Two distinct cell lines (OPM-1 and OPM-2) were established from the peripheral blood of a 56-year-old female myeloma patient at the stage of terminal leukemic evolution associated with loss of cytoplasmic immunoglobulin heavy chain (G lambda----lambda). The lines grew in suspension with a doubling time of 36-42 hr and 30-36 hr, respectively. EBNA was absent from both lines. The lines synthesized cytoplasmic lambda-chain, but had no detectable surface immunoglobulins. Fc receptors and complement receptors could not be detected in either line. The lines had very complex chromosomal abnormalities, but the patterns of chromosomes differed greatly between the two lines. The two lines, together with the RPMI 8226 line established by Matsuoka et al. (1967), were analyzed for phenotypic expression as defined by a panel of monoclonal antibodies to B cells (B1, BA-1, BA-2, BA-3, OKIa-1 and OKT10/BMA0100). Neither OPM-1 nor OPM-2 reacted with any of the antibodies tested except OKT10. OPM-1 cells reacted weakly (less than 30%) with OKT10/BMA0100, while OPM-2 cells showed a fluctuating reactivity, ranging from 40 to 80%, with OKT10/BMA0100. In contrast, RPMI 8226 reacted strongly with OKT10 and BA-2. These results demonstrate the presence of phenotypic heterogeneity in all 3 myeloma cell lines, suggesting that the lines might represent different stages of terminal B-cell development.

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We present an acute promyelocytic leukemia (APL) patient with two subtypes of IRF2BP2–RARA, in which the IRF2BP2 gene showed completely new breakpoints. Bone marrow examination revealed morphologic features indicative of APL. However, promyelocytic leukemia–RARA fusion was not detected. A paired‐end mRNA sequencing followed by RT‐PCR and direct sequencing revealed two types of fusion transcripts between exon 1B of IRF2BP2 and exon 3 of RARA. The patient received all‐trans retinoic acid and conventional chemotherapy, but showed resistance. This is the second report of IRF2BP2 involvement in APL, and we describe various breakpoints for the IRF2BP2–RARA fusion gene.

We describe a 69-year-old man with refractory relapsing thrombotic thrombocytopenic purpura (TTP) successfully treated with rituximab. The patient had once been successfully treated with plasmapheresis and vincristine, but he had relapsed after a short period. Although plasmapheresis, vincristine, and splenectomy could not achieve a consistent elevation of the platelet count, rituximab administration provided sustained remission for more than 7 months. Rituximab should be considered as a therapeutic alternative for refractory TTP.