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Blood, 1 June 2002, Vol. 99, No. 11, pp. 4094-4099
NEOPLASIA
Inactivating mutations of CASP10 gene in
non-Hodgkin lymphomas
Min Sun Shin,
Hong Sug Kim,
Chang Suk Kang,
Won Sang Park,
Su Young Kim,
Shi Nae Lee,
Jong Heun Lee,
Jik Young Park,
Ja June Jang,
Chul Woo Kim,
Sang Ho Kim,
Jung Young Lee,
Nam Jin Yoo, and
Sug Hyung Lee
From the Departments of Pathology, and Clinical
Pathology, College of Medicine, The Catholic University of Korea,
Seoul, Korea; and Department of Pathology and Cancer Research Center,
Seoul National University, College of Medicine, Seoul, Korea.
Caspase 10 (Mch4/FLICE2) is a caspase homologous to caspase 8. A
recent report described that inherited CASP10 gene
mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome (ALPS). In this study, to
explore the possibility that mutation of this gene might be involved in
the development of non-Hodgkin lymphoma (NHL), we have analyzed the
entire coding region and all splice sites of the CASP10
gene for the detection of somatic mutations in 117 human NHLs.
Overall, 17 NHLs (14.5%) were found to have CASP10 mutations, which were identified in the coding regions of the prodomain (n = 3), the p17 large protease subunit (n = 11), and the
p12 small protease subunit (n = 3). We expressed the tumor-derived caspase 10 mutants in 293 cells and found that apoptosis was
suppressed. These data suggest that the inactivating mutations of the
CASP10 gene might lead to the loss of its apoptotic
function and contribute to the pathogenesis of some human NHLs.
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