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Osteosarcoma ( OS ) is the most frequent primary solid malignant tumor of bone. Its prognosis remains poor in the substantial proportion of patients who do not respond to chemotherapy and novel therapeutic options are therefore needed. We previously established a mouse model that mimics the aggressive behavior of human  OS . Enzyme‐linked immunosorbent assay‐based screening of such mouse tumor lysates identified platelet‐derived growth factor– BB  ( PDGF ‐ BB ) as an abundant soluble factor, the gene for which was expressed dominantly in surrounding non‐malignant cells of the tumor, whereas that for the cognate receptor ( PDGF  receptor β) was highly expressed in  OS  cells. Platelet‐derived growth factor‐ BB  induced activation of both  MEK – ERK  and phosphatidylinositol 3‐kinase–protein kinase B signaling pathways and promoted survival in  OS  cells deprived of serum, and these effects were blocked by the  PDGF  receptor inhibitor imatinib. However, these actions of  PDGF ‐ BB  and imatinib were mostly masked in the presence of serum. Whereas imatinib alone did not manifest an antitumor effect in mice harboring  OS  tumors, combined treatment with imatinib and adriamycin exerted a synergistic antiproliferative effect on  OS  cells  in vivo . These results suggest that treatment of  OS  with imatinib is effective only when cell survival is dependent on  PDGF  signaling or when imatinib is combined with another therapeutic intervention that renders the tumor cells susceptible to imatinib action, such as by inducing cellular stress.

Synergistic antiproliferative effect of imatinib and adriamycin in platelet‐derived growth factor receptor‐expressing osteosarcoma cells