Abstract
Thyroid cancer remains the most common malignancy of the endocrine system worldwide. The indicators of its morbidity and mortality rates have been increasing rapidly over the last decades. Most cases of differentiated thyroid cancer (follicular and papillary histotypes) are clinically manifested by nodular goiter frequently combined with uncertain results of cytological diagnosis (categories III and IV according to the Bethesda (Bethesda System for Reporting Thyroid Cytopathology) classification). All of that makes it difficult to choose a proper tactic for patient treatment. It is known that the development, progression, invasion, and metastasis of cancer cells are regulated by a variety of molecular mechanisms. This review describes several molecular aspects of thyroid nodules oncogenesis, as well as its most promising diagnostic tumor markers. Following molecular pathways are described in particular: gene mutations, protein tumor markers, and epigenetic effects of micro-RNA, histones, as well as DNA methylation. The study of the pathogenesis of this disease has a prognostic value and contributes to the search for effective therapeutic and diagnostic methods and their improvement. That is why we also reviewed modern test panels aimed at preoperative differential diagnosis of thyroid nodules. Summarizing the results of world research on this topic allows us not only to expand the understanding of the fundamental processes of oncogenesis, but also to outline promising areas for future experimental research projects. All of that together will contribute to developing new prognostic, diagnostic and therapeutic technologies, and as a result, will improve the quality of medical care for patients with thyroid cancer.
Highlights
Contacts: Thyroid cancer remains the most common malignancy of the endocrine system worldwide
Most cases of differentiated thyroid cancer are clinically manifested by nodular goiter frequently combined with uncertain results of cytological diagnosis (categories III and IV according to the Bethesda (Bethesda System for Reporting Thyroid Cytopathology) classification)
This review describes several molecular aspects of thyroid nodules oncogenesis, as well as its most
Summary
Рак щитовидной железы – распространенное злокачественное новообразование эндокринной системы. Большинство случаев дифференцированного рака щитовидной железы (фолликулярного и папиллярного гистотипов) клинически проявляются как узловой зоб. В данной статье описываются некоторые молекулярные аспекты онкогенеза узловых образований щитовидной железы, а также наиболее перспективные диагностические онкомаркеры. В частности, рассматривается роль генных мутаций, белковых маркеров, эпигенетических воздействий микроРНК, гистонов и метилирования ДНК в патогенезе рака щитовидной железы. Поэтому в исследовании были рассмотрены применяемые в настоящий момент тест-панели, направленные на дооперационную дифференциальную диагностику узловых образований щитовидной железы. Анализ и обобщение результатов исследований по данной теме позволят не только расширить понимание фундаментальных процессов онкогенеза, но и наметить перспективные направления планирования экспериментальных научных работ для разработки новых прогностических, диагностических и терапевтических технологий с целью повышения качества медицинской помощи пациентам с раком щитовидной железы. Ключевые слова: рак щитовидной железы, онкомаркеры, эпигенетика, микроРНК, гистоны, метилирование. Современные концепции молекулярного патогенеза рака щитовидной железы.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.