Angiogenesis is closely related to
tumor development and
metastasis.
Osteosarcoma is an angiogenesis-dependent
tumor, and studies have shown that
chemotherapy often induces angiogenesis.
Endostatin is a broad spectrum
angiogenesis inhibitor and, while pre-clinical trials have shown that the combination of
endostatin with
chemotherapy can enhance anti-
tumor effects, this effect has not yet been shown in clinical trials. Here, we aimed to evaluate the clinical efficacy of
endostar (ES, human recombinant
endostatin) combined with
chemotherapy in the treatment of
osteosarcoma patients. A total of 116 newly diagnosed patients with
osteosarcoma were enrolled in this study. All patients received 4cycles of
chemotherapy with (54 cases) or without (62 cases) ES. ES was administered intravenously at a dose of 15mg/day for 2weeks during each cycle of
chemotherapy. The
tumors were removed by surgery after 2cycles of
chemotherapy treatment, and their histologic response to
chemotherapy was evaluated. Immunohistochemistry was used to measure
VEGF and CD 31 expression.
Chemotherapy increased
VEGF expression and the presence of microvessels in
osteosarcoma tissues compared with pre-
chemotherapy. No significant difference was observed in the histologic response between the ES treatment and non-treatment groups. However, ES treatment significantly inhibited the
chemotherapy-induced
VEGF expression and presence of microvessels. The ES treatment did not affect the overall survival rate but did increase the event-free survival rate and decreased the occurrence of
metastases. In conclusion, our results indicate that antiangiogenic
therapy using ES has the potential to prevent the progression of
metastases.