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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">ketendo</journal-id><journal-title-group><journal-title xml:lang="ru">Клиническая и экспериментальная тиреоидология</journal-title><trans-title-group xml:lang="en"><trans-title>Clinical and experimental thyroidology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">1995-5472</issn><issn pub-type="epub">2310-3787</issn><publisher><publisher-name>Endocrinology Research Centre</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.14341/ket20062116-20</article-id><article-id custom-type="elpub" pub-id-type="custom">ketendo-4513</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Articles</subject></subj-group></article-categories><title-group><article-title>КЛИНИКО-ГЕНЕТИЧЕСКИЕ АСПЕКТЫ СПОРАДИЧЕСКОГО НЕМЕДУЛЛЯРНОГО РАКА ЩИТОВИДНОЙ ЖЕЛЕЗЫ</article-title><trans-title-group xml:lang="en"><trans-title>Clinical and Genetic Aspects of Sporadic Non-Medullar Thyroid Cancer</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Rumjanzeva</surname><given-names>U</given-names></name></name-alternatives><bio xml:lang="ru"><p>Отделение радиохирургического лечения закрытыми радионуклидами</p></bio><email xlink:type="simple">-</email></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Rumjanzev</surname><given-names>P</given-names></name></name-alternatives><bio xml:lang="ru"><p>Отделение радиохирургического лечения закрытыми радионуклидами</p></bio><email xlink:type="simple">-</email></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Ilyin</surname><given-names>A</given-names></name></name-alternatives><bio xml:lang="ru"><p>Отделение радиохирургического лечения закрытыми радионуклидами</p></bio><email xlink:type="simple">-</email></contrib></contrib-group><pub-date pub-type="collection"><year>2006</year></pub-date><pub-date pub-type="epub"><day>15</day><month>03</month><year>2006</year></pub-date><volume>2</volume><issue>1</issue><issue-title>ТОМ 2, №1 (2006)</issue-title><fpage>16</fpage><lpage>20</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Rumjanzeva U., Rumjanzev P., Ilyin A., 2006</copyright-statement><copyright-year>2006</copyright-year><copyright-holder xml:lang="ru">Rumjanzeva U., Rumjanzev P., Ilyin A.</copyright-holder><copyright-holder xml:lang="en">Rumjanzeva U., Rumjanzev P., Ilyin A.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.cet-endojournals.ru/jour/article/view/4513">https://www.cet-endojournals.ru/jour/article/view/4513</self-uri><abstract><p>Роль соматических мутаций при спорадическом раке щитовидной железы (РЩЖ) в настоящее время изучена недостаточно. Вероятно, они не являются этиологическими факторами канцерогенеза, но, по данным многих исследователей, могут участвовать в патогенезе РЩЖ, определяя его клиническое течение и прогноз. На сегодняшний день основными протоонкогенами, участвующими в развитии злокачественных новообразований ЩЖ считаются RET/PTC, TRK, PTEN, P53, RAS, MET, PFARγ. С помощью генетического исследования ученые пытаются решать проблемы дифференциальной диагностики РЩЖ (цитокератин-19, цитокератин-20, антиген мезотелиальных клеток (Hector Battifora MEsotelial (cell), или HBME-1) и потери гетерозиготности (LOH) в коротком плече 3-й хромосомы (ген VHL - von Hippel Lindau, 3р26). Недавно в зарубежной литературе появились сообщения об обнаружении активирующих мутаций в гене BRAF, наиболее часто встречающихся при меланоме и папиллярном РЩЖ. Прогноз РЩЖ может отражать потеря гетерозиготности (Loss Of Heterozygosity, LOH) как биологическая поломка вообще, а также изменения в гене опухолевой супрессии P53, которые чреваты снижением дифференцировки опухоли, что значительно ухудшает прогноз заболевания. Таким образом, у генетиков и клиницистов остается еще много спорных вопросов о роли генома в патогенезе спорадических случаев РЩЖ. Необходимы дальнейшие исследования в данной области для уточнения влияния генетических поломок на активность опухолевого роста, и следовательно, для определения прогноза клинического течения заболевания с целью выбора адекватной тактики лечения в каждом конкретном случае.</p></abstract><trans-abstract xml:lang="en"><p>The role of somatic mutations in sporadic thyroid cancer is unclear today. Probably they coming out as aetiological factors in carcinogenesis as well as, respectfully to many authors, can to participate in TC pathogenesis and to determine the clinical course and prognosis of the disease. For today as main oncogenes taking part in initiation of thyroid malignant tumors are considered: RET/PTC, TRK, PTEN, P53, RAS, MET, PPARγ. By means of genetic investigations scientists are trying to solve problems with thyroid cancer differentiated diagnostics (cytokeratin-19, cytokeratin-20, mesothelial cells antigen (Hector Battifora MEsotelial (cell) or HBME-1), loss of heterozigitoty (LOH) in short arm of 3 chromosome (gene VHL -von Hippel Lindau, 3р26). Recently in foreign literature appeared reports of activated mutations in gene BRAF which most frequently are occurred in melanoma and papillary TC. Prognosis of thyroid cancer may reflected by the LOH as a biological breakage as well as changes of tumor suppressive gene P53 which fraught with decrease of disease prognosis. Thus, both researchers and clinicians have many questions concerning the role of genome, particularly in order to precise of genetic abnormality influence on tumor growth and therefore for assessment of clinical prognosis and with aim to chose adequate treatment tactic in each case.</p></trans-abstract></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Bevan S., Pal T., Greenberg C.R. et al. A comprehensive analysis of MNG1, TCO1, fPTC, PTEN, TSHR, and TRKA in familial non-medullary thyroid cancer: confirmation of linkage to TCO1 // J. Clin. Endocrnol. Metab. 2001. V. 86. N 8. P. 3701-3704.</mixed-citation><mixed-citation xml:lang="en">Bevan S., Pal T., Greenberg C.R. et al. 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