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Tiroid kanserinde moleküler etyolojik faktörler

Year 2014, , 128 - 146, 28.03.2014

Semra Özdemir , Öztürk Özdemir

https://doi.org/10.7197/cmj.v36i1.1008002565

Abstract

Özet

Tiroid kanseri en sık görülen endokrin kanserdir ve dünya çapında sıklığı giderek artmaktadır. Son zamanlardaki moleküler teknolojik çalışmalar, tiroid kanser tanı ve tedavisinin doğru yapılabilmesi için etyolojik parameterlere yoğunlaşmış durumdadır. Şimdiye kadar bu konuda üzerinde çalışılmış birçok moleküler ve immünohistokimyasal parametre bildirilmiştir. Son literatür bilgileri, tiroid kanseri ile genetik parametreler arasında güçlü bir ilişkinin olduğunu ortaya koymuştur. Normal tiroid dokusunda kanser tetiklenmesi ve ilerlemesi, nokta mutasyonlar, translokasyonlar, kromozomlararası yeniden düzenlemeler (rearrangements), aktif proto-onkogen ve inaktif tümör baskılayıcı gen şeklinde meydana gelen epigenetik alterasyonlar gibi çoklu genetik ve epigenetik değişikliklerle gerçekleşmektedir. Yine son rapor edilen literatür bilgileri, proto-onkogenlerin fonksiyon kazanarak ve tümör süpresör genlerin ise fonsiyon kaybederek tiroid kanserlerinin tetiklenmesinde ve/veya ilerlemesinde görev yapmaları bu gen ailelerinin karsinogenezisde antagonistik bir etkiye sahip olduklarını göstermektedir. Tiroid doku tümörleri ve nodüllerinin, moleküler genetik belirteçler açısından (somatik, germ-line) kimliklendirilmesinin malign-benign doku ayırt edilmesinde, kesin tanı ve etkin tedaviçin hayati öneme sahiptir. Her bir kanser olgusunda özgün moleküler genetik değişikliklerin neler olduğu öncelikle tespit edilmelidir. Ancak bu durumda kanser subtiplemesi doğru yapılabilir ve bu doğrultuda hastanın doğru ve etkin tedavi alması sağlanabilir. İlgili nodül ve tümör dokusunun neden kanserleştiğinin ipuçlarını yine içinde barındırmaktadır, bu moleküler etyolojik sebeplerin doğru tespiti tiroid kanserlerinin tedavisi için yeni ve etkin tedavi stratejilerinin geliştirilmesine olanak sağlar. Bu derleme makalesinde son literatür bilgileri ışığında tiroid kanserlerinde doğrudan ve/veya aracılık eden moleküler genetik paremetreler ve etki mekanizmaları olabildiğince geniş bir spektrumda ele alınmıştır.

Anahtar sözcükler: Tiroid kanseri, tanı, prognoz, moleküler belirteçler

 

Abstract

Thyroid cancer is a common endocrine malignancy its prevelance is increasing worldwide. Currently, the application of molecular technologies has focused on etiological parameters for the accurate diagnosis and therapy of thyroid cancer. Until now in this issue many molecular and immunohistochemical parameters have been reported. Recent literature show that strong association between genetic parameters and thyroid cancer. Initiation and progression of thyroid cancers arise as the consequence of multiple genetic and epigenetic alterations such as; structural point mutations, chromosomal rearrangements and epigenetic events that activate proto-oncogenes and inactivate tumor suppressor genes. There are lots of various tumor-suppressor genes are epigenetically silenced in thyroid cancers. Gain-of-function for proto-oncogenes and loss-of-function for tumour supressor genes have a crucial role in the initiation and/or progression of the thyroid carcinogenesis. The determining of somatic and/or germline molecular alterations have been recognized as helpful diagnostic and prognostic markers and valuable tools for the management of tumoural/nontumuoral nodules in thyroid cancer patients. Known details about those molecular etiological parameters provide further research and clinical development targets, novel diagnostic and therapeutic strategies for thyroid cancers treatment. Current article reviews the molecular etiological alterations in thyroid cancer that help identify relevant biologic pathways to drive cancer development. Direct and undirect moleculer ethiological parametes and action mechanisims that play crucial role in the thyroid cancers widely reviewed in the currenr report.

