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A Case of monoclonal gammopathy associated with acute myelomonocytic leukemia with eosinophilia suggested to be the result of lineage infidelity
Author(s) -
Nagata Toshihito,
Mugishima Hideo,
Yoden Atsushi,
Yoshikawa Kenji,
Oguni Tatsuya,
Yamashiro Kuniaki,
Yamamori Shiyunji,
Harada Kensuke
Publication year - 2000
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/1096-8652(200009)65:1<66::aid-ajh12>3.0.co;2-t
Subject(s) - monoclonal gammopathy , acute myelomonocytic leukemia , eosinophilia , medicine , lineage (genetic) , immunology , monoclonal , pathology , chronic myelomonocytic leukemia , leukemia , monoclonal antibody , bone marrow , biology , genetics , gene , myelodysplastic syndromes , antibody
Acute myelomonocytic leukemia (AMMoL) accompanied by monoclonal gammopathy is a rare condition, and its pathogenesis and the cytogenetic mechanism of such leukemogenesis have not been determined in detail. A case of AMMoL with eosinophilia accompanied by immunoglobulin G κ monoclonal gammopathy is described. Immunophenotypic studies of the peripheral blood and bone marrow mononuclear cells revealed no evidence of abnormally proliferating cells of B‐lineage. DNA analyses of bone marrow mononuclear cells containing leukemic cells revealed rearrangement of the κ‐light chain ( Igκ ) gene and c‐ myc and c‐ jun proto‐oncogenes. The intensities of the rearranged bands for these genes on Southern blot analysis suggested the existence of a major population of leukemic cells with rearranged Igκ gene and minor population(s) of leukemic cells with rearranged c‐ myc and/or c‐ jun proto‐oncogene(s) in the patient's bone marrow and indicated the occurrence of genetic evolutionary changes in leukemic cells in this patient before starting chemotherapy. These results suggest that these leukemic cells are the most likely candidate for immunoglobulin G κ monoclonal protein production, and structural abnormalities of c‐ myc and c‐ jun proto‐oncogenes may have contributed to the evolution of leukemic cells in this patient. Am. J. Hematol. 65:66–71, 2000. © 2000 Wiley‐Liss, Inc.