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[1]McLeod DS, Sawka AM, Cooper DS: Controversies in primary treatment of low-risk papillary thyroid cancer. Lancet 381:1046-1057 (2013)
[2]The People’s Goverment of Beijing Municipality: The report of health and population health in Beijing (2011)
[3]Mazzaferri EL, Jhiang SM: Long-term impact of initial surgical and medical therapy on papillary and follicular thyroid cancer. Am J Med 97:418-428 (1994)
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[5]Haugen BR, Kane MA: Approach to the thyroid cancer patient with extracervical metastases. J Clin Endocrinol Metab 95:987-993. (2010)
[6]Nixon IJ, Whitcher MM, Palmer FL, Tuttle RM, Shaha AR. The impact of distant metastases at presentation on prognosis in patients with differentiated carcinoma of the thyroid gland. Thyroid 22:884-889 (2012)
[7]Turner HE, Harris AL, Melmed S, Wass JA: Angiogenesis in endocrine tumors. Endocr Rev 24:600-632 (2003)
[8]Nikiforova MN, Kimura ET, Gandhi M, Biddinger PW, Knauf JA. BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas. J Clin Endocrinol Metab 88:5399-5404 (2003)
[9]Xing M, Westra WH, Tufano RP, Cohen Y, Rosenbaum E: BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancer. J Clin Endocrinol Metab 90:6373-6379 (2005)
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[12]Kimura ET, Nikiforova MN, Zhu Z, Knauf JA, Nikiforov YE. High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma. Cancer Res 63:1454-1457 (2003)
[13]Knauf JA, Ma X, Smith EP, Zhang L, Mitsutake N. Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiation. Cancer Res 65:4238-4245 (2005)
[14]Kim TY, Kim WB, Song JY, Rhee YS, Gong G. The BRAF mutation is not associated with poor prognostic factors in Korean patients with conventional papillary thyroid microcarcinoma. Clin Endocrinol (Oxf) 63:588-593 (2005)
[15]Xing M: Molecular pathogenesis and mechanisms of thyroid cancer. Nat Rev Cancer 13:184-199 (2013)
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[19]Liu Z, Hou P, Ji M, Guan H, Studeman K. Highly prevalent genetic alterations in receptor tyrosine kinases and phosphatidylinositol 3-kinase/akt and mitogen-activated protein kinase pathways in anaplastic and follicular thyroid cancers. J Clin Endocrinol Metab 93:3106-3116 (2008)
[20]Nikiforov YE: RET/PTC rearrangement in thyroid tumors. Endocr Pathol 13:3-16 (2002)
[21]Al-Nedawi K, Meehan B, Rak J: Microvesicles: messengers and mediators of tumor progression. Cell Cycle 8:2014-2018 (2009)
[22]Castellone MD, De Falco V, Rao DM, Bellelli R, Muthu M: The beta-catenin axis integrates multiple signals downstream from RET/papillary thyroid carcinoma leading to cell proliferation. Cancer Res 69:1867-1876 (2009)
[23]Miyagi E, Braga-Basaria M, Hardy E, Vasko V, Burman KD. Chronic expression of RET/PTC 3 enhances basal and insulin-stimulated PI3 kinase/AKT signaling and increases IRS-2 expression in FRTL-5 thyroid cells. Mol Carcinog 41:98-107 (2004)
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Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Molecular mechanisms in differentiated thyroid cancer
1 Center of Thyroid and Parathyroid, Department of General Surgery, Shanghai Sixth People’s Hospital, Shanghai Jiaotong University of Medicine, Shanghai, China
2 Department of Nuclear Medicine, Shanghai 10th People’s Hospital, Tongji University School of Medicine, Shanghai, China
3 Institute of Intervention Vessel, Tongji University, North Zhongshan Road, Shanghai, China
Abstract
Thyroid cancer is a common endocrine malignancy. The tumorigenesis of thyroid tumours has been identified in recent years, including numerous genetic alterations and several major signalling pathways. However, the molecular mechanisms involved in thyroid cancer metastasis remain controversial. Studies in thyroid cancer metastasis suggested that reactivation of several pathways, including epithelial to mesenchymal transition and microenvironment change, may be involved in thyroid cancer migration. The previously identified thyroid oncogenes, BRAF, RET/PTC and Ras, play important roles in regulating the metastatic process. Here, we review the recent knowledge eon molecular mechanisms involved in thyroid cancer metastasis.
