PRDM1 expression on the epithelial component but not on ectopic lymphoid tissues of Warthin tumour
Objective To determine the role of PRDM1, a key molecule for modulating the immune cells, in Warthin tumour (WT) pathogenesis. Subjects and methods Forty paraffin‐embedded parotid tissues of patients (mean age: 62.08 ± 11.90) with WT were retrieved from the pathology archives of Qindu Hospital from...
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Published in | Oral diseases Vol. 21; no. 4; pp. 432 - 436 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Denmark
Blackwell Publishing Ltd
01.05.2015
Wiley Subscription Services, Inc |
Subjects | |
Online Access | Get full text |
ISSN | 1354-523X 1601-0825 1601-0825 |
DOI | 10.1111/odi.12294 |
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Summary: | Objective
To determine the role of PRDM1, a key molecule for modulating the immune cells, in Warthin tumour (WT) pathogenesis.
Subjects and methods
Forty paraffin‐embedded parotid tissues of patients (mean age: 62.08 ± 11.90) with WT were retrieved from the pathology archives of Qindu Hospital from January 2012 to December 2012. The PRDM1 expression was investigated in a cohort of WT by immunohistochemistry.
Results
PRDM1 was expressed only on the epithelial component but not on ectopic lymphoid tissue of the tumour. Statistically, PRDM1 expression rates between WT glandular epithelial cells (40/40 cases) and the tumour‐adjacent tissues (0/9 cases), and WT germinal centres (0/34 cases) and tonsil tissues (10/10 cases) were significantly different (P < 0.001), respectively.
Conclusions
The PRDM1 expression appeared to play an essential role in WT pathogenesis. A better understanding of it might give options for revealing possible novel management strategies. |
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Bibliography: | ArticleID:ODI12294 istex:3911E3B848697473A63B91B2B02D3FB24A0FF645 National Natural Science Foundation of China - No. 81272134; No. 81171804 ark:/67375/WNG-P8PCJWX1-N ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1354-523X 1601-0825 1601-0825 |
DOI: | 10.1111/odi.12294 |