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Content available remote Sirt7 an emerging sirtuin: deciphering newer roles
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EN
A pilot study on relationships of selected molecular factors [erbB-1, erbB-2, erbB-3, and c-myc oncogene average gene copy numbers (AGCN); steroid receptors and pS2 gene expression; tumor cells' DNA values] to the ex vivo chemosensitivity of ovarian cancer in a modified adenosine triphosphate cell viability chemosensitivity assay (ATP-CVA), was performed. Despite the relatively small number of patients, numerous correlations among the factors tested were found. Nevertheless, only c-myc gene dosage positively affected ex vivo chemosensitivity of tumors tested.
EN
 The exact function of the protein product of N-myc downstream regulated 1 gene (NDRG1) is unclear. Depending on the tissue type the NDRG1 protein is localized in the cytoplasm, nucleus, mitochondrion or membranes. Moreover, the expression of NDRG1 may be altered by several factors such as hypoxia, heavy metals, DNA damage, hormones, oncogene, and tumor-suppressor genes. A number of studies emphasize the role of NDRG1 in cancerogenesis. Presumably NDRG1 participates in angiogenesis, metastases, and mechanisms leading to anti-cancer drug resistance. This review summarizes current knowledge about the NDRG1 gene and the position of NDRG1 protein in the cellular machinery. The role of NDRG1 in cancer pathogenesis and its possible usefulness as a prognostic factor for patients with cancer is also discussed.
EN
The relationship between HPV (Human Papillomavirus) and cervical carcinoma is very strong, causal, constant, specific and universal. HPV infection precedes the occurrence of preinvasive carcinoma and the evidence for biological probability of such relationship does not leave any doubt. Out of high-risk HPV types, the most often occurring in cervical infections types 16 and 18 were placed in the first group of human carcinogens. However, HPV infection is not the only factor of malignant neoplasm development. Neuroplastic transformation of cervical epithelium requires the presence of cofactors. In recent years, higher role is ascribed to the influences of steroid hormones, including estradiol and progesterone. In normal and neoplastic cells of uterine cervix, the occurrence of receptors for steroid hormones was described. In the regulatory region of oncogenic HPV hormone response elements were found. Receptors combined with steroid hormones functioning as transcription factors may influence the expression of viral oncogens E6 and E7 through stimulation of proliferation and transformation. The aim of this study was to analyse the influence of 17ß-estradiol on the amount of proteins E6 and E7 HPV 18 and to evaluate the transcript E6/E7 after incubation of HeLa line cells with 17ß-estradiol. The results revealed stimulating influence of the hormone on the expression of proteins and mRNA at concentrations of lx10-7M. At high concentrations of 1x10- 4M, estradiol was inhibiting transcription and expression of oncoproteins.
EN
Many models of tumour formation have been put forth so far. In general they involve mutations in at least three elements within the cell: oncogenes, tumour suppressors and regulators of telomere replication. Recently numerous mutations in mitochondria have been found in many tumours, whereas they were absent in normal tissues from the same individual. The presence of mutations, of course, does not prove that they play a causative role in development of neoplastic lesions and progression; however, the key role played by mitochondria in both apoptosis and generation of DNA-damaging reactive oxygen species might indicate that the observed mutations contribute to tumour development. Recent experiments with nude mice have proven that mtDNA mutations are indeed responsible for tumour growth and exacerbated ROS production. This review describes mtDNA mutations in main types of human neoplasia.
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