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Fibroblasts from metastatic sites induce broad-spectrum drug desensitization via modulation of mitochondrial priming

Benjamin D. Landry, Thomas Leete, Ryan Richards, Peter Cruz-Gordillo, Gary Ren, Alyssa D. Schwartz, Shelly R. Peyton, Michael J. Lee
doi: https://doi.org/10.1101/197376
Benjamin D. Landry
Program in Systems Biology; Program in Molecular Medicine; and Department of Molecular>, Cell and Cancer Biology University of Massachusetts Medical School Worcester, MA 01605
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Thomas Leete
Program in Systems Biology; Program in Molecular Medicine; and Department of Molecular>, Cell and Cancer Biology University of Massachusetts Medical School Worcester, MA 01605
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Ryan Richards
Program in Systems Biology; Program in Molecular Medicine; and Department of Molecular>, Cell and Cancer Biology University of Massachusetts Medical School Worcester, MA 01605
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Peter Cruz-Gordillo
Program in Systems Biology; Program in Molecular Medicine; and Department of Molecular>, Cell and Cancer Biology University of Massachusetts Medical School Worcester, MA 01605
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Gary Ren
Program in Systems Biology; Program in Molecular Medicine; and Department of Molecular>, Cell and Cancer Biology University of Massachusetts Medical School Worcester, MA 01605
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Alyssa D. Schwartz
Department of Chemical Engineering University of Massachusetts, Amherst Amherst, MA 01003
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Shelly R. Peyton
Department of Chemical Engineering University of Massachusetts, Amherst Amherst, MA 01003
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Michael J. Lee
Program in Systems Biology; Program in Molecular Medicine; and Department of Molecular>, Cell and Cancer Biology University of Massachusetts Medical School Worcester, MA 01605
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  • For correspondence: michael.lee@umassmed.edu
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ABSTRACT

Due to tumor heterogeneity, most believe that effective treatments should be tailored to the features of an individual tumor or tumor subclass. It is still unclear what information should be considered for optimal disease stratification, and most prior work focuses on tumor genomics. Here, we focus on the tumor micro-environment. Using a large-scale co-culture assay optimized to measure drug-induced cell death, we identify tumor-stroma interactions that modulate drug sensitivity. Our data show that the chemo-insensitivity typically associated with aggressive subtypes of breast cancer is not cell intrinsic, but rather a product of tumor-fibroblast interactions. Additionally, we find that fibroblast cells influence tumor drug response in two distinct and divergent manners, which were predicable based on the anatomical origin from which the fibroblasts were harvested. These divergent phenotypes result from modulation of “mitochondrial priming” of tumor cells, caused by secretion of inflammatory cytokines, such as IL6 and IL8, from stromal cells.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted October 02, 2017.
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Fibroblasts from metastatic sites induce broad-spectrum drug desensitization via modulation of mitochondrial priming
Benjamin D. Landry, Thomas Leete, Ryan Richards, Peter Cruz-Gordillo, Gary Ren, Alyssa D. Schwartz, Shelly R. Peyton, Michael J. Lee
bioRxiv 197376; doi: https://doi.org/10.1101/197376
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Fibroblasts from metastatic sites induce broad-spectrum drug desensitization via modulation of mitochondrial priming
Benjamin D. Landry, Thomas Leete, Ryan Richards, Peter Cruz-Gordillo, Gary Ren, Alyssa D. Schwartz, Shelly R. Peyton, Michael J. Lee
bioRxiv 197376; doi: https://doi.org/10.1101/197376

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