Inflammatory breast cancer (IBC) is an aggressive disease with poor prognosis, accounting for 10% of breast cancer mortality. A contributing factor to this is the lack of therapeutics targeting IBC. IBC exhibits clinical features that differentiate it from non inflammatory breast cancers (nIBC) including swollen and enlarged breasts, skin redness, and diffuse distribution of IBC cells through the breast tissue. Even with the mentioned distinguishing features, as of now there are no differentiating molecular or histological markers that separate IBC from nIBC. Recent research has shown tumor stromal interactions to be the driving force in IBC with roles in promoting tumor development and growth, angiogenesis, and metastasis to distant tissues. Better understanding of these interactions is necessary for discovery of IBC distinct targeting markers and development of IBC specific treatments. We developed an in vitro vascularized IBC platform that allows for investigation of tumor-stromal interactions in IBC, specifically, we focused on the interactions between IBC cells, tumor associated macrophages (TAMs), and blood and lymphatic vasculatures. The platform allowed for spatiotemporal tracking of cellular interactions and responses in a physiologically relevant setting. Using the in vitro vascularized IBC platform, we showed the presence of triple negative IBC cells SUM149 resulted in a permeable blood vessel vasculature and decreased endothelial coverage of the vessel lumen while HER2+ IBC cells MDA-IBC3 promoted and supported angiogenic sprouting of the blood vessel and increased expression of angiogenic cytokines. Lymphatic vessels showed an increased permeability compared to blood vessels both with and without IBC cells as well as a lack of angiogenic sprouting and decreased matrix remodeling. When TAMs were incorporated into the blood vessel platforms, we observed an increase in the number of new vessel sprouts, increased permeability of the vessel, increased matrix porosity, and intravasation of MDA-IBC3 cells. In the in vitro IBC platforms with lymph vessels, TAMs induced lymphangiogenesis, albeit at a slower rate compared to blood vessel platforms, and increased matrix porosity. In conclusion, the work presented here brings us closer to uncovering the mechanisms that drive IBC and discovery of IBC specific therapeutic targets.