SUMMARYCancer chemoprevention is defined as the use of natural, synthetic or biological chemical agents to reverse, suppress or prevent carcinogenic progression of invasive cancer. Carcinogenesis is a complex multi-step process; therefore, it is necessary to attack cell proliferation, stimulate apoptosis and inhibit angiogenesis. There have been more than 60 randomised trials using chemopreventive potential agents.The success of several recent clinical trials in preventing cancer in high-risk populations suggests that chemoprevention is a rational and appealing strategy. In this review, we describe the conceptual basis for the chemoprevention of cancer, proven concepts of efficiency and current trends in the use of chemopreventive agents according to place and mechanism of action. We classify chemopreventive substances into seven groups based on their chemical structure and their effects, namely, deltanoids (paracalcitriol), retinoids (13-cis retinoic acid), non-steroidal anti-rheumatics (Deguelin), antiestrogens (genistein), polyphenols (curcumin), sulphur containing compounds (sulforaphane) and terpenes (lycopene). Chemoprevention is one of several promising strategies for reducing the incidence of malignant tumours or helping to prolong the time before recurrence.
Clinical diagnosis of gynaecological malignancies is usually successful in the advanced stages of the tumour, and this has a major impact on the success of therapy. Therefore, in the last few years, cancer research has tried to identify and characterise new biochemical and molecular markers needed as predictive indicators for the diagnosis of cancer. Our aim has been to search the molecular changes in gene expression of death receptor 6, glycoprotein M6B (Gpm6B) and genes associated with tumours of the female genital system. After isolation of messenger RNA (mRNA), transcription of mRNA into the cDNA was performed. The quantification of gene expression changes was detected using the reverse transcription polymerase chain reaction (RT-PCR) method. Analysis at the protein level was performed using the Western blot method. In both methods, we used actin as a housekeeping gene for normalisation. Numerical quantification of changes in expression and in the level of the specific proteins was evaluated using the Data Syngene program. Significant changes in the levels of protein and mRNA expression were detected, mainly in the death receptor 6 (Dr6) gene of patients suffering from cancer of the corpus and cervix uteri and ovarian cancer, which also corresponded with the level of protein Dr6. At the level of transcription, a significant increase in the expression levels of mRNA for the Gpm6B gene was detected, which led to an increase in corresponding protein in the peripheral blood of patients with gynaecological tumours against the healthy control group. This article could help to find an adequate marker for clinical application that will enable more sensitive detection of the early stages of gynaecological malignancies from the peripheral blood of patients.
The incidence of malignant melanoma worldwide continues to grow despite the enormous advances in topical and systemic therapy. This increase is recorded regularly even in countries where, as a result of public health campaigns, dermatological examination and subsequent treatment have become more frequent. However, there have been reports of a stable or even decreasing mortality rate that seem to contradict the objective increase in its incidence. The well-known risk factors for malignant melanoma include sunburns and occasional sunbathing, whereas regular sunbathing is associated with a lower incidence. Besides DNA damage, exposure to the sun also results in the synthesis of vitamin D (cholecalciferol) in the skin, which contributes to over 90% of circulating Calcidiol (25 (OH) D) in serum. Current cultural norms (dressing, working indoors, avoiding sun exposure, and dietary choices) affect the serum vitamin D level, resulting in severely low serum levels of vitamin D in some sectors of todays society. Emerging data suggests that mild, unprotected exposure to UV radiation or dietary supplementation with oral vitamin D can reduce cancer mortality. Supplementation with vitamin D or alternatively UV exposure may be regarded as an adjuvant for the treatment of many types of tumors (e.g. tumors of the colon, prostate, and breast). The effect of vitamin D on malignant melanoma may be due to its non-calcemic systemic effects. Additionally, vitamin D may have more pronounced effects locally in the skin because of the unique ability of keratinocytes to synthesize the active form of vitamin D.Key words: malignant melanoma - vitamin D - adjuvant treatment therapy - clinical oncology The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study. The Editorial Board declares that the manuscript met the ICMJE recommendation for biomedical papers.Submitted: 7. 10. 2016Accepted: 26. 7. 2017.
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