BCL-6 expression in mesenchymal tumours

An immunohistochemical and fluorescence in situ hybridisation study

Matthew P. Walters, Ellen McPhail, Mark E. Law, Andrew L. Folpe

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

The BCL-6 proto-oncogene encodes a transcriptional repressor protein. Among normal tissues, BCL-6 expression is confined to germinal center B-cells and a subpopulation of T-helper cells. Little is known about BCL-6 expression in mesenchymal tissues. We examined a series of solitary fibrous tumor (SFT) and other mesenchymal tumors for BCL-6 expression. Immunohistochemistry for BCL-6 was performed on 64 mesenchymal tumors [26 SFT (19 benign/uncertain, 7 malignant), 6 synovial sarcomas (SS), 5 gastrointestinal stromal tumors (GIST), 5 malignant peripheral nerve sheath tumors (MPNST), 5 leiomyosarcomas (LMS), 9 leiomyomas (LM) 4 desmoid tumors (DT), 4 perineuriomas (PN)]. Nuclear immunoreactivity was considered positive. Six BCL-6 positive SFT were also tested for BCL-6 gene rearrangement/amplification by FISH. Nuclear expression of BCL-6 was seen in 13/26 SFT, 5/5 LMS, 1/9 LM, 5/6 SS, 1/5 GIST, 1/5 MPNST, 1/4 PN, and 0/5 DT. BCL-6 expression was significantly more frequent in malignant (6/7) as compared with benign/uncertain SFT (6/19) (p=0.02) and in LMS (5/5) as compared with LM (1/9) (p=0.003). FISH for BCL-6 rearrangement/amplification was negative in all tested cases. We have observed BCL-6 expression in 50% or more of SFT, SS, and LMS, and in a lesser percentage of LM, GIST, MPNST and PN. Significantly more frequent expression of BCL-6 in malignant compared with benign/uncertain SFT and in LMS compared with LM suggests abnormalities in the BCL-6 signaling pathway may contribute to malignant transformation in at least some mesenchymal tumors. It is unlikely that BCL-6 expression in mesenchymal tumors is due to BCL-6 gene amplification or rearrangement. amplification or rearrangement.

Original languageEnglish (US)
Pages (from-to)866-869
Number of pages4
JournalJournal of Clinical Pathology
Volume64
Issue number10
DOIs
StatePublished - Oct 2011

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Solitary Fibrous Tumors
Fluorescence In Situ Hybridization
Leiomyosarcoma
Leiomyoma
Nerve Sheath Neoplasms
Synovial Sarcoma
Gastrointestinal Stromal Tumors
Neurilemmoma
Neoplasms
Aggressive Fibromatosis
Gene Rearrangement
Gene Amplification
Repressor Proteins
Germinal Center
Proto-Oncogenes
Helper-Inducer T-Lymphocytes
B-Lymphocytes
Immunohistochemistry

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Medicine(all)

Cite this

BCL-6 expression in mesenchymal tumours : An immunohistochemical and fluorescence in situ hybridisation study. / Walters, Matthew P.; McPhail, Ellen; Law, Mark E.; Folpe, Andrew L.

In: Journal of Clinical Pathology, Vol. 64, No. 10, 10.2011, p. 866-869.

Research output: Contribution to journalArticle

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abstract = "The BCL-6 proto-oncogene encodes a transcriptional repressor protein. Among normal tissues, BCL-6 expression is confined to germinal center B-cells and a subpopulation of T-helper cells. Little is known about BCL-6 expression in mesenchymal tissues. We examined a series of solitary fibrous tumor (SFT) and other mesenchymal tumors for BCL-6 expression. Immunohistochemistry for BCL-6 was performed on 64 mesenchymal tumors [26 SFT (19 benign/uncertain, 7 malignant), 6 synovial sarcomas (SS), 5 gastrointestinal stromal tumors (GIST), 5 malignant peripheral nerve sheath tumors (MPNST), 5 leiomyosarcomas (LMS), 9 leiomyomas (LM) 4 desmoid tumors (DT), 4 perineuriomas (PN)]. Nuclear immunoreactivity was considered positive. Six BCL-6 positive SFT were also tested for BCL-6 gene rearrangement/amplification by FISH. Nuclear expression of BCL-6 was seen in 13/26 SFT, 5/5 LMS, 1/9 LM, 5/6 SS, 1/5 GIST, 1/5 MPNST, 1/4 PN, and 0/5 DT. BCL-6 expression was significantly more frequent in malignant (6/7) as compared with benign/uncertain SFT (6/19) (p=0.02) and in LMS (5/5) as compared with LM (1/9) (p=0.003). FISH for BCL-6 rearrangement/amplification was negative in all tested cases. We have observed BCL-6 expression in 50{\%} or more of SFT, SS, and LMS, and in a lesser percentage of LM, GIST, MPNST and PN. Significantly more frequent expression of BCL-6 in malignant compared with benign/uncertain SFT and in LMS compared with LM suggests abnormalities in the BCL-6 signaling pathway may contribute to malignant transformation in at least some mesenchymal tumors. It is unlikely that BCL-6 expression in mesenchymal tumors is due to BCL-6 gene amplification or rearrangement. amplification or rearrangement.",
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