Shen, KeyueLuk, SamanthaHicks, Daniel FElman, Jessica SBohr, StefanIwamoto, YoshikoMurray, RyanPena, KristenWang, FangjingSeker, ErkinWeissleder, RalphYarmush, MartinToner, MehmetSgroi, DennisParekkadan, Biju2015-07-132014Shen, K., S. Luk, D. F. Hicks, J. S. Elman, S. Bohr, Y. Iwamoto, R. Murray, et al. 2014. “Resolving Cancer-Stroma Interfacial Signaling and Interventions with Micropatterned Tumor-Stromal Assays.” Nature communications 5 (1): 5662. doi:10.1038/ncomms6662. http://dx.doi.org/10.1038/ncomms6662.2041-1723http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295619Tumor-stromal interactions are a determining factor in cancer progression. In vivo, the interaction interface is associated with spatially-resolved distributions of cancer and stromal phenotypes. Here, we establish a micropatterned tumor-stromal assay (μTSA) with laser capture microdissection to control the location of co-cultured cells and analyze bulk and interfacial tumor-stromal signaling in driving cancer progression. μTSA reveals a spatial distribution of phenotypes in concordance with human estrogen receptor-positive (ER+) breast cancer samples, and heterogeneous drug activity relative to the tumor-stroma interface. Specifically, an unknown mechanism of reversine is shown in targeting tumor-stromal interfacial interactions using ER+ MCF-7 breast cancer and bone marrow-derived stromal cells. Reversine suppresses MCF-7 tumor growth and bone metastasis in vivo by reducing tumor stromalization including collagen deposition and recruitment of activated stromal cells. This study advocates μTSA as a platform for studying tumor microenvironmental interactions and cancer field effects with applications in drug discovery and development.en-USJournal Article2015-07-1310.1038/ncomms6662