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bcl‐2 and p53 protein expression in follicular lymphoma
Author(s) -
Cooper Kumarasen,
Haffajee Zenobia
Publication year - 1997
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199707)182:3<307::aid-path873>3.0.co;2-6
Subject(s) - follicular lymphoma , protein expression , cancer research , lymphoma , p53 protein , follicular phase , expression (computer science) , biology , computational biology , pathology , medicine , immunohistochemistry , genetics , computer science , gene , programming language
Recent studies have shown bcl‐2 to be regulated by p53. Other studies have suggested an inverse relationship between p53 and bcl‐2 protein expression in breast and colonic cancers and in a variety of subtypes of non‐Hodgkin's lymphoma. This study investigates the relationship between bcl‐2 and p53 protein expression and the correlation between these findings and the grade and cell type of follicular lymphomas according to the REAL classification. Paraffin‐embedded nodal follicular lymphomas ( n =37) were subjected to bcl‐2 and p53 immunohistochemistry on tissue sections using a three‐step ABC system. Positive immunostaining for both oncoproteins was scored using a three‐tiered scale: +, <10 per cent cells; ++, 10–50 per cent cells; and +++, >50 per cent cells (<10 per cent was used as a cut‐off to define negative tumours). Ninety‐seven per cent (36/37) of follicular lymphomas expressed bcl‐2 protein in all three grades, manifesting in the small cell (grade 1) through to the large cell (grade 3). p53 protein expression showed a pattern of increasing immunostaining with progression towards the high‐grade follicular lymphoma: grade 1=6 per cent (1/16); grade 2=48 per cent (10/21); grade 3=100 per cent (6/6). Five cases comprised varying combinations of grades. This latter finding suggests a role for p53 mutation in the progression/transformation of follicular lymphoma. The mechanism, however, differs from that suggested in breast and colonic cancers, since an inverse relationship between bcl‐2 and p53 was not demonstrated in the present study. © 1997 John Wiley & Sons, Ltd.