Keywords
- hyroid Cancer
- Lymphaticand Distant Metastasis
- Oncogenes
- MicroRNA
References
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- [2] The People’s Goverment of Beijing Municipality: The report of health and population health in Beijing (2011)
- [3] Mazzaferri EL, Jhiang SM: Long-term impact of initial surgical and medical therapy on papillary and follicular thyroid cancer. Am J Med 97:418-428 (1994)
- [4] Sherman SI, Brierley JD, Sperling M, Ain KB, Bigos ST: Prospective multicenter study of thyroiscarcinoma treatment: initial analysis of staging and outcome. National Thyroid Cancer Treatment Cooperative Study Registry Group. Cancer 83:1012-1021 (1998)
- [5] Haugen BR, Kane MA: Approach to the thyroid cancer patient with extracervical metastases. J Clin Endocrinol Metab 95:987-993. (2010)
- [6] Nixon IJ, Whitcher MM, Palmer FL, Tuttle RM, Shaha AR. The impact of distant metastases at presentation on prognosis in patients with differentiated carcinoma of the thyroid gland. Thyroid 22:884-889 (2012)
- [7] Turner HE, Harris AL, Melmed S, Wass JA: Angiogenesis in endocrine tumors. Endocr Rev 24:600-632 (2003)
- [8] Nikiforova MN, Kimura ET, Gandhi M, Biddinger PW, Knauf JA. BRAF mutations in thyroid tumors are restricted to papillary carcinomas and anaplastic or poorly differentiated carcinomas arising from papillary carcinomas. J Clin Endocrinol Metab 88:5399-5404 (2003)
- [9] Xing M, Westra WH, Tufano RP, Cohen Y, Rosenbaum E: BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancer. J Clin Endocrinol Metab 90:6373-6379 (2005)
- [10] Kebebew E, Weng J, Bauer J, Ranvier G, Clark OH: The prevalence and prognostic value of BRAF mutation in thyroid cancer. Ann Surg 246:466-470; discussion 470-461 (2007)
- [11] Huber MA, Kraut N, Beug H: Molecular requirements for epithelial-mesenchymal transition during tumor progression. Curr Opin Cell Biol 17:548-558 (2005)
- [12] Kimura ET, Nikiforova MN, Zhu Z, Knauf JA, Nikiforov YE. High prevalence of BRAF mutations in thyroid cancer: genetic evidence for constitutive activation of the RET/PTC-RAS-BRAF signaling pathway in papillary thyroid carcinoma. Cancer Res 63:1454-1457 (2003)
- [13] Knauf JA, Ma X, Smith EP, Zhang L, Mitsutake N. Targeted expression of BRAFV600E in thyroid cells of transgenic mice results in papillary thyroid cancers that undergo dedifferentiation. Cancer Res 65:4238-4245 (2005)
- [14] Kim TY, Kim WB, Song JY, Rhee YS, Gong G. The BRAF mutation is not associated with poor prognostic factors in Korean patients with conventional papillary thyroid microcarcinoma. Clin Endocrinol (Oxf) 63:588-593 (2005)
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- [19] Liu Z, Hou P, Ji M, Guan H, Studeman K. Highly prevalent genetic alterations in receptor tyrosine kinases and phosphatidylinositol 3-kinase/akt and mitogen-activated protein kinase pathways in anaplastic and follicular thyroid cancers. J Clin Endocrinol Metab 93:3106-3116 (2008)
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- [29] Shevde LA, Welch DR: Metastasis suppressor pathways--an evolving paradigm. Cancer Lett 198:1-20 (2003)
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- [31] Horak CE, Lee JH, Marshall JC, Shreeve SM, Steeg PS: The role of metastasis suppressor genes in metastatic dormancy. APMIS 116:586-601 (2008)
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- [33] Arai T, Yamashita T, Urano T, Masunaga A, Itoyama S: Preferential reduction of nm23-H1 gene product in metastatic tissues from papillary and follicular carcinomas of the thyroid. Mod Pathol 8:252-256 (1995)
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- [35] von Wasielewski R, Rhein A, Werner M, Scheumann GF, Dralle H: Immunohistochemical detection of E-cadherin in differentiated thyroid carcinomas correlates with clinical outcome. Cancer Res 57:2501-2507 (1997)
- [36] Ringel MD, Hardy E, Bernet VJ, Burch HB, Schuppert F: Metastin receptor is overexpressed in papillary thyroid cancer and activates MAP kinase in thyroid cancer cells. J Clin Endocrinol Metab 87:2399 (2002)
- [37] Stathatos N, Bourdeau I, Espinosa AV, Saji M, Vasko VV: KiSS-1/G protein-coupled receptor 54 metastasis suppressor pathway increases myocyte-enriched calcineurin interacting protein 1 expression and chronically inhibits calcineurin activity. J Clin Endocrinol Metab 90:5432-5440 (2005)
- [38] Espinosa AV, Shinohara M, Porchia LM, Chung YJ, McCarty S: Regulator of calcineurin 1 modulates cancer cell migration in vitro. Clin Exp Metastasis 26:517-526 (2009)
- [39] Ito Y, Yoshida H, Uruno T, Nakano K, Takamura Y: KAI1 expression in thyroid neoplasms: its linkage with clinicopathologic features in papillary carcinoma. Pathol Res Pract 199:79-83 (2003)
- [40] Arai T, Watanabe M, Onodera M, Yamashita T, Masunaga A: Reduced nm 23-H1 messenger RNA expression in metastatic lymph nodes from patients with papillary carcinoma of the thyroid. Am J Pathol 142:1938-1944 (1993)
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- [46] Zhang X, Mao H, Lv Z: MicroRNA role in thyroid cancer pathogenesis. Front Biosci (Landmark Ed)18:734-739 (2013)
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