Platinum complexes are widely administrated in cancer therapy. A conjugate of selenite with diammineplatinum [(NH 3 ) 2 Pt(SeO 3 ) 2 ] is a novel potential anticancer drug. Using alkaline single cell gel electrophoresis (comet assay), we showed that the drug at 5-30 µM induced concentration-dependent damage to DNA of endometrial cancer cells derived from tumor samples. Sodium ascorbate at 10 and 50 µM reduced the extent of the DNA damage evoked by the drug. (NH 3 ) 2 Pt(SeO 3 ) reduced telomerase activity in the cells in a concentration-dependent manner as measured by using the telomere repeat amplification protocol (TRAP) assay. This effect was independent of sodium ascorbate. Therefore, mutagenic effects of the conjugate can be reduced by well-recognized antimutagen, sodium ascorbate, but it can still retain ability to affect neoplastic transformation. The results obtained indicate that (NH 3 ) 2 Pt(SeO 3 ) may specifically inhibit telomerase activity in endometrial cancer cells. Teratogenesis Carcinog. Mutagen. 22:73-82, 2002.