Author of

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  P3.01 - Poster Session 3 - Cancer Biology (ID 147)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Biology
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/30/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

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    P3.01-005 - Efficacy of Arsenic Trioxide in the Treatment of Malignant Pleural Effusion caused by Pleural Metastasis of Lung Cancer (ID 821)

    09:30 - 09:30  |  Author(s): B. Li
    • Abstract

    Background
    Arsenic trioxide (As~2~O~3~), an ancient drug used in traditional Chinese medicine with the characteristics of high effectiveness and low toxicity, was used to treat acute promyelocytic leukemia at the beginning . Over the past decade, in our clinical practice, local injection of As~2~O~3~ into pleural cavity has been successfully used for more than 80 patients with malignant pleural effusions(MPE) caused by pleural metastasis of lung cancer. And interestingly, after local administration of As~2~O~3~, the composition of blood cells in pleural effusion was reduced and the color of MPE changed from red to light yellow in the majority of patients, indicating that As~2~O~3~ could be considered as an effective approach for the treatment of MPE, but the underlying mechanism remains unclear . The aim of this study was to investigate the mechanism of arsenic trioxide (As~2~O~3~) in the treatment of malignant pleural effusion (MPE) caused by pleural metastasis of lung cancer.

    Methods
    A mouse model of MPE caused by pleural metastasis of lung cancer was first established in our study, and then As~2~O~3~ was intraperitoneally injected to treat MPE. Those mice treated with bevacizumab and bleomycin were included as positive control animals, and placebo equivalents were also employed as negative control. The effects of As~2~O~3 ~on MPE volume, pleural vessel density, vascular permeability, expression of angiogenic function related factors including VEGF and TNF-α, as well as NF-κB activity in pleural carcinomatosis were observed.

    Results
    Intraperitoneal injection of As~2~O~3~ could reduce the volume of MPE and decrease vascular density and vascular permeability in pleural metastatic nodules, in a dose-dependent manner. Moreover, the dose-dependent decrease in VEGF and TNF-α expression in MPE and NF-κB activity in pleural carcinomatosis were also found after As~2~O~3 ~treatment.

    Conclusion
    Our work demonstrated that As~2~O~3~ could down-regulate the VEGF expression through NF-κB inhibition, and then decrease vascular density and permeability in pleural metastatic nodules, thereby playing its effects on MPE caused by pleural metastasis of lung cancer. Our results could provide a foundation for As~2~O~3~-based clinical treatment program.