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EN
Introduction. Estrogen receptors (ER) are members of nuclear receptors that act in the ER signaling pathway regulating the pathophysiology of hormone-responsive target cells including breast tissue. Aim. This detailled review literature was written on the pathophysiology of ER signaling as well as the effect altered ERα and associated pathway derangement in the oncogenesis of breast cancer. Material and methods. This review was performed according to systematic literature search of three major bibliographic databases (Scopus, PubMed, and Cochran). Analysis of the literature. In this pathway, estrogen receptor alpha (ERα) is a key estradiol-17β (E2) induced transcription factor that has been implicated in the initiation and development of the major fraction of breast cancers. Hence understanding the ERα-mediated ER signaling that results in alterations from normal phenotypic features of breast tissue to the oncogenic features of breast cancer is important. The oncogenic effect of ERα in ER signaling is driven by combinations of molecular assets within the cancer cells. Normally, the transcriptional activity of ERα is controlled by tight regulation of its protein level inside the cells. Altered stability and activity of ERα due to its phosphorylation, ubiquitination, glycosylation, sumoylation, and acetylation events can trigger oncogenic ER signaling. Conclusion. The function and activity of ERα is also modulated by its interaction with coregulators as well as crosstalk with oncogenic factors from other oncogenic pathways. These all events increase the complexity of the progression of ER+ breast cancer and its response to endocrine therapy
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EN
Introduction and aim. Paired box 8 (PAX-8) is a specific transcription factor known as a protein product gene that plays an essential role in organogenesis and oncogenesis. The aim of this paper was to discuss structure and function of PAX-8. The aim of this study is to determine the utility of PAX-8 in cytology effusions with metastatic tumor. Material and methods. This article is a review done in regards to discuss the role knowledge on PAX-8 especially in oncogenesis and organogenesis. Analysis of the literature. Current information about PAX-8 is presented. Conclusion. The PAX family of genes plays an important role in the formation of tissues and organs during embryonic development and in maintaining the proper functioning of certain cells after birth.
EN
ras-encoded p21 protein expression was investigated immunohistochemically in 10 specimens of human endometrial adenocarcinoma. The control group consisted of 5 proliferative endometrium slides. The analysis was performed by using the biotin-streptavidin-peroxidase AEC detection system. An immunohistochemical histologic H- score according to Nyholm et al. [1] was calculated in a semiquantitative fashion incorporating intensity and distribution of staining. Adenocarcinoma glandular cells stained positively in 6 out of 10 specimens (n=6; H-score 0.71; range 0.3-1.15), whereas adenocarcinoma stromal cells exhibited a reddish-brown color in all specimens analyzed (n=10; H-score 0.83; range 0.3-1.5). Only one out of 5 proliferative endometrium slides stained positively for ras p21 (H-score 0.3). Our observations suggest that in human endometrial adenocarcinomas not only glandular but also stromal cells reacted strongly with monoclonal antibody NCC-RAS-001 raised against ras p21 protein. Enhanced ras p21 expression adenocarcinoma stromal cells in comparison with adenocarcinoma glandular cells may suggest that stromal cells are involved strongly in the neoplasm formation.
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tom 57
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nr 4
375-383
EN
Leptin is an adipocyte-derived hormone regulating energy homeostasis and body weight. Leptin also plays a role in hematopoesis, cell cycle regulation, and in oncogenesis. The leptin receptor is a single transmembrane protein belonging to the superfamily of cytokine receptors, structurally related to the hemopoietin receptor family. The aim of the study was to evaluate bone marrow and peripheral blood leptin level and frequency of distribution of leptin receptor gene polymorphism Gln223Arg in children with acute leukemia. The examined group included 92 children with acute leukemia (83 ALL and 9 AML) and 39 non-leukemic control children. Leptin level was measured by ELISA method at the day of leukemia diagnosis. Genomic DNA was isolated with the use of a column method and the genotyping of DNA sequence variation was carried out by the restriction enzyme analysis of PCR – amplified DNA. The samples were then electrophoresed on 2.5% agarose gel. Leptin level in leukemic children was lower than in healthy children. Bone marrow leptin level was significantly lower than that in the blood in leukemic children with ALL-T and AML. An analysis of frequency distribution of the Gln233Arg polymorphism in the leptin receptor gene in leukemic children showed lack of differences between the patients and controls. There was no difference in the genotype frequencies between the leukemic AML and ALL groups either. The results indicate a possible relation between the leptin level and leukemia development in children. The effectory effect of the hormone seems not related to Gln223Arg polymorphism of its receptor.
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2005
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tom 56
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nr 1
1-14
PL
Na podstawie piśmiennictwa omówiono podstawy epigenetycznych zmian metylacji DNA, jako alternatywnego mechanizmu transformacji nowotworowej komórki Przedstawiono rolą metylacji DNA w regulacji ekspresji genów w aspekcie rakotwórczego działania związków chemicznych nie wywołujących bezpośrednich uszkodzeń DNA.
EN
It is increasingly accepted that the initiation of chemical carcinogenesis should be considered as a transformation process of a normal cell caused by genetic changes, i.e. mutational DNA damage and/or epigenetic changes, which render normal gene expression impossible with the preservation of the DNA sequence intact. Epigenetic DNA methylation changes have been among the most extensively investigated processes in the recent years. Many types of cancer cells have been found to exhibit an increased or reduced level of CpG sequence methylation in promoter regions of genes, especially the genes whose protein products take part in the control of cell cycle regulation. In view of the fact that DNA methylation is thought to play a role in gene expression, its abnormal level in the genes that encode proteins participating in the control of the cell cycle and apoptosis regulation may disturb cell homeostasis resulting in pathologies that may, in turn, lead to neoplastic transformation. Although changes in the mechanisms of transcriptional activity caused by methylation of cytosine in CpG sequences have not been completely elucidated, it has been determined that this relationship is associated with a decreased level of histone acetylation, which induced a more densely-packaged chromatin structures in the methylated regions of chromosomal DNA. A large proportion of chemical carcinogens consists of chemicals whose carcinogenic activity is not related to direct damage of the genetic material. The changes in DNA methylation are being considered as one mechanism of action for non-genotoxic carcinogens (NGCs). The significance of nongenotoxic agents in the development of the carcinogenesis rocess indicate that their mechanisms of the action should be investigated in terms of health hazards they pose to humans exposed to this type of environmental pollutants.
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