Abstract

Abstract It has been shown that CD24 drives lung metastasis formation of bladder cancer and might be a good candidate for mAb-dependent therapy. We tested whether mAb SWA11 to CD24 would be effective in preventing tumor growth in xenotransplanted mice. In an A549 lung carcinoma model cells were implanted s.c. into SCID/beige mice followed by multiple injections of mAb over 37 days. Therapy with anti-CD24 mAb SWA11 lead to substantially reduced tumor load. The final tumor mass of treated animals was significantly smaller compared to isotype-control mAb treated animals. Similar observations were made in therapy models of CD24-positive BxPC3 pancreatic adenocarcioma cells in NOD/SCID mice and SKOV-3ip ovarian carcinoma cells in CD1 mice. The therapeutic effects were associated with changes in tumor cell proliferation, apoptosis and angiogenesis. Surprisingly, we found that SWA11 mAb treatment significantly altered cytokine tumor microenvironment. Also the mAb treatment lead to the increased infiltration of tumor tissue with immune cells suggesting involvement of ADCC. Addition of SWA11 mAb to the gemcitabine treatment strongly potentiated its anti-cancer efficacy in A549 lung cancer model. Our data demonstrate that targeting of CD24 could be beneficial for the anti-cancer treatment using standard chemotherapy regimes. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2011 Nov 12-16; San Francisco, CA. Philadelphia (PA): AACR; Mol Cancer Ther 2011;10(11 Suppl):Abstract nr C59.

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