© 2003 by Oxford University Press
Journal of the National Cancer Institute, Vol. 95, No. 8, 625-627,
April 16, 2003
© 2003 Oxford University Press
BRIEF COMMUNICATION |
BRAF Mutation in Papillary Thyroid Carcinoma
Affiliations of authors: Y. Cohen, E. Mambo, Z. Guo, G. Wu, B. Trink, W. H. Westra, D. Sidransky (Division of Head and Neck Cancer Research, Department of Otolaryngology–Head and Neck Surgery), M. Xing, P. W. Ladenson (Division of Endocrinology and Metabolism), The Johns Hopkins University School of Medicine, Baltimore, MD; U. Beller, Department of Obstetrics and Gynecology, Shaare Zedek Medical Center, Ben-Gurion University of the Negev, Jerusalem, Israel.
Correspondence to: David Sidransky, M.D., Division of Head and Neck Cancer Research, Department of Otolaryngology–Head and Neck Surgery, The Johns Hopkins University School of Medicine, 720 Rutland Ave., Ross Bldg. 818, Baltimore, MD 21205-2196 (e-mail: dsidrans{at}jhmi.edu).
ABSTRACT
The BRAF gene has been found to be activated by mutation in human cancers, predominantly in malignant melanoma. We tested 476 primary tumors, including 214 lung, 126 head and neck, 54 thyroid, 27 bladder, 38 cervical, and 17 prostate cancers, for the BRAF T1796A mutation by polymerase chain reaction (PCR)–restriction enzyme analysis of BRAF exon 15. In 24 (69%) of the 35 papillary thyroid carcinomas examined, we found a missense thymine (T)
adenine (A) transversion at nucleotide 1796 in the BRAF gene (T1796A). The T1796A mutation was detected in four lung cancers and in six head and neck cancers but not in bladder, cervical, or prostate cancers. Our data suggest that activating BRAF mutations may be an important event in the development of papillary thyroid cancer.
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