Variation in BCL2 protein expression in follicular lymphomas without t(14;18) chromosomal translocations

Noraidah Masir, Margaret Jones, Faridah Abdul-Rahman, Chandramaya S. Florence, David Y. Mason

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Aim: The hallmark of follicular lymphoma is the t(14;18) (q32;q21) chromosomal translocations that lead to deregulation of BCL2 expression in tumour cells. However, not all cases of follicular lymphoma express BCL2, nor is the t(14;18) translocation always present. Follicular lymphomas lacking the BCL2 rearrangement are less well studied with regards to their immunohistochemical and molecular features. This study aims to investigate the BCL2 protein expression pattern in t(14;18) negative follicular lymphomas. Methods: BCL2 protein expression pattern was analysed in 26 cases of t(14;18) negative follicular lymphoma [determined by fluorescence in situ hybridisation (FISH)], using antibodies against two-different epitopes, i.e., the widely-used antibody BCL2/124 and an alternative antibody E17. Results: Two of the t(14;18) negative cases showed evidence of BCL2 amplification and trisomy 18. A total of 13 cases (50%) lacked BCL2 expression. In 10 cases (38%) the expression was heterogeneous and in only three cases (12%) the BCL2 expression was strongly positive. These cases could thus be subdivided into three subgroups: Group I, normal BCL2 genes (i.e., no evidence of translocation or amplification), and BCL2 protein negative; Group II, normal BCL2 genes but BCL2 protein positive; and Group III, presence of other genetic alterations, i.e., BCL2 amplification and trisomy 18, and BCL2 protein positive. Conclusions: This study suggests that it may be possible on the basis of staining to predict that the t(14;18) translocation is absent if a case is either negative for BCL2 protein with different antibodies or has heterogeneous BCL2 expression, possibly acquired through a physiological process of differentiation.

Original languageEnglish
Pages (from-to)228-233
Number of pages6
JournalPathology
Volume44
Issue number3
DOIs
Publication statusPublished - Apr 2012

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Proto-Oncogene Proteins c-bcl-2
Genetic Translocation
Follicular Lymphoma
Antibodies
Physiological Phenomena
Fluorescence In Situ Hybridization
Epitopes
Staining and Labeling

Keywords

  • BCL2 expression
  • Follicular lymphoma
  • T(14;18) negative

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Variation in BCL2 protein expression in follicular lymphomas without t(14;18) chromosomal translocations. / Masir, Noraidah; Jones, Margaret; Abdul-Rahman, Faridah; Florence, Chandramaya S.; Mason, David Y.

In: Pathology, Vol. 44, No. 3, 04.2012, p. 228-233.

Research output: Contribution to journalArticle

Masir, Noraidah ; Jones, Margaret ; Abdul-Rahman, Faridah ; Florence, Chandramaya S. ; Mason, David Y. / Variation in BCL2 protein expression in follicular lymphomas without t(14;18) chromosomal translocations. In: Pathology. 2012 ; Vol. 44, No. 3. pp. 228-233.
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AB - Aim: The hallmark of follicular lymphoma is the t(14;18) (q32;q21) chromosomal translocations that lead to deregulation of BCL2 expression in tumour cells. However, not all cases of follicular lymphoma express BCL2, nor is the t(14;18) translocation always present. Follicular lymphomas lacking the BCL2 rearrangement are less well studied with regards to their immunohistochemical and molecular features. This study aims to investigate the BCL2 protein expression pattern in t(14;18) negative follicular lymphomas. Methods: BCL2 protein expression pattern was analysed in 26 cases of t(14;18) negative follicular lymphoma [determined by fluorescence in situ hybridisation (FISH)], using antibodies against two-different epitopes, i.e., the widely-used antibody BCL2/124 and an alternative antibody E17. Results: Two of the t(14;18) negative cases showed evidence of BCL2 amplification and trisomy 18. A total of 13 cases (50%) lacked BCL2 expression. In 10 cases (38%) the expression was heterogeneous and in only three cases (12%) the BCL2 expression was strongly positive. These cases could thus be subdivided into three subgroups: Group I, normal BCL2 genes (i.e., no evidence of translocation or amplification), and BCL2 protein negative; Group II, normal BCL2 genes but BCL2 protein positive; and Group III, presence of other genetic alterations, i.e., BCL2 amplification and trisomy 18, and BCL2 protein positive. Conclusions: This study suggests that it may be possible on the basis of staining to predict that the t(14;18) translocation is absent if a case is either negative for BCL2 protein with different antibodies or has heterogeneous BCL2 expression, possibly acquired through a physiological process of differentiation.

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