Molecular genetics of medullary thyroid carcinoma: the quest for novel therapeutic targets

被引：61

作者：

Cerrato, Aniello ^{[1
]}

De Falco, Valentina ^{[1
]}

Santoro, Massimo ^{[1
]}

机构：

[1] Univ Naples Federico II, Dipartimento Biol & Patol Cellulare & Mol L Calif, CNR, Ist Endocrinol & Oncol Sperimentale, I-80131 Naples, Italy

来源：

JOURNAL OF MOLECULAR ENDOCRINOLOGY | 2009年 / 43卷 / 3-4期

关键词：

NEOPLASIA TYPE 2A; RET TYROSINE KINASE; C-CELL HYPERPLASIA; GROWTH-FACTOR RECEPTOR; GERM-LINE MUTATIONS; FACTOR-KAPPA-B; ENDOCRINE-NEOPLASIA; TRANSGENIC MICE; NEUROTROPHIC FACTOR; SIGNALING PATHWAY;

D O I：

10.1677/JME-09-0024

中图分类号：

R5 [内科学];

学科分类号：

100201 [内科学];

摘要：

Medullary thyroid carcinoma (MTC) is a rare tumour arising from neural crest-derived parafollicular C-cells. Metastatic MTC patients are incurable because the cancer does not respond to radiotherapy or chemotherapy. The REarranged during Transfection (RET) proto-oncogene plays a key role in the development of MTC. However, one-half of the sporadic MTC do not carry RET mutations. Mice models and early evidence obtained in human samples suggest that other genes, including those encoding components of the RB1 (retinoblastoma) and TP53 tummour-suppressor pathways, may be involved in MTC formation. Here, we review the data on the involvement of genes acting in the RET and RB1/TP53 pathways in MTC. Understanding genetic lesions that occur in MTC is a prerequisite to identifying molecular therapeutic targets in MTC and in improving the efficacy of RET-targeted therapies. Journal of Molecular Endocrinology (2009) 43, 143-155

引用

页码：143 / 155

页数：13

共 158 条

[1]

Multiple endocrine neoplasia type 2B mutation in human RET oncogene induces medullary thyroid carcinoma in transgenic mice [J].