Molecular Genetic Aspects of Thyroid Carcinogenesis
About the author:
Mugychuk O. V., Vinnyk U. O., Vasko A. R., Gorbenko V. M., Gargin V. V.
Heading:
CONTENTS
Type of article:
Scentific article
Annotation:
Thyroid cancer is considered one of the most common endocrine malignancy, with a characteristic tendency to increase the frequency of the disease in both industrialized countries and in the Third World. According to medical statistics, Ukraine is not an exception in this list. Given the complexity and depth to the problem, consider only some aspects of carcinogenesis that are being discussed currently in the academic world. Oncogenes – a family of genes that are present in normal body cells and potentially (after mutation) in coopera tion with each other neoplastic transformed cells. Oncogenes encode a particular protein, the activity of which is associated with one of the stages of carcinogenesis, that none of oncogenes not able to make the entire process of carcinogenesis, and causes only a stage of neoplastic transformation – immortality, promotion, induction of tumor phenotype, support the transformation of the state and others. The main distinction of oncogenes and antionco genes is phenotypical effect – oncogene causes neoplastic transformation and immortality and antioncogen rather inhibits division and causes reversal. Protooncogene – normal gene cells that are involved in the regulation of proliferation and differentiation, activation of which can cause neoplastic transformation. Activated protooncogene called cellular oncogenes. 4 basic mechanisms of oncogene activation are known: 1) insertional activation (embedded in the cell’s genome viral genes); 2) chromosome translocation sites that are protooncogene; 3) amplification of genes; 4) onepoint mutations. Tumor growth is the result of an irreversible disruption of the stages of regulation that may arise or increase the activity of the mechanisms of stimulation, or with the loss of activity of inhibitors of cell growth. It is believed that the critical stage of neoplastic transformation is to delay the normal differentiation with excessive stimulation to divi sion. So as a result of genetic damage in malignant cells is unregulated expression of growth factors or components of their signaling pathway or inhibition mechanisms of inactivation. The present level of development of medicine leaves no doubt that the leading role in the genesis of neoplastic transformation played a violation of genetic information, and adverse environmental conditions affect the process indirectly contributing to the accumulation of mutations. There are several factors that may increase the likelihood of cancer, but most cancer patients have no obvious risk factors. Due to the discovery protooncogene, oncogene and tumor suppressor has made substantial progress in understanding the mechanisms of carcinogenesis, which gained molecular oncology. Thus, conducted studies help us to understand the mechanism of carcinogenesis in the thyroid gland. However, the practical aspects of these studies used small, although implementing them in practical medicine can help not only the primary diagnosis, such as anaplastic and poorly differentiated thyroid cancers, and in the timely diagnosis of distant metastases and pathogenetic treatment, especially locallyadvanced and generalized forms of thyroid cancer.
Tags:
thyroid cancer, cell proliferation factors, oncogenes, protooncogene, tumor suppressor
Bibliography:
- афанасьева з. а. иммуноморфологические исследования в диагностике опухолей щитовидной железы / з. а. афанасьева, C. B. петров, р. Ш. Хасанов // российский онкологический журнал. – 2005. № 5. – с. 5054.
- генетические аспекты рака щитовидной железы / р. Ф. гарькавцева, т. п. казубская, и. е. лиснянский [и др.] // про блемы эндокринологии. – 2002. – т. 48, № 4. – с. 1620.
- гистологические и молекулярнобиологические маркеры злокачественности в различных вариантах папиллярного рака щитовидной железы / т. е. свиридова, е. а. коган, М. а. пальцев [и др.] // архив патологии. – 2002. – № 6. – с. 1923.
- заридзе д. г. канцерогенез / д. г. заридзе. – Москва : «Медицина», 2004. – 576 с
- иммуногистохимическая характеристика инфильтративного роста высокодифференцированных карцином щитовид ной железы / т. а. чипышева, М. и. бронштейн, В. д. ермилова [и др.] / архив патологии. – 2002. – № 3. – с. 2025.
- Молекулярногенетические аспекты новообразований щитовидной железы / дедов и. и., трошина е. а., Мазурина н. В. [и др.] // проблемы эндокринологии. – 2000. – № 2. – с. 2230.
- петров C. B. руководство по иммуногистохимической диагностике опухолей человека. издание 3е, дополненное и переработанное / C. B. петров, н. т. райхлин. – казань, 2004. – 456 с.
- прогностическое значение экспрессии тиреоглобулина и онкомаркеров (р53, EGFR, RETонкогена) в различных ва риантах папиллярного рака щитовидной железы (клиникоморфологическое и иммуногистохимическое исследова ние) / е. а. коган, е. б рожкова., В. п. [середин и др.] // архив патологии. – 2006. – № 4. – с. 811.
- профилактика и ранняя диагностика злокачественных новообразований. пособие для врачей / В. и. чиссов, В. В. старинский, A. C. Мамонтов [и др.]. – Москва, 2007. – 31 с.
- Хмельницкий O. K. Цитологическая и гистологическая диагностика заболеваний щитовидной железы. руководство / O. K. Хмельницкий. – спб.: сотис, 2002. – 288 с
- Galectin3 interaction with ThomsenFriedenreich disaccharide on cancer associated MUC1 causes increased cancer cell endothelial adhesion / L. G. Yu, N. Andrews, Q. Zhao [et al.] // Journal of Biological Chemistry. – 2007. – Vol. 282, № 1. – P. 773781
- High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTCRASBRAF signaling pathway in papillary thyroid carcinoma / E. T. Kimura, M. N. Nikiforova, Z. Zhu [et al.] // Cancer Research. – 2003. – Vol. 63, № 7. – P. 14541457
- Immunoexpression of HBME1, High Molecular Weight Cytokeratin, Cytokeratin 19, Thyroid Transcription Factor1, and E cadherin in Thyroid Carcinomas / Y. L. Choi, M. K. Kim, J. W. Suh [et al.] // Journal Korean Academy of Medical Sciences. – 2005. – Vol. 20, № 5. – P. 853859.
- Overexpression of p53 protein and MDM2 in papillary carcinomas of the thyroid: Correlations with clinicopathologic features / S. Horie, H Maeta., K. Endo [et al.] // Pathology International. – 2008. – Vol. 51, № 1. – P. 1115.
- Rosai J. Pitfalls in thyroid tumor pathology / J. Rosai, E. Kuhn, M. L. Carcangiu // Histopathology. – 2006. – Vol. 49, № 2. – P. 107120
- Said S. Oncogenes and antioncogenes in human epithelial thyroid tumours / S. Said, M. Schlumberger, H. G. Suarez // Jour nal of Endocrinology Investigation. – 1994. – Vol. 17, № 5. P. 371379
- Vielh P. Immunocytochemistry and molecular pathology of follicular lesion of the thyroid / P. Vielh // 21st European Congress of Pathology. – 2007. – P. 36.
- Wang H. G. Mechanisms of Bcl2 protein function / H. G. Wang, J. C. Reed // Histology & Histopathology. – 1998. – Vol. 13, № 2. – P. 521530.
- Xing M. BRAF mutation in thyroid cancer / M. Xing // EndocrineRelated Cancer. – 2005. – Vol. 12, № 2. – P. 245262.
Publication of the article:
«Bulletin of problems biology and medicine» Issue 3 part 2 (111), 2014 year, 44-49 pages, index UDK 616006. 6091: 616. 441006. 6