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TGF-&bgr; Isoform and Receptor Expression in Giant Cell Tumor and Giant Cell Lesions of Bone

TGF-&bgr; Isoform and Receptor Expression in Giant Cell Tumor and Giant Cell Lesions of Bone The authors examined the distribution of tumor growth factor-&bgr; (TGF-&bgr;) isoforms and receptors in 35 giant cell tumor (GCT) of bone in comparison with a group of benign giant cell-containing lesions of bone, including 5 aneurysmal bone cysts, 2 cases of brown tumor of hyperparathyroidism, 3 nonossifying fibromas, and 7 cases of giant cell reparative granuloma. The results of immunohistochemical analysis of GCT showed a complete absence of TGF-&bgr;1 expression in both mononuclear tumor cells and giant cells. Only reactive bone present within the tumor showed an intense immunoreactivity. Transforming growth factor-&bgr;2 and TGF-&bgr;3 were detected in the majority of cases (97.1% and 82.8%, respectively), whereas TGF-&bgr; receptor type I (TGF-&bgr; RI) and type II (TGF-&bgr; RII) were diffusely expressed in all cases. Reverse transcription-polymerase chain reaction (RT-PCR) analysis performed on 10 GCTs with specific oligonucleotide primers demonstrated the presence of mRNA transcripts for TGF-&bgr;1, 2, 3, and for TGF-&bgr; RI and RII. Quantitative measurements of TGF-&bgr;1 in conditioned media from primary cultures of GCT showed undetectable or very low amounts of the cytokine (0–23 pg/mL). The results of immunohistochemical analysis showed that all giant cell-containing lesions of bone were at least focally positive for the 3 isoform of TGF-&bgr;, with positivity present both in osteoclast-like giant cells and mononuclear cells, and diffusely positive for TGF-&bgr; RI and RII. Reverse transcription-polymerase chain reaction analysis conducted on samples from 3 nonossifying fibromas and 1 giant cell reparative granuloma confirmed the expression of the corresponding mRNA. In conclusion, according to the current data, GCT of bone can be distinguished from other giant cell-containing lesions of bone on the basis of the absence of TGF- β1 expression at the protein level, which appears to be the result of posttranslational regulation processes. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Applied Immunohistochemistry & Molecular Morphology Wolters Kluwer Health

TGF-&bgr; Isoform and Receptor Expression in Giant Cell Tumor and Giant Cell Lesions of Bone

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ISSN
1541-2016

Abstract

The authors examined the distribution of tumor growth factor-&bgr; (TGF-&bgr;) isoforms and receptors in 35 giant cell tumor (GCT) of bone in comparison with a group of benign giant cell-containing lesions of bone, including 5 aneurysmal bone cysts, 2 cases of brown tumor of hyperparathyroidism, 3 nonossifying fibromas, and 7 cases of giant cell reparative granuloma. The results of immunohistochemical analysis of GCT showed a complete absence of TGF-&bgr;1 expression in both mononuclear tumor cells and giant cells. Only reactive bone present within the tumor showed an intense immunoreactivity. Transforming growth factor-&bgr;2 and TGF-&bgr;3 were detected in the majority of cases (97.1% and 82.8%, respectively), whereas TGF-&bgr; receptor type I (TGF-&bgr; RI) and type II (TGF-&bgr; RII) were diffusely expressed in all cases. Reverse transcription-polymerase chain reaction (RT-PCR) analysis performed on 10 GCTs with specific oligonucleotide primers demonstrated the presence of mRNA transcripts for TGF-&bgr;1, 2, 3, and for TGF-&bgr; RI and RII. Quantitative measurements of TGF-&bgr;1 in conditioned media from primary cultures of GCT showed undetectable or very low amounts of the cytokine (0–23 pg/mL). The results of immunohistochemical analysis showed that all giant cell-containing lesions of bone were at least focally positive for the 3 isoform of TGF-&bgr;, with positivity present both in osteoclast-like giant cells and mononuclear cells, and diffusely positive for TGF-&bgr; RI and RII. Reverse transcription-polymerase chain reaction analysis conducted on samples from 3 nonossifying fibromas and 1 giant cell reparative granuloma confirmed the expression of the corresponding mRNA. In conclusion, according to the current data, GCT of bone can be distinguished from other giant cell-containing lesions of bone on the basis of the absence of TGF- β1 expression at the protein level, which appears to be the result of posttranslational regulation processes.

Journal

Applied Immunohistochemistry & Molecular MorphologyWolters Kluwer Health

Published: Jun 1, 2001

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