Effect of Recombinant Human Endostatin on Angiogenesis and Treatment Response of Chemoradiation Therapy for Patients With Esophageal Squamous Carcinoma

Abstract

Purpose/Objective(s)Recombinant human endostatin has been documented to be an inhibitor of tumor angiogenesis. We investigated the treatment response to anti-angiogenic therapy of recombinant human endostatin combined with chemoradiation therapy (CRT) for patients with esophageal cell squamous carcinoma (ESCC).Materials/MethodsA total of 37 ESCC patients with UICC2002 stage T1-T4 were randomly studied. Twenty-one patients were simultaneously treated with recombinant human endostatin combined with docetaxel (75 mg/m2 on day 1)/CDDP (25 mg/m2 on day 1-3)-based intensity-modulated radiation therapy (IMRT, 60-66 Gy/30-33 f/6-7 wks), and 16 patients were treated with docetaxel/CDDP-based IMRT alone. CT perfusion imaging responses of tumor blood vessels, and immunohistochemical staining of tumor microvessel density (MVD) before treatment and radiation therapy DT 20 Gy, and treatment-related complications were assessed during and after treatment.ResultsRecombinant human endostatin combined with CRT led to a marked decrease in tumor blood flow (BF) and blood volume (BV) with correction of MVD, compared to the CRT alone group (P < 0.05) was found. Our findings showed a slight improvement in overall response rate (ORR) (61.5% vs 54.5% in the CRT alone group), and no treatment-related toxicities that could be attributed specifically to recombinant human endostatin, and the common toxicities observed across the two groups are probably due to the CRT itself in the present study.ConclusionsRecombinant human endostatin combined with CRT can reduce tumor angiogenesis, and the effects of recombinant human endostatin combined with CRT were a potential improvement over that of CRT alone. Further prospective randomized control studies are needed to evaluate conclusively the clinical efficacy of this combined treatment modality for ESCC. Purpose/Objective(s)Recombinant human endostatin has been documented to be an inhibitor of tumor angiogenesis. We investigated the treatment response to anti-angiogenic therapy of recombinant human endostatin combined with chemoradiation therapy (CRT) for patients with esophageal cell squamous carcinoma (ESCC). Recombinant human endostatin has been documented to be an inhibitor of tumor angiogenesis. We investigated the treatment response to anti-angiogenic therapy of recombinant human endostatin combined with chemoradiation therapy (CRT) for patients with esophageal cell squamous carcinoma (ESCC). Materials/MethodsA total of 37 ESCC patients with UICC2002 stage T1-T4 were randomly studied. Twenty-one patients were simultaneously treated with recombinant human endostatin combined with docetaxel (75 mg/m2 on day 1)/CDDP (25 mg/m2 on day 1-3)-based intensity-modulated radiation therapy (IMRT, 60-66 Gy/30-33 f/6-7 wks), and 16 patients were treated with docetaxel/CDDP-based IMRT alone. CT perfusion imaging responses of tumor blood vessels, and immunohistochemical staining of tumor microvessel density (MVD) before treatment and radiation therapy DT 20 Gy, and treatment-related complications were assessed during and after treatment. A total of 37 ESCC patients with UICC2002 stage T1-T4 were randomly studied. Twenty-one patients were simultaneously treated with recombinant human endostatin combined with docetaxel (75 mg/m2 on day 1)/CDDP (25 mg/m2 on day 1-3)-based intensity-modulated radiation therapy (IMRT, 60-66 Gy/30-33 f/6-7 wks), and 16 patients were treated with docetaxel/CDDP-based IMRT alone. CT perfusion imaging responses of tumor blood vessels, and immunohistochemical staining of tumor microvessel density (MVD) before treatment and radiation therapy DT 20 Gy, and treatment-related complications were assessed during and after treatment. ResultsRecombinant human endostatin combined with CRT led to a marked decrease in tumor blood flow (BF) and blood volume (BV) with correction of MVD, compared to the CRT alone group (P < 0.05) was found. Our findings showed a slight improvement in overall response rate (ORR) (61.5% vs 54.5% in the CRT alone group), and no treatment-related toxicities that could be attributed specifically to recombinant human endostatin, and the common toxicities observed across the two groups are probably due to the CRT itself in the present study. Recombinant human endostatin combined with CRT led to a marked decrease in tumor blood flow (BF) and blood volume (BV) with correction of MVD, compared to the CRT alone group (P < 0.05) was found. Our findings showed a slight improvement in overall response rate (ORR) (61.5% vs 54.5% in the CRT alone group), and no treatment-related toxicities that could be attributed specifically to recombinant human endostatin, and the common toxicities observed across the two groups are probably due to the CRT itself in the present study. ConclusionsRecombinant human endostatin combined with CRT can reduce tumor angiogenesis, and the effects of recombinant human endostatin combined with CRT were a potential improvement over that of CRT alone. Further prospective randomized control studies are needed to evaluate conclusively the clinical efficacy of this combined treatment modality for ESCC. Recombinant human endostatin combined with CRT can reduce tumor angiogenesis, and the effects of recombinant human endostatin combined with CRT were a potential improvement over that of CRT alone. Further prospective randomized control studies are needed to evaluate conclusively the clinical efficacy of this combined treatment modality for ESCC.