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This Article Full Text Full Text (PDF) All Versions of this Article: JME-09-0024v1 43/4/143    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Cerrato, A. Articles by Santoro, M. PubMed PubMed Citation Articles by Cerrato, A. Articles by Santoro, M.

Istituto di Endocrinologia ed Oncologia Sperimentale CNR c/o Dipartimento di Biologia e Patologia Cellulare e Molecolare, ‘L. Califano’, Università Federico II di Napoli, via S. Pansini 5, 80131 Naples, Italy

(Correspondence should be addressed to M Santoro; Email: masantor{at}unina.it)

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 tumour-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.