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Progenitors of blast cell colonies have been identified in acute leukemia. The peripheral blood of 18 of 25 patients with preleukemic states yielded low numbers of blast cell colonies, and the colony-forming cells were in an active proliferative state when assessed using short-term exposure to tritiated thymidine. The clinical significance of blast cell colonies is uncertain, but we suggest that further analysis of this cultural abnormality may lead to a better understanding of mechanisms and management in preleukemia.

SummaryA compulsory programme of proficiency testing in immunohaematology has been conducted for the last 4 years. The collection, processing and analysis of testing data reported by participating laboratories depends on a computer‐based system, which allows the generation of reports for participants and working documents essential to the functioning of a committee which supervises the operation of the programme. The options open to the committee in coping with laboratories with poor performance are summarized.

Summary. An analysis of the results of a compulsory proficiency testing programme in immunohaematology is presented. Error rates have been calculated for the determination of ABO and Rh(D) groups, the direct antiglobulin test and antibody detection according to defined criteria. The introduction of proficiency testing has been associated with alterations in error rates for some determinations. An educational programme introduced for laboratories with poor performance has proved effective in improving their results in the proficiency testing programme.

Sex-linked hypochromic anemia is the result of iron deficiency, apparently caused by malabsorption of iron. Progenitor cells in marrow and spleen of male anemic (genotype, sla/-) and normal (+/-) littermate mice were studied by quantitative transplantation into irradiated, but otherwise normal, recipient mice. The progeny of grafted cells were assessed by isotope uptake technics. Progenitor cells of sla/- mice were capable of extensive production of erythroid cells, which synthesized DNA and hemoglobin, and of leukocytic elements, which synthesized DNA but not hemoglobin. Proliferation of the latter cell types was assayed in recipient mice rendered polycythemic with red cell infusions to suppress erythropoiesis. The mature red cells produced by transplanted sla/- marrow and spleen were normal with respect to volume, size, and hemoglobin content. The grossly enlarged spleens of sla/- mice contained 20 times the normal number of erythropoietic progenitor units (EPU); parenteral iron therapy cured the anemia and caused the spleen to revert to normal. The ratio of EPU to leukopoietic progenitor units (LPU) was abnormally high in marrow and spleen of sla/- mice; in addition, the EPU:LPU ratio was higher in spleen than in marrow of normal and anemic mice. The high EPU:LPU ratio of sla/- bone marrow persisted after transplantation to a lesser, but significant, extent for at least 52 days. We conclude that: 1) the sla mutant gene does not affect hemopoietic cells directly, but that iron deficiency alters the ratio of EPU to LPU by committing more primitive pluripotent stem cells to erythropoiesis, and 2) EPU and LPU are separate progenitor cells with restricted potential for differentiation. Persistence of the altered EPU:LPU ratio in sla/- marrow chimeras may be explained by extensive and independent self-replication of EPU and/or LPU, especially after grafting relatively small numbers (1.6 million) of marrow cells into irradiated mice.