¹Divisions of Endocrinology and Oncology, Department of Medicine, The Ohio State University College of Medicine and Arthur G. James Comprehensive Cancer Center, Columbus, OH, USA

Correspondence: Dr MD Ringel, 445D McCampbell Hall, 1581 Dodd Drive, Columbus, OH 43210, USA. E-mail: matthew.ringel@osumc.edu

Received 12 September 2006; Revised 9 November 2006; Accepted 10 November 2006; Published online 19 December 2006.

Abstract

Activating mutations in the gene encoding BRAF are the most commonly identified oncogenic abnormalities in papillary thyroid cancer. In vitro and in vivo models have demonstrated that overexpression of activated BRAF induces malignant transformation and aggressive tumour behaviour. BRAF and other RAF kinases are frequently activated by other thyroid oncogenes and are important mediators of their biological effects including dedifferentiation and proliferation. Because current therapeutic options for patients with thyroid cancers that are aggressive and/or do not respond to standard therapies are limited, BRAF and its downstream effectors represent attractive therapeutic targets. In this review, data supporting a role for BRAF activation in thyroid cancer development and establishing the potential therapeutic efficacy of BRAF-targeted agents in patients with thyroid cancer will be reviewed.