Recruitment of circulating monocytes is critical for tumor angiogenesis. However, a recent study emphasized the high risk of developing breast cancer metastasis after cessation of CCL2 inhibition therapy, designed to target pan-monocyte and macrophage mobilization. The outcome of this study suggests that future strategies need to focus on targeting the recruitment and function of better defined monocyte subsets. Therefore defining human monocyte subsets with proangiogenic and protumorigenic functions as well as understanding their extravasation cascade would present opportunity for rapid clinical translation. How human monocyte subpopulations extravasate to tumors is unclear. In this study we show mechanisms of extravasation of human CD14dimCD16+ patrolling and CD14+CD16+ intermediate proangiogenic monocytes (HPMo), using human tumor xenograft models and live imaging of transmigration of isolated human monocytes. IFNγ promotes an increase of the chemokine CX3CL1 on vessel lumen, imposing continuous crawling to HPMo and making these monocytes insensitive to chemokines required for their extravasation. Expression of the angiogenic factor VEGF and the inflammatory cytokine TNF by tumor cells enables HPMo extravasation by inducing GATA3-mediated repression of CX3CL1 expression. Recruited HPMo boosts angiogenesis by secreting MMP9 leading to release of matrix-bound VEGF-A, which amplifies the entry of more HPMo into tumors. Uncovering the extravasation cascade of HPMo sets the stage for future tumor therapies.