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<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Bone and soft tissue sarcomas, tumors of the skin</journal-id><journal-title-group><journal-title xml:lang="en">Bone and soft tissue sarcomas, tumors of the skin</journal-title><trans-title-group xml:lang="ru"><trans-title>Саркомы костей, мягких тканей и опухоли кожи</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2219-4614</issn><issn publication-format="electronic">2782-3687</issn><publisher><publisher-name xml:lang="en">Publishing House ABV Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">187</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>EXPERIMENTAL ONCOLOGY</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>ЭКСПЕРИМЕНТАЛЬНАЯ ОНКОЛОГИЯ</subject></subj-group><subj-group subj-group-type="article-type"><subject></subject></subj-group></article-categories><title-group><article-title xml:lang="en">Molecular biomarkers oftypel neurofibromatosis</article-title><trans-title-group xml:lang="ru"><trans-title>Молекулярно-биологические маркеры неврофиброматоза I типа</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Stepanova</surname><given-names>E. V.</given-names></name><name xml:lang="ru"><surname>Степанова</surname><given-names>Е. В.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>e_stepanova@nm.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Lichinitser</surname><given-names>M. R.</given-names></name><name xml:lang="ru"><surname>Личиницер</surname><given-names>М. Р.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Bokhyan</surname><given-names>B. Y.</given-names></name><name xml:lang="ru"><surname>Бохян</surname><given-names>В. Ю.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Fedenko</surname><given-names>A. A.</given-names></name><name xml:lang="ru"><surname>Феденко</surname><given-names>А. А.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Charatishvili</surname><given-names>T. K.</given-names></name><name xml:lang="ru"><surname>Харатишвили</surname><given-names>Т. К.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Aliev</surname><given-names>M. D.</given-names></name><name xml:lang="ru"><surname>Алиев</surname><given-names>М. Д.</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">N.N. Blokhin Russian Cancer Research Center, Russian Academy of Medical Sciences</institution></aff><aff><institution xml:lang="ru">Российский онкологический научный центр им. Н.Н. Блохина РАМН</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2010-11-11" publication-format="electronic"><day>11</day><month>11</month><year>2010</year></pub-date><volume>2</volume><issue>4</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>55</fpage><lpage>58</lpage><history><date date-type="received" iso-8601-date="2022-01-11"><day>11</day><month>01</month><year>2022</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2010, Stepanova E.V., Lichinitser M.R., Bokhyan B.Y., Fedenko A.A., Charatishvili T.K., Aliev M.D.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2010, Степанова Е.В., Личиницер М.Р., Бохян В.Ю., Феденко А.А., Харатишвили Т.К., Алиев М.Д.</copyright-statement><copyright-year>2010</copyright-year><copyright-holder xml:lang="en">Stepanova E.V., Lichinitser M.R., Bokhyan B.Y., Fedenko A.A., Charatishvili T.K., Aliev M.D.</copyright-holder><copyright-holder xml:lang="ru">Степанова Е.В., Личиницер М.Р., Бохян В.Ю., Феденко А.А., Харатишвили Т.К., Алиев М.Д.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://sarbon.abvpress.ru/jour/article/view/187">https://sarbon.abvpress.ru/jour/article/view/187</self-uri><abstract xml:lang="en"><p>Neurofibromatosis type I is a autosomal dominant hereditary disorder caused by NF1 gene mutations. The main molecular mechanisms contributes to tumor formation in neurofibromatosis type I is angiogenesis stimulation and ras, AKT-mTOR signaling pathways activation. We show that these tumors expressed c-kit and VEGF. Information about clinical trials of target therapy for neurofibromatosis I type patient treatment is cited.</p></abstract><trans-abstract xml:lang="ru"><p>Нейрофиброматоз I типа - аутосомно-доминантное наследственное заболевание, связанное с мутациями в гене NF1. Основными молекулярными механизмами развития опухолей при нейрофиброматозе I типа является стимуляция ангиогенеза и сигнальных путей ras, AKT-mTOR. Нами показано, что в этих опухолях экспрессируется c-kit и VEGF. Приводятся данные о клинических испытаниях таргетных препаратов у больных нейрофиброматозом I типа.</p></trans-abstract><kwd-group xml:lang="en"><kwd>molecular biomarkers</kwd><kwd>neutofibromatosis I type</kwd><kwd>target therapy</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>молекулярно-биологические маркеры</kwd><kwd>нейрофиброматоз I типа</kwd><kwd>таргетная терапия</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Korf B.R. Clinical Features and Pathobiology of Neurofibromatosis 1. J. Child Neurol. 2002, v. 17, p. 573-577.</mixed-citation></ref><ref id="B2"><label>2.</label><mixed-citation>Ferner R.E. Neurofibromatosis type 1. Eur. J. Hum. Genet. 2007, v. 15, № 2, p. 131-8.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Korf B.R. Plexiform neurofibromas. Am. J. Med. Genet. 1999, v. 89, p. 31-37.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Korf B.R. 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