Smad3 Promotes Cancer‐Associated Fibroblasts Generation via Macrophage–Myofibroblast Transition (Adv. Sci. 1/2022)
Macrophage‐Myofibroblast Transition In article number 2101235 Philip Chiu‐Tsun Tang, Patrick Ming‐Kuen Tang, Hui‐Yao Lan, and co‐workers discovered that tumor‐associated macrophages are capable for de novo generating pathogenic cancer‐associated fibroblasts via a direct mechanism macrophage‐myofibro...
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creator | Tang, Philip Chiu‐Tsun Chung, Jeff Yat‐Fai Xue, Vivian Wei‐wen Xiao, Jun Meng, Xiao‐Ming Huang, Xiao‐Ru Zhou, Shuang Chan, Alex Siu‐Wing Tsang, Anna Chi‐Man Cheng, Alfred Sze‐Lok Lee, Tin‐Lap Leung, Kam‐Tong Lam, Eric W.‐F. To, Ka‐Fai Tang, Patrick Ming‐Kuen Lan, Hui‐Yao |
description | Macrophage‐Myofibroblast Transition
In article number 2101235 Philip Chiu‐Tsun Tang, Patrick Ming‐Kuen Tang, Hui‐Yao Lan, and co‐workers discovered that tumor‐associated macrophages are capable for de novo generating pathogenic cancer‐associated fibroblasts via a direct mechanism macrophage‐myofibroblast transition (MMT), representing a novel therapeutic target in the tumor microenvironment of solid cancers. Here, the macrophages undergoing MMT were coexpressing CAF (α‐SMA, red) and macrophage marker (F4/80, green) with nuclei staining (blue), visualized by immunofluorescence with an experimental Lewis lung carcinoma (LLC) model. |
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In article number 2101235 Philip Chiu‐Tsun Tang, Patrick Ming‐Kuen Tang, Hui‐Yao Lan, and co‐workers discovered that tumor‐associated macrophages are capable for de novo generating pathogenic cancer‐associated fibroblasts via a direct mechanism macrophage‐myofibroblast transition (MMT), representing a novel therapeutic target in the tumor microenvironment of solid cancers. Here, the macrophages undergoing MMT were coexpressing CAF (α‐SMA, red) and macrophage marker (F4/80, green) with nuclei staining (blue), visualized by immunofluorescence with an experimental Lewis lung carcinoma (LLC) model.</description><identifier>ISSN: 2198-3844</identifier><identifier>EISSN: 2198-3844</identifier><identifier>DOI: 10.1002/advs.202270005</identifier><language>eng</language><publisher>Weinheim: John Wiley & Sons, Inc</publisher><subject>Frontispiece</subject><ispartof>Advanced science, 2022-01, Vol.9 (1), p.n/a</ispartof><rights>2022 Wiley‐VCH GmbH</rights><rights>Copyright John Wiley & Sons, Inc. Jan 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2575-62f4111c5cf07ab117a4bb9e206909ccf55be1bbe42a9a84d332689144c005fd3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8728852/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8728852/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1002%2Fadvs.202270005$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc></links><search><creatorcontrib>Tang, Philip Chiu‐Tsun</creatorcontrib><creatorcontrib>Chung, Jeff Yat‐Fai</creatorcontrib><creatorcontrib>Xue, Vivian Wei‐wen</creatorcontrib><creatorcontrib>Xiao, Jun</creatorcontrib><creatorcontrib>Meng, Xiao‐Ming</creatorcontrib><creatorcontrib>Huang, Xiao‐Ru</creatorcontrib><creatorcontrib>Zhou, Shuang</creatorcontrib><creatorcontrib>Chan, Alex Siu‐Wing</creatorcontrib><creatorcontrib>Tsang, Anna Chi‐Man</creatorcontrib><creatorcontrib>Cheng, Alfred Sze‐Lok</creatorcontrib><creatorcontrib>Lee, Tin‐Lap</creatorcontrib><creatorcontrib>Leung, Kam‐Tong</creatorcontrib><creatorcontrib>Lam, Eric W.‐F.</creatorcontrib><creatorcontrib>To, Ka‐Fai</creatorcontrib><creatorcontrib>Tang, Patrick Ming‐Kuen</creatorcontrib><creatorcontrib>Lan, Hui‐Yao</creatorcontrib><title>Smad3 Promotes Cancer‐Associated Fibroblasts Generation via Macrophage–Myofibroblast Transition (Adv. Sci. 1/2022)</title><title>Advanced science</title><description>Macrophage‐Myofibroblast Transition
In article number 2101235 Philip Chiu‐Tsun Tang, Patrick Ming‐Kuen Tang, Hui‐Yao Lan, and co‐workers discovered that tumor‐associated macrophages are capable for de novo generating pathogenic cancer‐associated fibroblasts via a direct mechanism macrophage‐myofibroblast transition (MMT), representing a novel therapeutic target in the tumor microenvironment of solid cancers. 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In article number 2101235 Philip Chiu‐Tsun Tang, Patrick Ming‐Kuen Tang, Hui‐Yao Lan, and co‐workers discovered that tumor‐associated macrophages are capable for de novo generating pathogenic cancer‐associated fibroblasts via a direct mechanism macrophage‐myofibroblast transition (MMT), representing a novel therapeutic target in the tumor microenvironment of solid cancers. Here, the macrophages undergoing MMT were coexpressing CAF (α‐SMA, red) and macrophage marker (F4/80, green) with nuclei staining (blue), visualized by immunofluorescence with an experimental Lewis lung carcinoma (LLC) model.</abstract><cop>Weinheim</cop><pub>John Wiley & Sons, Inc</pub><doi>10.1002/advs.202270005</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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title | Smad3 Promotes Cancer‐Associated Fibroblasts Generation via Macrophage–Myofibroblast Transition (Adv. Sci. 1/2022) |
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