Abstract: The present invention is based on the finding that CD11b signaling inhibits immune suppression, modulates neovascularization and promotes anti-tumor immune responses in models of murine and human cancer. As such, provided herein are methods of treating cancer using an antibody, protein or small molecule that modulates CD11b activity or expression. Also provided are methods of identifying cancer that is amenable to such treatment and/or increasing susceptibility of cancer cells to treatment with a chemotherapeutic agent.

Abstract: The present invention is based on the finding that CD11b signaling inhibits immune suppression, modulates neovascularization and promotes anti-tumor immune responses in models of murine and human cancer. As such, provided herein are methods of treating cancer using an antibody, protein or small molecule that modulates CD11b activity or expression. Also provided are methods of identifying cancer that is amenable to such treatment and/or increasing susceptibility of cancer cells to treatment with a chemotherapeutic agent.

Abstract: This invention relates to the discovery of the convergence of diverse receptors and signaling pathways on the PI3gamma dependent activation of VLA4 (integrin a4b1). In particular, the invention relates to the role of myeloid cells in tumor inflammation and metastasis. The invention provides methods for inhibiting cancer in a subject comprising administering to a subject having cancer that comprises endothelial cells a therapeutically effective amount of a PI-3-kinase gamma inhibitor that reduces at least one of (a) adhesion of myeloid cells to the endothelial cells, (b) migration of myeloid cells into the cancer, (c) growth of the cancer, (d) activation of integrin a4b1 that is comprised on the myeloid cells, and (e) clustering of integrin a4b1 that is comprised on the myeloid cells.