Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/40387
DC FieldValueLanguage
dc.contributor.authorYuan, A.en_US
dc.contributor.author陳健尉zh_TW
dc.contributor.authorChen, J.J.W.en_US
dc.contributor.authorYang, P.C.en_US
dc.date2008zh_TW
dc.date.accessioned2014-06-06T08:03:41Z-
dc.date.available2014-06-06T08:03:41Z-
dc.identifier.issn0065-2423zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/40387-
dc.description.abstractThe macrophage is an important component of the human immune defense mechanism. Cancer cells secrete a variety of chemoattractants that attract macrophages and cause them to accumulate in the tumor tissue, wherein the macrophage becomes a tumor-associated macrophage (TAM). Recent evidence has shown that the function of tumor stromal TAMs can be modified by cancer cells and the factors they secrete. TAMs are directed toward stimulating tumor growth and progression and thus have protumorigenesis activity. However, there is also limited evidence that TAMs still play an important role in the killing and destruction of cancer cells, inhibit cancer metastasis, and have antitumor activity. Whether TAMs show protumorigenesis or antitumor activity depends on interaction with cancer cells, other stromal cells, and the tumor microenvironment. Gene expression profiles of TAMs, cancer cells, and other stromal cells are altered by cell-cell interactions. This phenomenon results in positive or negative regulation of angiogenesis, tumor cell proliferation, apoptosis, cancer cell migration and invasion, and the secretion of a variety of cytokines or factors. Whether TAMs have a positive or negative effect also depends on the macrophage activation state, the status of tumor development, and the anatomic locus of macrophage infiltration. Understanding of the mechanisms that regulate TAM function is essential in designing therapies to promote antitumor activity in humans. Although limited evidence from both animal and human studies indicates a potential role for TAMs in cancer treatment, the clinical usefulness of these therapies require further studies.en_US
dc.language.isoen_USzh_TW
dc.relationAdvances in Clinical Chemistryen_US
dc.relation.ispartofseriesAdvances in Clinical Chemistry, Volume 45, Page(s) 199-223.en_US
dc.relation.urihttp://dx.doi.org/10.1016/s0065-2423(07)00008-xen_US
dc.subjectcolony-stimulating factoren_US
dc.subjectcell lung-canceren_US
dc.subjecthuman prostate-canceren_US
dc.subjectendothelial growth-factoren_US
dc.subjectmonocyte-mediated cytotoxicityen_US
dc.subjecturokinase-receptor expressionen_US
dc.subjectinvasive breast-carcinomaen_US
dc.subjectnecrosis-factor-alphaen_US
dc.subjectb kinase-activityen_US
dc.subjectcolorectal-canceren_US
dc.titlePathophysiology of tumor-associated macrophagesen_US
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/s0065-2423(07)00008-xzh_TW
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en_US-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.fulltextno fulltext-
item.cerifentitytypePublications-
Appears in Collections:生物醫學研究所
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