2016
DOI: 10.18632/oncotarget.10364
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Sunitinib enhances the antitumor responses of agonistic CD40-antibody by reducing MDSCs and synergistically improving endothelial activation and T-cell recruitment

Abstract: CD40-activating immunotherapy has potent antitumor effects due to its ability to activate dendritic cells and induce cytotoxic T-cell responses. However, its efficacy is limited by immunosuppressive cells in the tumor and by endothelial anergy inhibiting recruitment of T-cells. Here, we show that combining agonistic CD40 monoclonal antibody (mAb) therapy with vascular targeting using the tyrosine kinase inhibitor sunitinib decreased tumor growth and improved survival in B16.F10 melanoma and T241 fibrosarcoma. … Show more

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Cited by 37 publications
(40 citation statements)
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“…The clinically approved cancer therapeutics ibrutinib and sunitinib inhibited tyrosine kinases present in MDSCs and prevented MDSC generation, migration, and function in several murine tumor models (64,145).…”
Section: Direct Targeting Of Mdscs In Vivomentioning
confidence: 99%
“…The clinically approved cancer therapeutics ibrutinib and sunitinib inhibited tyrosine kinases present in MDSCs and prevented MDSC generation, migration, and function in several murine tumor models (64,145).…”
Section: Direct Targeting Of Mdscs In Vivomentioning
confidence: 99%
“…Reduction or removal of MDSCs could be a new strategy for effective treatment of cancers. In fact, several agents have been found to reduce the proliferation of MDSCs or to target MDSCs' trafficking in mouse and human tumors, for example, the inhibitor of CXCR2 (43), the CXCR4 antagonist AMD3100 (44), and the chemotherapeutic drugs doxorubicin (45), sunitinib (tyrosine kinase inhibitor) (46), and Avastin (VEGF-specific monoclonal antibody) (47). Whether the combination of drugs inhibiting MDSC proliferation with hypofractionated IR could enhance the efficacy of antitumor and antimetastasis drugs needs to be studied.…”
Section: Discussionmentioning
confidence: 99%
“…In our experimental model, the combination of Sunitinib with pro-inflammatory cytokines present in the cytokine-treated keratinocyte medium or expressed by ECs exposed to the keratinocyte supernatants, could result into ICAM-1 up-regulation as well. A recent paper by van Hooren and colleagues [40] demonstrated the up-regulation of ICAM-1 expression on tumor ECs treated with Sunitinib and an agonistic anti-CD40 monoclonal antibody. CD40 is a member of the TNF super family and, in immune cells, its expression is induced by several pro-inflammatory cytokines such as IL-36γ itself.…”
Section: Discussionmentioning
confidence: 99%