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9p21 deletion in the diagnosis of malignant mesothelioma, using fluorescence in situ hybridization analysis
Author(s) -
Takeda Maiko,
Kasai Takahiko,
Enomoto Yasunori,
Takano Masato,
Morita Kouhei,
Kadota Eiji,
omura Akitaka
Publication year - 2010
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1111/j.1440-1827.2010.02534.x
Subject(s) - pathology , fluorescence in situ hybridization , adenomatoid tumor , in situ hybridization , mesothelioma , biology , locus (genetics) , mesothelial cell , hyperplasia , atypical hyperplasia , comparative genomic hybridization , immunohistochemistry , medicine , gene , gene expression , chromosome , biochemistry
Homozygous deletion of 9p21, the locus harboring the p16 gene, has been reported as one of the most common genetic alterations in malignant mesotheliomas (MMs). Previous studies showed that this alteration might be useful for differentiating benign from malignant mesothelial tumors in cytology and surgical specimens. Although the diagnostic utility of 9p21 homozygous deletion by fluorescence in situ hybridization (FISH) analysis has been reported only recently, it has not been well demonstrated. The purpose of this study is to evaluate the diagnostic utility of 9p21 homozygous deletion assessed by FISH in mesothelial neoplasm and hyperplasia of Japanese patients using paraffin‐embedded tissue. Simultaneously, p16 protein immunoexpression was explored as a potential diagnostic aid. FISH analysis demonstrated 9p21 deletion in 35 of 40 cases with MM (88%) ( P < 0.001). In contrast, no cases of adenomatoid tumor, benign mesothelial multicystic tumor, reactive mesothelial hyperplasia or pleuritis showed 9p21 deletion ( P < 0.005). 9p21 homozygous deletion correlated well with p16 protein expression in the tumor cells. Our study suggests that 9p21 homozygous deletion assessed by FISH on paraffin‐embedded tissue may be very useful for differentiating MM from reactive mesothelial proliferation.