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10.1038/ncomms6662

http://scihub22266oqcxt.onion/10.1038/ncomms6662
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C4261930!4261930!25489927
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suck abstract from ncbi


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pmid25489927      Nat+Commun 2014 ; 5 (ä): 5662
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  • Resolving Cancer-Stroma Interfacial Signaling and Interventions with Micropatterned Tumor-Stromal Assays #MMPMID25489927
  • Shen K; Luk S; Hicks DF; Elman JS; Bohr S; Iwamoto Y; Murray R; Pena K; Wang F; Seker E; Weissleder R; Yarmush ML; Toner M; Sgroi D; Parekkadan B
  • Nat Commun 2014[]; 5 (ä): 5662 PMID25489927show ga
  • Tumor-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 (?TSA) with laser capture microdissection to control the location of co-cultured cells and analyze bulk and interfacial tumor-stromal signaling in driving cancer progression. ?TSA 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 ?TSA as a platform for studying tumor microenvironmental interactions and cancer field effects with applications in drug discovery and development.
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