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Merck
  • Tumor-specific cytolysis caused by an E1B55K-attenuated adenovirus in nasopharyngeal carcinoma is augmented by cisplatin.

Tumor-specific cytolysis caused by an E1B55K-attenuated adenovirus in nasopharyngeal carcinoma is augmented by cisplatin.

Anatomical record (Hoboken, N.J. : 2007) (2013-10-19)
Ran-Yi Liu, Ji-Lin Peng, Yong-Qiang Li, Bi-Jun Huang, Huan-Xin Lin, Ling Zhou, Hui-Ling Luo, Wenlin Huang
要旨

An E1B55K-attenuated adenovirus, dl1520, has been shown to replicate selectively in and lyse tumor cells. In this study, the antitumor activities of dl1520, alone or in combination with the chemotherapeutic agent cisplatin, were investigated in nasopharyngeal carcinoma (NPC) cells. The results demonstrated that dl1520 replicated in and destroyed NPC cells, and induced apoptosis in vitro. In a nude mouse xenograft model, dl1520 significantly inhibited the growth of NPC cell xenografts, and the viral replication was associated with tumor regression. Importantly, the antitumor activity of dl1520 was augmented by the addition of cisplatin both in vitro and in vivo, showing that dl1520 and cisplatin have a synergistic anti-NPC effect. These data suggest that dl1520 exerts an efficient anti-NPC activity through oncolysis and the induction of apoptosis, which is enhanced synergistically by cisplatin. These findings indicate that oncolytic viral therapeutics using the E1B55K-attenuated adenovirus dl1520 could be promising in the comprehensive treatment of NPC, especially in combination with platinum-based chemotherapy.

材料
製品番号
ブランド
製品内容

Sigma-Aldrich
抗アデノウイルス(ブレンド)コーティング抗体、クローン2/6、20/11, ascites fluid, Chemicon®, from mouse