AML blast cell adhesion to endothelium is in all likelihood a prerequi
site for blast cell migration across the vascular wall in the peripher
y and the subsequent establishment of leukemic extravascular disease.
A general feature of malignant cells is their acquisition of altered o
r aberrant adhesive capabilities which appear to be associated with th
eir ability to metastasize. Aberrant expression of integrin adhesion m
olecules and of membrane oligosaccharide structures is found in AML an
d various solid tumors. With respect to AML, these alterations in adhe
sive phenotype may confer a proliferative advantage on the malignant c
ells in the marrow, may facilitate egress from the bone marrow into th
e peripheral vasculature and may enable AML blast cells to traverse th
e vessel wall and so establish extravascular disease. Oncogenes may be
directly involved in the acquisition of such aberrant adhesive phenot
ypes. Neutrophil extravasation is described as a model for leukocyte m
igration across the vessel wall and brief summaries of experimental wo
rk involving aspects of AML blast cell and normal CD34+ bone marrow ce
ll adhesion to endothelium in vitro are described.