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|a dc
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|a Hayakawa, Yoku
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|a Massachusetts Institute of Technology. Department of Biological Engineering
|e contributor
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|a Massachusetts Institute of Technology. Division of Comparative Medicine
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|a Shen, Zeli
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|a Fox, James G
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|a Ariyama, Hiroshi
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|a Stancikova, Jitka
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|a Sakitani, Kosuke
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|a Asfaha, Samuel
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|a Renz, Bernhard W.
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|a Dubeykovskaya, Zinaida A.
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|a Shibata, Wataru
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|a Wang, Hongshan
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|a Westphalen, Christoph B.
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|a Chen, Xiaowei
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|a Takemoto, Yoshihiro
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|a Kim, Woosook
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|a Khurana, Shradha S.
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|a Tailor, Yagnesh
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|a Nagar, Karan
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|a Tomita, Hiroyuki
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|a Hara, Akira
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|a Sepulveda, Antonia R.
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|a Setlik, Wanda
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|a Gershon, Michael D.
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|a Saha, Subhrajit
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|a Ding, Lei
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|a Friedman, Richard A.
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|a Konieczny, Stephen F.
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|a Worthley, Daniel L.
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|a Korinek, Vladimir
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|a Wang, Timothy C.
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|a Shen, Zeli
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|a Fox, James G
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|a Mist1 Expressing Gastric Stem Cells Maintain the Normal and Neoplastic Gastric Epithelium and Are Supported by a Perivascular Stem Cell Niche
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|b Elsevier,
|c 2017-03-29T16:17:09Z.
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|z Get fulltext
|u http://hdl.handle.net/1721.1/107766
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|a The regulation and stem cell origin of normal and neoplastic gastric glands are uncertain. Here, we show that Mist1 expression marks quiescent stem cells in the gastric corpus isthmus. Mist1⁺ stem cells serve as a cell-of-origin for intestinal-type cancer with the combination of Kras and Apc mutation and for diffuse-type cancer with the loss of E-cadherin. Diffuse-type cancer development is dependent on inflammation mediated by Cxcl12⁺ endothelial cells and Cxcr4⁺ gastric innate lymphoid cells (ILCs). These cells form the perivascular gastric stem cell niche, and Wnt5a produced from ILCs activates RhoA to inhibit anoikis in the E-cadherin-depleted cells. Targeting Cxcr4, ILCs, or Wnt5a inhibits diffuse-type gastric carcinogenesis, providing targets within the neoplastic gastric stem cell niche.
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|a National Institutes of Health (U.S.) (Grants 54CA126513, R01CA093405, R01CA120979, and R01DK052778)
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|a en_US
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|a Article
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|t Cancer Cell
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