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Volume 291, Issue 1, Pages 31-38 (1 May 2010)


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Deletion of the WWOX gene and frequent loss of its protein expression in human osteosarcoma

Jilong Yangae, David Cogdelle, Da Yangb, Limei Hue, Haixin Lib, Hong Zhengb, Xiaoling Dud, Yi Pangc, Jonathan Trentf, Kexin Chenb, Wei ZhangeCorresponding Author Informationemail address

Received 23 September 2009; accepted 28 September 2009. published online 09 November 2009.

Abstract 

To evaluate the role of WWOX gene in human osteosarcoma, array comparative genomic hybridization on 10 frozen osteosarcoma specimens and immunohistochemical staining of 55 formalin-fixed and paraffin-embedded tissues for WWOX was performed. Deletion of the WWOX gene was observed in 3 of 10 samples and the WWOX protein was undetectable in 34 of 55 osteosarcomas. This is the first investigation of the role of WWOX gene in human osteosarcoma. The WWOX gene deletion, loss of its protein expression, and lack of correlation of WWOX expression with patient survival suggest loss of WWOX expression is an early event in the pathogenesis of osteosarcoma and the phenotypic results of its deletion do not imminently result in patient death.

a Department of Bone and Soft Tissue Tumors, Tianjin Medical University Cancer Hospital and Institute, Tianjin 30060, China

b Department of Epidemiology and Biostatistics, Tianjin Medical University Cancer Hospital and Institute, Tianjin 30060, China

c Department of Pathology, Tianjin Medical University Cancer Hospital and Institute, Tianjin 30060, China

d Department of Diagnostics, Tianjin Medical University, Tianjin 30060, China

e Department of Pathology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA

f Department of Sarcoma Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX 77030, USA

Corresponding Author InformationCorresponding author. Address: Department of Pathology, Unit 85, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, Texas 77030, USA. Tel.: +1 713 745 1103; fax: +1 713 792 5549.

PII: S0304-3835(09)00617-X

doi:10.1016/j.canlet.2009.09.018


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