DEVELOPMENT OF MYELOMA AND SECONDARY MYELODYSPLASTIC SYNDROME FROM A COMMON CLONE

Citation
Hm. Schmetzer et al., DEVELOPMENT OF MYELOMA AND SECONDARY MYELODYSPLASTIC SYNDROME FROM A COMMON CLONE, Cancer genetics and cytogenetics, 100(1), 1998, pp. 31-35
Citations number
12
Categorie Soggetti
Oncology,"Genetics & Heredity
ISSN journal
01654608
Volume
100
Issue
1
Year of publication
1998
Pages
31 - 35
Database
ISI
SICI code
0165-4608(1998)100:1<31:DOMASM>2.0.ZU;2-#
Abstract
We report the case of a 49-year-old woman who presented with a monoclo nally IgG kappa expressing myeloma since October 1989. Four years late r, after 24 cycles of Melphalan-containing chemotherapy, bone marrow ( BM) cells of the patient cytologically revealed myelodysplastic change s for the first lime. Cytogenetic examination of the BM obtained in Ja nuary 1994 showed two clonally aberrant main lines. Each of them repre sented one of the hematological neoplastic diseases. The quantitativel y major clone (MDS-clone) showed a deletion of the long arm of chromos ome 7, typical for secondary myeloid disorders. The other clone (myelo ma (MM) clone) was characterized by a reciprocal translocation between the short arm of chromosome 8, band q24, a region known to contain th e c-myc gene, and the long arm of chromosome 2, band p12, where the 1g kappa gene is located. An unusual finding, however, was that an abnor mality of the long arm of chromosome 16 could be detected in both obvi ously unrelated clones. In the further course of the disease, the MDS and MM clones could be detected, both of them showing cytogenetically a clonal evolution characterized by additional clonal abnormalities. O ur data stress the significance of cytogenetics in detecting typical c lonal abnormalities in different malignant hematological disorders and in detecting ''clonal evolution'' as an indicator of the progress of the disease. Moreover, our data suggest that MM and MDS may arise from a common stem cell, which may be characterized by a clonal cytogeneti c abnormality. (C) Elsevier Science Inc., 1998.