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High prevalence of immunoglobulin light chain gene aberrations as revealed by FISH in multiple myeloma and MGUS
Author(s) -
Türkmen Seval,
Binder Anastasia,
Gerlach Antje,
Niehage Sylke,
Theodora Melissari Maria,
Inandiklioglu Nihal,
Dörken Bernd,
Burmeister Thomas
Publication year - 2014
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/gcc.22175
Subject(s) - immunoglobulin light chain , chromosomal translocation , multiple myeloma , monoclonal gammopathy of undetermined significance , biology , antibody , immunoglobulin heavy chain , gene rearrangement , plasma cell neoplasm , myeloma protein , microbiology and biotechnology , chromosome , cancer research , bone marrow , gene , plasmacytoma , genetics , monoclonal , immunology , monoclonal antibody
Multiple myeloma (MM) is a malignant B‐cell neoplasm characterized by an uncontrolled proliferation of aberrant plasma cells in the bone marrow. Chromosome aberrations in MM are complex and represent a hallmark of the disease, involving many chromosomes that are altered both numerically and structurally. Nearly half of the cases are nonhyperdiploid and show IGH translocations with the following partner genes: CCND1 , FGFR3 and MMSET , MAF , MAFB , and CCND3 . The remaining 50% are grouped into a hyperdiploid group that is characterized by multiple trisomies involving chromosomes 3, 5, 7, 9, 11, 15, 19, and 21. In this study, we analyzed the immunoglobulin light chain kappa ( IGK , 2p12) and lambda ( IGL , 22q11) loci in 150 cases, mostly with MM but in a few cases monoclonal gammopathy of undetermined significance (MGUS), without IGH translocations. We identified aberrations in 27% (= 40 patients) including rearrangements (12%), gains (12%), and deletions (4.6%). In 6 of 18 patients with IGK or/and IGL rearrangements, we detected a MYC rearrangement which suggests that MYC is the translocation partner in the majority of these cases. © 2014 Wiley Periodicals, Inc.