Potential role of OPN in ALL cell dormancy. In the marrow microenvironment, HPCs are maintained in perivascular and endosteal niches, which also can be occupied by ALL and other leukemia cells. In the osteoblast niches, osteoblasts and ALL cells secrete OPN, which becomes part of the extracellular matrix and builds a bridge between ALL cells and osteoblasts/the bone (left). Adherence of ALL cells to OPN via adhesion molecules causes ALL cell dormancy, which makes ALL cells less susceptible to cytotoxic drugs, such as Ara-C. ALL cell dormancy can be reversed by OPN neutralization (right), which causes an increase in dividing/cycling ALL cells. This reversal of ALL cell dormancy by OPN neutralization can potentially be used for “chemosensitization” to target dormant ALL cells that otherwise survive conventional polychemotherapy.

Potential role of OPN in ALL cell dormancy. In the marrow microenvironment, HPCs are maintained in perivascular and endosteal niches, which also can be occupied by ALL and other leukemia cells. In the osteoblast niches, osteoblasts and ALL cells secrete OPN, which becomes part of the extracellular matrix and builds a bridge between ALL cells and osteoblasts/the bone (left). Adherence of ALL cells to OPN via adhesion molecules causes ALL cell dormancy, which makes ALL cells less susceptible to cytotoxic drugs, such as Ara-C. ALL cell dormancy can be reversed by OPN neutralization (right), which causes an increase in dividing/cycling ALL cells. This reversal of ALL cell dormancy by OPN neutralization can potentially be used for “chemosensitization” to target dormant ALL cells that otherwise survive conventional polychemotherapy.

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