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Disrupting tumour vasculature and recruitment of aPDL1-loaded platelets control tumour metastasis.

Hongjun LiZe-Jun WangZhaowei ChenTianyuan CiGuojun ChenDi WenRuoxin LiJinqiang WangHuan MengRichard B BellZhi-Feng GuGianpietro DottiZhen Gu
Published in: Nature communications (2021)
Although therapies of cancer are advancing, it remains challenging for therapeutics to reach the sites of metastasis, which accounts for majority of cancer associated death. In this study, we have developed a strategy that guides an anti-programmed cell death-ligand 1 (aPDL1) antibody to accumulate in metastatic lesions to promote anti-tumour immune responses. Briefly, we have developed a combination in which Vadimezan disrupts tumour blood vessels of tumour metastases and facilitates the recruitment and activation of adoptively transferred aPDL1-conjugated platelets. In situ activated platelets generate aPDL1-decorated platelet-derived microparticles (PMP) that diffuse within the tumour and elicit immune responses. The proposed combination increases 10-fold aPDL1 antibody accumulation in lung metastases as compared to the intravenous administration of the antibody and enhances the magnitude of immune responses leading to improved antitumour effects.
Keyphrases
  • immune response
  • small cell lung cancer
  • toll like receptor
  • dendritic cells
  • cancer therapy
  • gold nanoparticles
  • inflammatory response
  • high dose
  • low grade
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  • childhood cancer