Keywords: Thyroid cancer, diagnosis, prognosis, molecular markers

Keywords

Tiroid kanseri tanı prognoz moleküler belirteçler

References

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-

Year 2014, , 128 - 146, 28.03.2014

Semra Özdemir , Öztürk Özdemir

https://doi.org/10.7197/cmj.v36i1.1008002565

Abstract

Thyroid cancer is a common endocrine malignancy its prevelance is increasing worldwide. Currently, the application of molecular technologies has focused on etiological parameters for the accurate diagnosis and therapy of thyroid cancer. Until now in this issue many molecular and immunohistochemical parameters have been reported. Recent literature show that strong association between genetic parameters and thyroid cancer. Initiation and progression of thyroid cancers arise as the consequence of multiple genetic and epigenetic alterations such as; structural point mutations, chromosomal rearrangements and epigenetic events that activate proto-oncogenes and inactivate tumor suppressor genes. There are lots of various tumor-suppressor genes are epigenetically silenced in thyroid cancers. Gain-of-function for proto-oncogenes and loss-offunction for tumour supressor genes have a crucial role in the initiation and/or progression of the thyroid carcinogenesis. The determining of somatic and/or germline molecular alterations have been recognized as helpful diagnostic and prognostic markers and valuable tools for the management of tumoural/nontumuoral nodules in thyroid cancer patients. Known details about those molecular etiological parameters provide further research and clinical development targets, novel diagnostic and therapeutic strategies for thyroid cancers treatment. Current article reviews the molecular etiological alterations in thyroid cancer that help identify relevant biologic pathways to drive cancer development. Direct and undirect moleculer ethiological parametes and action mechanisims that play crucial role in the thyroid cancers widely reviewed in the currenr report.

