Clinical Orthopaedics and Related Research®
© The Association of Bone and Joint Surgeons® 2009
10.1007/s11999-009-1134-x

Erratum

Erratum to: PATCHED-ONE or SMOOTHENED Gene Mutations Are Infrequent in Chondrosarcoma

Taiqiang Yan1, Mark Angelini2, 3, Benjamin A. Alman4, Irene L. Andrulis2 and Jay S. Wunder2, 3 Contact Information

(1)  Department of Orthopaedic Oncology, People’s Hospital, Beijing University, Beijing, China
(2)  Program in Molecular Biology and Cancer, Samuel Lunenfeld Research Institute, Toronto, Canada
(3)  University Musculoskeletal Oncology Unit, Mount Sinai Hospital, University of Toronto, 476-600 University Avenue, Toronto, ON, Canada, M5G 1X5
(4)  Division of Orthopaedics and Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, University of Toronto, Toronto, Canada

Contact Information Jay S. Wunder
Email: jwunder@mtsinai.on.ca

Published online: 22 October 2009

Without Abstract
The online version of the original article can be found under doi:10.1007/s11999-008-0332-2.
Erratum to: Clin Orthop Relat Res DOI 10.1007/s11999-008-0332-2

The Abstract for this article was incorrectly identified and typeset as the first of two Introductions. Reprinted below is the Abstract in its entirety:

Abstract Constitutive hedgehog signaling has been implicated in the tumorigenesis of cartilaginous neoplasia; however, a common mutational mechanism remains unknown. Some tumors exhibiting hedgehog pathway activation such as basal cell cancer frequently harbor PATCHED-ONE (PTCH-1) or SMOOTHENED (SMO) gene mutations. We therefore asked whether mutations of the hedgehog receptor genes PTCH-1 or SMO occur in cartilage tumors. Singlestrand conformation polymorphism (SSCP) analysis with subsequent manual sequencing was performed to detect alterations of PTCH-1 and SMO in 46 cartilage tumors. SSCP detected five shifts in the PTCH-1 gene and two shifts in SMO. Direct DNA sequencing revealed the five shifts in PTCH-1 were caused by silent nucleotide alterations. The two SMO shifts were the result of the same missense mutation (783G>A) and occurred in one dedifferentiated chondrosarcoma and a synovial chondromatosis. The patient with chondromatosis also carried this same mutation in the germline. However, this mutation was also identified in leukocyte DNA from three of 127 (2.4%) control subjects without cartilage tumors, suggesting it may represent a rare SMO variant. Constitutive activation of the hedgehog signaling pathway in chondrosarcoma is rarely caused by PTCH-1 or SMO mutations.

CORR and Springer regret this error.