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甲状腺癌分子生物学的最新进展及其临床意义。

Recent advances in molecular biology of thyroid cancer and their clinical implications.

作者信息

Xing Mingzhao

机构信息

Department of Medicine and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA.

出版信息

Otolaryngol Clin North Am. 2008 Dec;41(6):1135-46, ix. doi: 10.1016/j.otc.2008.07.001.

DOI:10.1016/j.otc.2008.07.001
PMID:19040974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2615411/
Abstract

Thyroid cancer is the most common endocrine malignancy. With a rapidly rising incidence in recent years, novel efficient management strategies are increasingly needed for this cancer. Remarkable advances have occurred in understanding several major biologic areas of thyroid cancer, including the molecular alterations for the loss of radioiodine avidity of thyroid cancer, the pathogenic role of the MAP kinase and PI3K/Akt pathways and their related genetic alterations, and the aberrant methylation of functionally important genes in thyroid tumorigenesis and pathogenesis. These exciting advances provide unprecedented opportunities for the development of molecular-based novel diagnostic, prognostic, and therapeutic strategies for thyroid cancer.

摘要

甲状腺癌是最常见的内分泌恶性肿瘤。近年来其发病率迅速上升,因此越来越需要针对这种癌症的新型有效管理策略。在理解甲状腺癌的几个主要生物学领域方面已经取得了显著进展,包括甲状腺癌碘摄取能力丧失的分子改变、MAP激酶和PI3K/Akt信号通路的致病作用及其相关基因改变,以及甲状腺肿瘤发生和发病机制中功能重要基因的异常甲基化。这些令人振奋的进展为开发基于分子的甲状腺癌新型诊断、预后和治疗策略提供了前所未有的机会。

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本文引用的文献

1
Association of PTEN gene methylation with genetic alterations in the phosphatidylinositol 3-kinase/AKT signaling pathway in thyroid tumors.甲状腺肿瘤中PTEN基因甲基化与磷脂酰肌醇3-激酶/AKT信号通路基因改变的相关性
Cancer. 2008 Nov 1;113(9):2440-7. doi: 10.1002/cncr.23869.
2
BRAFV600E mutation, but not RET/PTC rearrangements, is correlated with a lower expression of both thyroperoxidase and sodium iodide symporter genes in papillary thyroid cancer.BRAFV600E突变而非RET/PTC重排与甲状腺乳头状癌中甲状腺过氧化物酶和钠碘同向转运体基因的低表达相关。
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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.间变性甲状腺癌和滤泡状甲状腺癌中受体酪氨酸激酶、磷脂酰肌醇3激酶/蛋白激酶B及丝裂原活化蛋白激酶信号通路中高度普遍的基因改变
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4
Hypermethylation of the DNA mismatch repair gene hMLH1 and its association with lymph node metastasis and T1799A BRAF mutation in patients with papillary thyroid cancer.DNA错配修复基因hMLH1的高甲基化及其与甲状腺乳头状癌患者淋巴结转移和T1799A BRAF突变的相关性
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BRAF mutation in papillary thyroid cancer: pathogenic role, molecular bases, and clinical implications.甲状腺乳头状癌中的BRAF突变:致病作用、分子基础及临床意义。
Endocr Rev. 2007 Dec;28(7):742-62. doi: 10.1210/er.2007-0007. Epub 2007 Oct 16.
6
Inhibitory effects of the mitogen-activated protein kinase kinase inhibitor CI-1040 on the proliferation and tumor growth of thyroid cancer cells with BRAF or RAS mutations.丝裂原活化蛋白激酶激酶抑制剂CI-1040对具有BRAF或RAS突变的甲状腺癌细胞增殖和肿瘤生长的抑制作用。
J Clin Endocrinol Metab. 2007 Dec;92(12):4686-95. doi: 10.1210/jc.2007-0097. Epub 2007 Oct 2.
7
Molecular characteristics in papillary thyroid cancers (PTCs) with no 131I uptake.无 131I 摄取的甲状腺乳头癌(PTC)的分子特征。
Clin Endocrinol (Oxf). 2008 Jan;68(1):108-16. doi: 10.1111/j.1365-2265.2007.03008.x. Epub 2007 Sep 14.
8
BRAF mutations in papillary thyroid carcinomas inhibit genes involved in iodine metabolism.甲状腺乳头状癌中的BRAF突变会抑制参与碘代谢的基因。
J Clin Endocrinol Metab. 2007 Jul;92(7):2840-3. doi: 10.1210/jc.2006-2707. Epub 2007 May 8.
9
High prevalence and mutual exclusivity of genetic alterations in the phosphatidylinositol-3-kinase/akt pathway in thyroid tumors.甲状腺肿瘤中磷脂酰肌醇-3-激酶/蛋白激酶B通路基因改变的高发生率及相互排斥性
J Clin Endocrinol Metab. 2007 Jun;92(6):2387-90. doi: 10.1210/jc.2006-2019. Epub 2007 Apr 10.
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BRAF V600E maintains proliferation, transformation, and tumorigenicity of BRAF-mutant papillary thyroid cancer cells.BRAF V600E维持BRAF突变型甲状腺乳头状癌细胞的增殖、转化和致瘤性。
J Clin Endocrinol Metab. 2007 Jun;92(6):2264-71. doi: 10.1210/jc.2006-1613. Epub 2007 Mar 20.