Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/26973
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dc.contributor.authorWang, Kai-
dc.contributor.authorHe, Hong-
dc.date.accessioned2021-07-05T06:11:05Z-
dc.date.available2021-07-05T06:11:05Z-
dc.date.issued2020-
dc.identifier.citationAdvances in Experimental Medicine and Biology 2020; 1296: 243-257en
dc.identifier.issn0065-2598
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/26973-
dc.description.abstractThe pancreatic ductal adenocarcinoma (PDAC) microenvironment is a diverse and complex milieu of immune, stromal, and tumor cells and is characterized by a dense stroma, which mediates the interaction between the tumor and the immune system within the tumor microenvironment (TME). The interaction between stromal and tumor cells signals and shapes the immune infiltration of TME. The desmoplastic compartment contains infiltrated immune cells including tumor-associated macrophages (TAMs) and large numbers of fibroblasts/myofibroblasts dominated by pancreatic stellate cells (PSCs) which contribute to fibrosis. The highly fibrotic stroma with its extensive infiltration of immunosuppressive cells forms the major component of the pro-tumorigenic microenvironment (Laklai et al. Nat Med 22:497-505, 2016, Zhu et al. Cancer Res 74:5057-5069, 2014) provides a barrier to the delivery of cytotoxic agents and limits T-cell access to tumor cells (Feig et al. Proc Natl Acad Sci USA 110:20212-20217, 2013, Provenzano et al Cancer Cell 21:418-429, 2012). Activated PSCs reduced infiltration of cytotoxic T cells to the juxtatumoral stroma (immediately adjacent to the tumor epithelial cells) of PDAC (Ene-Obong et al. Gastroenterology 145:1121-1132, 2013). M1 macrophages activate an immune response against tumor, but M2 macrophages are involved in immunosuppression promoting tumor progression (Noy and Pollard Immunity 41:49-61, 2014, Ruffell et al. Trends Immunol 33:119-126, 2012). The desmoplastic stroma is reported to protect tumor cells against chemotherapies, promoting their proliferation and migration. However, experimental depletion of the desmoplastic stroma has led to more aggressive cancers in animal studies (Nielsen et al. World J Gastroenterol 22:2678-2700, 2016). Hence reprogramming rather than simple depletion of the PDAC stroma has the potential for developing new therapeutic strategies for PC treatment. Modulation of PSCs/fibrosis and immune infiltration/inflammation composes the major aspects of TME reprogramming.en
dc.language.isoeng
dc.subjectAlpha-smooth muscle actin (α-SMA)en
dc.subjectCollagensen
dc.subjectCytotoxic T cellsen
dc.subjectExtracellular matrix (ECM)en
dc.subjectGemcitabineen
dc.subjectHypoxiaen
dc.subjectHypoxia-inducible factors (HIFs)en
dc.subjectImmune checkpoint proteinsen
dc.subjectMyeloid-derived suppressor cells (MDSCs)en
dc.subjectPancreatic ductal adenocarcinoma (PDAC)en
dc.subjectPancreatic stellate cells (PSCs)en
dc.subjectTumor immune responseen
dc.subjectTumor infiltrating lymphocytes (TILs)en
dc.subjectTumor microenvironment (TME)en
dc.subjectTumor-associated macrophages (TAMs)en
dc.titlePancreatic Tumor Microenvironment.en
dc.typeJournal Articleen
dc.identifier.journaltitleAdvances in Experimental Medicine and Biologyen
dc.identifier.affiliationSurgery (University of Melbourne)en
dc.identifier.doi10.1007/978-3-030-59038-3_15en
dc.type.contentTexten
dc.identifier.pubmedid34185297
local.name.researcherHe, Hong
item.openairetypeJournal Article-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
crisitem.author.deptSurgery (University of Melbourne)-
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