Abstract

Markedly increased numbers of CFU‐C are characteristically found in the peripheral blood of patients with chronic granulocytic leukaemia (CGL). The likely sources of these circulating CFU‐C are the spleen and/or bone marrow. Using the double layer agar technique we measured peripheral blood cloning efficiency serially, prior to and after splenectomy in a man with CGL. In addition we measured cloning efficiencies of splenic venous blood, spleen cell suspensions, and marrow cell suspensions on the day of surgery. In order to estimate the proliferative status of CFU‐C, peripheral blood cells as well as spleen and marrow cell suspensions were exposed to cytosine arabino‐side for 60 min prior to culture.Peripheral blood cloning efficiency (155 ± 8 colonies / 2 times 105 cells) decreased markedly (10 ± 3) after splenectomy. Cloning efficiency of splenic venous blood (288 ± 34) was twice that of peripheral venous blood. The surviving fraction of splenic CFU‐C after exposure to cytosine arabinoside was 16 % compared to survivals of 67 % and 66 % for marrow and peripheral blood CFU‐C respectively. We conclude that the spleen was primarily responsible for the release of CFU‐C into the peripheral blood and that the splenic microenvironment may have exerted a more marked stimulatory effect on the replicative activity of CFU‐C than did the microenvironment of the marrow.

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