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A comparison has been made of the capacities of chloroquine and quinine to serve as companions to primaquine in curing established infections with sporozoites of the M or B strains of Plasmodium cynomolgi in rhesus monkeys. The results indicated that chloroquine was slightly but consistently more effective than quinine in this role. This finding provides support for use of chloroquine as the companion blood schizonticide in the current experimental animal-based search for improved tissue schizonticidal drugs, and bolsters the rather tenuous base for clinical use of this 4-aminoquinoline, rather than quinine, as a companion to primaquine in suppressive-curative and radical-curative regimens.

Long-term outcome of acute megakaryoblastic leukemia (AMKL) patients without Down's syndrome remains poor. Founding mutations and chimeric oncogenes characterize various AMKL subtypes. However, for around one third of all cases the underlying mechanisms of AMKL leukemogenesis are still largely unknown. Recently, an in-frame fusion of meningeoma 1–friend leukemia virus integration 1 (MN1–Fli1) gene was detected in a child with AMKL. We intended to investigate the potential role of this oncofusion in leukemogenesis of acute myeloid leukemia. Strikingly, expression of MN1–Fli1 in murine hematopoietic progenitor cells was sufficient to induce leukemic transformation generating immature myeloid cells with cytomorphology and expression of surface markers typical for AMKL. Systematic structure function analyses revealed FLS and 3′ETS domains of Fli1 as decisive domains for the AMKL phenotype. Our data highlight an important role of MN1–Fli1 in AMKL leukemogenesis and provide a basis for research assessing the value of this oncofusion as a future diagnostic marker and/or therapeutic target in AMKL patients.

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