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IgG1‐κ biclonal gammopathy associated with multiple myeloma suggests a regulatory mechanism
Author(s) -
Marco Pizzolato,
G Bragantini,
Pablo Diego Bresciani,
Santiago Pavlovsky,
Joseph V. Chuba,
Rubén Vidal,
Agueda Rostagno,
Jorge Ghiso
Publication year - 1998
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.1998.00805.x
Subject(s) - multiple myeloma , clone (java method) , bence jones protein , antibody , plasma cell , melphalan , plasmacytoma , myeloma protein , immunology , biology , microbiology and biotechnology , immunoglobulin light chain , cancer research , genetics , gene
Multiclonal gammopathies associated with multiple myeloma may result either from a neoplastic transformation of a cell clone undergoing immunoglobulin class switching or from independent transforming events yielding proliferation of unrelated plasma cell clones. The simultaneous presence of more than one neoplastic clone may possess regulatory implications in terms of cell proliferation, clonal expansion, secretion of M‐components or response to chemotherapy. We report a patient, diagnosed with multiple myeloma stage IIIa, who presented with two well‐defined homogenous IgG1‐κ components in the serum (designated WER‐1 and WER‐2) with striking differences in their plasma concentration and response to the classic melphalan/prednisone treatment. Immunochemical characterization and amino terminal sequence analysis of both the heavy and light chains of each M‐component undoubtedly determined their biclonal origin. WER‐1 was identified as IgG1(VHII)‐κI while WER‐2 was classified as IgG1(VHIII)‐κIII. The plateau phase was characterized by very low or undetectable levels of WER‐2, a high, almost constant, concentration of WER‐1 and the absence of Bence Jones proteinuria, whereas these parameters were completely reversed during the escape phase with levels resembling those observed at the time of diagnosis. The statistically significant negative correlation between the biclonal components and the different susceptibility to the treatment clearly suggests regulatory interactions between the clones WER‐1 and WER‐2.