Keywords

Thyroid cancer diagnosis prognosis molecular markers

References

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  • Morris LG, Sikora AG, Tosteson TD, Davies L. The increasing incidence of thyroid cancer: the influence of access to care. Thyroid 2013; 23: 885-91.
  • Boufraqech M, Patel D, Xiong Y, Kebebew E. Diagnosis of thyroid cancer: state of art. Expert Opin Med Diagn 2013; 7: 331-42.
  • Zimmerman D. Thyroid carcinoma in children and adolescents: diagnostic implications of analysis of the tumor genome. Curr Opin Pediatr 2013; 25: 528
  • Kleinau G, Neumann S, Grüters A, Krude H, Biebermann H. Novel insights on thyroid-stimulating hormone receptor signal transduction. Endocr Rev 2013; 34: 691-7
  • Fay DS. Cancer metabolism: feeding a worm to starve a tumor. Curr Biol 2013; 23: R557-9.
  • Nagayama Y. Thyroid cancer. Nihon Rinsho 2012; 70: 436-40.
  • Dvorkin S, Robenshtok E, Hirsch D, Strenov Y, Shimon I, Benbassat CA. Differentiated thyroid cancer is associated with less aggressive disease and better outcome in patients with coexisting hashimotos thyroiditis. J Clin Endocrinol Metab 2013; 98: 2409-14.
  • Nagarkatti SS, Faquin WC, Lubitz CC, Garcia DM, Barbesino G, Ross DS, Hodin RA, Daniels GH, Parangi S. Management of thyroid nodules with atypical cytology on fine-needle aspiration biopsy. Ann Surg Oncol 2013; 20: 60-5.
  • Figlioli G, Landi S, Romei C, Elisei R, Gemignani F. Medullary thyroid carcinoma (MTC) and RET proto-oncogene: mutation spectrum in the familial cases and a meta-analysis of studies on the sporadic form. Mutat Res 2013; 752: 36Makki FM, Taylor SM, Shahnavaz A, Leslie A, Gallant J, Douglas S, Teh E, Trites J, Bullock M, Inglis K, Pinto DM, Hart RD. Serum biomarkers of papillary thyroid cancer. J Otolaryngol Head Neck Surg 2013; 42: 16.
  • Papale F, Cafiero G, Grimaldi A, Marino G, Rosso F, Mian C, Barollo S, Pennelli G, Sorrenti S, De Antoni E, Barbarisi A. Galectin-3 expression in thyroid fine needle cytology (t-FNAC) uncertain cases: Validation of molecular markers and technology innovation. J Cell Physiol 2013; 228: 968-74.
  • Cui W, Sang W, Zheng S, Ma Y, Liu X, Zhang W. Usefulness of cytokeratin-19, galectin-3, and Hector Battifora mesothelial-1 in the diagnosis of benign and malignant thyroid nodules. Clin Lab 2012; 58: 673-80.
  • Rossi ED, Straccia P, Palumbo M, Stigliano E, Revelli L, Lombardi CP, Santeusanio G, Pontecorvi A, Fadda G. Diagnostic and prognostic role of HBME-1, galectin-3, and β-catenin in poorly differentiated and anaplastic thyroid carcinomas. Appl Immunohistochem Mol Morphol 2013; 21: 237-41.
  • Griffith OL, Chiu CG, Gown AM, Jones SJ, Wiseman SM.Biomarker panel diagnosis of thyroid cancer: a critical review. Expert Rev Anticancer Ther 2008; 8: 1399-413.
  • Cochand-Priollet B, Dahan H, Laloi-Michelin M, Polivka M, Saada M, Herman P, Guillausseau PJ, Hamzi L, Poté N, Sarfati E, Wassef M, Combe H, RaulicRaimond D, Chedin P, Medeau V, Casanova D, Kania R. Immunocytochemistry with cytokeratin 19 and anti-human mesothelial cell antibody (HBME1) increases the diagnostic accuracy of thyroid fine-needle aspirations: preliminary report of 150 liquid-based fine-needle aspirations with histological control. Thyroid 2011; 21: 1067-73.
  • Rosário PW, Penna GC, Brandão K, Souza BÉ. Usefulness of preoperative serum calcitonin in patients with nodular thyroid disease without suspicious history or cytology for medullary thyroid carcinoma. Arq Bras Endocrinol Metabol 2013; 57: 312-6.
  • Duntas LH. Clinical comments related to medullary thyroid cancer diagnosis and management. Thyroid Res 2013; 6 Suppl 1:S6.
  • Taccaliti A, Boscaro M. Genetic mutations in thyroid carcinoma. Minerva Endocrinol 2009; 34: 11-28.
  • Fusco A, Grieco M, Santoro M, Berlingieri MT, Pilotti S, Pierotti MA, Della Porta G, Vecchio G. A new oncogene in human thyroid papillary carcinomas and their lymph-nodal metastases. Nature 1987; 328: 170-2.
  • Vander Poorten V, Hens G, Delaere P. Thyroid cancer in children and adolescents. Curr Opin Otolaryngol Head Neck Surg 2013; 21: 135-42.
  • Li C, Lee KC, Schneider EB, Zeiger MA. BRAF V600E mutation and its association with clinicopathological features of papillary thyroid cancer: a metaanalysis. J Clin Endocrinol Metab 2012; 97: 4559-70.
  • Fernandez IJ, Piccin O, Sciascia S, Cavicchi O, Repaci A, Vicennati V, Fiorentino M. Clinical significance of BRAF mutation in thyroid papillary cancer. Otolaryngol Head Neck Surg 2013; 148: 919-25.
  • Ward LS, Kloos RT. Molecular markers in the diagnosis of thyroid nodules. Arq Bras Endocrinol Metabol 2013; 57: 89-97.
  • Cappola AR, Mandel SJ. Molecular testing in thyroid cancer: BRAF mutation status and mortality. JAMA 2013; 309: 1529-30.
  • Rosove MH, Peddi PF, Glaspy JA. BRAF V600E inhibition in anaplastic thyroid cancer. N Engl J Med 2013; 368: 684-5.
  • Park SJ, Sun JY, Hong K, Kwak JY, Kim EK, Chung WY, Choi JR. Application of BRAF, NRAS, KRAS mutations as markers for the detection of papillary thyroid cancer from FNAB specimens by pyrosequencing analysis. Clin Chem Lab Med 2013; 51: 1673-80.
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There are 68 citations in total.

Details

Primary Language Turkish
Journal Section Reviews
Authors

Semra Özdemir

Öztürk Özdemir

Publication Date March 28, 2014
Published in Issue Year 2014

Cite

AMA Özdemir S, Özdemir Ö. Tiroid kanserinde moleküler etyolojik faktörler. CMJ. March 2014;36(1):128-146. doi:10.7197/cmj.v36i1.1008002565