Abstract
Variation of laminin receptor levels (LNR) during myeloid‐cell differentiation and in acute leukemia were investigated by ^125^I‐laminin‐binding determination during HL60 cell differentiation and in cells of patients with different types of leukemia, characterized according to the FAB classification. LNR levels in HL60 cells increased during differentiation, being significantly higher in cells exposed to phorbol myristate acetate (PMA) and ethanol (55,391 ± 27,845 and 29,314 ± 6,435 sited cell respectively) as compared with HL60 controls (8,549 ± 4,000 siteskell). The control cells do not adhere to laminin‐coated surfaces, but differentiation with PMA results in their rapid adherence on this substratum. Short treatment with PMA does not increase the number of adherent cells or the receptor expression. Granulocytes also presented equally high LNR concentration (29,739 ± 13,516 sites/cell). The lymphoid cells (lymphocyte, acute lymphoid leukemia and chronic lymphocytic leukemia) shared low LNR numbers (<6,500 sites/cell). Myeloid cells displayed a wide range of LN receptors with higher levels being associated with the more differentiated FA9 subgroups. ^125^I‐laminin binding to lymphoid or myeloid leukemic cells was mainly inhibited by P~1~ fragments, whereas granulocytes and differentiated HL60 cells displayed a dual binding pattern for laminin fragments P~1~ and E~8~. These results were confirmed by assays using 125I‐labelled P~1~ and E~8~ fragments. We conclude that magnitude of LNR levels and variation in expression of P~1~ and E~8~ receptors appear to be linked to lineage and maturation status in hematopoietic cells.