Online ISSN: 3007-0244,
Print ISSN:  2410-4280
FORMATION OF FOCI OF P53 BOUND PROTEIN 1 IN THYROID TUMORS: ACTIVATION OF GENETIC INSTABILITY DURING THYROID CARCINOGENESIS. LITERATURE REVIEW
Introduction: In our days big successes have been reached in studying of molecular–cellular mechanisms in carcinogenesis, establishing the role of oncogens and antioncogens in the development of tumors with various localization, including thyroid cancer. The vast majority of benign and malignant tumors of the thyroid gland develops from the follicular epithelium, which have different degrees of differentiation, different morphogenetic and biochemical features, clinical course and prognosis. Objective: to conduct a search for scientific information on the activation of genetic instability in the course of thyroid carcinogenesis. Search strategy: The search for sources was carried out on the basis of Pubmed (https://www.ncbi.nlm.nih.gov/pubmed/), using the specialized search engine Google Scholar and in the electronic scientific library CyberLeninka. Search depth was 13 years: from 2004 till 2017. The following key queries were used: adenoma, oncocytes, expression, thyroid, 53BP1. Inclusion criteria: publications that are in full-text access; articles in English, Russian, studies conducted in the near and far abroad. Exclusion criteria: articles describing isolated cases; articles published before 1991; summary of reports. A total of 1533 sources were found, of which 75 were selected for further analysis. Search results: Analysis of the literature data showed that follicular adenoma (FA) is the most common form of thyroid tumors and occurs in 4-7% of the adult population [12]. FA develops both in the intact organ and on the background of any pathological changes, especially nodular goiter and chronic autoimmune thyroiditis [49]. One of the most difficult aspects of studying Hurthle’s cell tumors is to determine whether the lesion is benign or malignant. Initially, it was believed that Hurthle's cell is the result of senile changes in the thyroid follicular-epithelial cell, because Hurthle’s cells are more common in the elderly. Most likely, this assumption is not far from the truth. Hurthle’s cells are less active than follicular cells, their production of thyroglobulin is limited. At the same time, they demonstrate a high level of oxidative enzymes [41]. Numerous studies have shown that all forms of thyroid neoplasia are likely to have an oncocytic component. In particular, Trovisco V et al. (2004) it was found that BRAF FV600E mutations are found in many common types of PTCs and in oncocyte variants of PTC, while this anomaly is not detected in oncocytic follicular variants of papillary cancer [65,66]. Discussion of the search results: For prognosis improving of oncocyte follicular adenomas of the thyroid glands with traditional methods, it is necessary to include molecular genetics methods, create possibilities to diagnose diseases at the level of altered DNA structure, allow to determine localization of hereditary disorders. Molecular genetic methods can identify mutations which connected associated even with the replacement of one / single basis.
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Козыкенова Ж.У., Жетписбаев Б.А., Нурмадиева Г.Т., Уразалина Н.М., Ибрагимова Л.А. Формирование очагов Р53 связанного белка 1 в опухолях щитовидной железы: активация генетической нестабильности в течении канцерогенеза щитовидной железы. Обзор литературы // Наука и Здравоохранение. 2019. 2 (Т.21). С. 25-37. Коzykenova Zh.U., Zhetpisbaev B.А., Nurmadieva G.Т., Urazalina N.М., Ibraqimova L.А. Formation of foci of P53 bound protein 1 in thyroid tumors: activation of genetic instability during thyroid carcinogenesis. Literature review. Nauka i Zdravookhranenie [Science & Healthcare]. 2019, (Vol.21) 2, pp. 25-37. Козыкенова Ж.У., Жетписбаев Б.А., Нурмадиева Г.Т., Уразалина Н.М., Ибрагимова Л.А. Қалқанша безі ісіктерінде р53-байланыстырушы нәруыз 1 ошақтарының қалыптасуы: қалқанша безі канцерогенезінде геномды тұрақсыздықтың белсенділігі. Әдебиеттерді шолу // Ғылым және Денсаулық сақтау. 2019. 2 (Т.21). Б. 25-37.

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