Waldenström's macroglobulinemia with the AML/MDS-associated t(1;3)(p36;q21).
Two unusual, and perhaps causally related, clinical and cytogenetic features in a patient with Waldenström's macroglobulinemia are presented. Firstly, during the progression of the primary macroglobulinemia bone destruction and hypercalcemia occurred. Secondly, a t(1;3)(p36;q21) was found as the sole clonal chromosomal abnormality. This translocation is characteristic of acute myeloid leukemia (AML) and myelodysplastic syndromes with a high propensity for progressing to AML. The t(1;3) has previously never been reported in a lymphoproliferative disorder. Since the abnormality is associated with acute transformation of cells of the myelopoietic lineages, it is possible that the t(1;3), found in cells of lymphoid origin in the present case, not only induced the neoplastic process as such but also brought about the unusually malignant tumor progression.
Johansson
B
B
Department of Clinical Genetics, Lund University Hospital, Sweden.
Waldenström
J
J
Hasselblom
S
S
Mitelman
F
F
D002878:Chromosomes, Human, Pair 1; D002893:Chromosomes, Human, Pair 3; D005260:Female; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology; D007621:Karyotyping; D015470:Leukemia, Myeloid, Acute / Q000235:genetics*; D008875:Middle Aged; D009190:Myelodysplastic Syndromes / Q000235:genetics*; D010014:Osteolysis / Q000209:etiology; D014178:Translocation, Genetic; D008258:Waldenstrom Macroglobulinemia / Q000150:complications / Q000235:genetics*