Enhanced radioresponse with a novel recombinant human endostatin protein via tumor vasculature remodeling: experimental and clinical evidence

Radiother Oncol. 2013 Jan;106(1):130-7. doi: 10.1016/j.radonc.2012.10.022. Epub 2013 Jan 23.

Abstract

Purpose: This study aimed to examine the effect of the novel recombinant human endostatin (rh-Endo) protein on tumor vasculature, and to explore and evaluate the optimal scheduling of rh-Endo and radiotherapy (RT).

Methods: Tumor-perfusion parameters and hypoxia were monitored after rh-Endo treatment in 10 non-small cell lung-cancer (NSCLC) patients. Eight-week female C57BL/6J mice were randomized to receive rh-Endo or control (saline) once daily for 12 days when Lewis lung carcinoma (LLC) reached approximately 100-150 mm(3). On planned days, tumors were measured for cell apoptosis, microvessel density, pericytes, blood-vessel morphology, and tumor hypoxia. The tumor response under different combinations of rh-Endo and RT schedules was evaluated.

Results: Tumor hypoxia was significantly reduced 5 days after rh-Endo in NSCLC patients, and a similar result was found in the LLC mouse model. The anti-tumor effect was markedly enhanced when RT was administered within the remodeling period compared to any other treatment schedule. rh-Endo treatment remodeled the tumor vasculature after 5 days by reducing microvessel density and increasing pericytic coverage of the vessel endothelium.

Conclusion: This study demonstrated decreased hypoxia in animals and patients upon rh-Endo treatment, which also enhanced the radioresponse within the vasculature-remodeling period. The optimal clinical combination of rh-Endo and RT warrants further investigation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / analysis
  • Actins / genetics
  • Adolescent
  • Adult
  • Aged
  • Animals
  • Apoptosis / drug effects
  • Carcinoma, Non-Small-Cell Lung / blood supply
  • Carcinoma, Non-Small-Cell Lung / radiotherapy*
  • Cell Hypoxia
  • Endostatins / pharmacology*
  • Endothelial Cells / physiology
  • Female
  • Humans
  • Lung Neoplasms / blood supply
  • Lung Neoplasms / radiotherapy*
  • Mice
  • Mice, Inbred BALB C
  • Middle Aged
  • Platelet Endothelial Cell Adhesion Molecule-1 / genetics
  • RNA, Messenger / analysis
  • Radiation-Sensitizing Agents / pharmacology*
  • Recombinant Proteins / pharmacology

Substances

  • ACTA2 protein, human
  • Actins
  • Endostatins
  • Platelet Endothelial Cell Adhesion Molecule-1
  • RNA, Messenger
  • Radiation-Sensitizing Agents
  • Recombinant Proteins