Abstract
Selective homing of hemopoietic progenitor cells to hemopoietic organs is the initial event in hemopoiesis. At a molecular level, it is mediated by a membrane receptor on the surface of hemopoietic progenitor cells. The receptor molecule then binds selectively to a glycoconjugate on the surface of bone marrow stromal cells. The molecular nature of this receptor has been shown previously to be a lectin with specificity for an as yet unknown configuration of galactosyl and mannosyl residues of the glycoconjugate. Normal murine progenitor cell lines, FDCP-1 and B6SUT, were found to possess this homing receptor on their cell membrane, and they also bind well to hemopoietic stroma. However, when three human leukemic cell lines, U937, HL60 and K562, were probed for the presence of this receptor, they were found to be deficient in the homing protein. Further, these cells showed little ability to bind the hemopoietic stromal cell line, GB1/6. These findings suggest that leukemic cells experience a loss, or at least alteration, of homing receptor molecule during leukemic transformation. This can result in a diminished ability to bind to marrow stroma. The lack of homing function may be of pathogenetic significance in the lack of differentiation of leukemic cells and may also contribute to the dissemination of leukemic cells in the circulation.
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