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Lack of BCL10 mutations in multiple myeloma and plasma cell leukemia
Author(s) -
Shih LeeYung,
Fu JenFen,
Shurtleff Sheila A.,
Morris Stephan W.,
Downing James R.
Publication year - 2001
Publication title -
genes, chromosomes and cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.754
H-Index - 119
eISSN - 1098-2264
pISSN - 1045-2257
DOI - 10.1002/1098-2264(2001)9999:9999<::aid-gcc1106>3.0.co;2-f
Subject(s) - plasma cell , plasma cell dyscrasia , carcinogenesis , biology , single strand conformation polymorphism , dyscrasia , multiple myeloma , intron , plasma cell leukemia , exon , leukemia , microbiology and biotechnology , genetics , bone marrow , gene , mutation , missense mutation , immunoglobulin light chain , immunology , antibody
To determine whether the BCL10 mutation plays a role in the oncogenesis of plasma cell dyscrasias, we used polymerase chain reaction–single‐strand conformation polymorphism (PCR‐SSCP) and direct sequencing analysis and examined the genomic BCL10 mutations in 57 patients with multiple myeloma or plasma cell leukemia and 52 normal bone marrow samples. We found three polymorphic sequence variants, either alone or in combination, at codons 5 and 8, and in intron 1 at base 58 of the BCL10 gene in 37 patients with plasma cell dyscrasia. Identical aberrant band shifts were also observed in 34 normal marrow samples. No polymorphic variants were identified in exon 2 or 3 in either patient or control samples, and no pathogenic mutations were detected. Patients with plasma cell dyscrasias in Taiwan appeared to have a higher frequency of polymorphisms at codon 5 and intron 1 at base 58, and a lower frequency at codons 8 and 213. Our results suggest that BCL10 is not involved in the oncogenesis of plasma cell dyscrasias. © 2001 Wiley‐Liss, Inc.