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Verfasst von:Kovaleva, Olga V. [VerfasserIn]   i
 Gratchev, Alexei [VerfasserIn]   i
Titel:Tumor associated macrophages in kidney cancer
Verf.angabe:Olga V. Kovaleva, Daria V. Samoilova, Maria S. Shitova, and Alexei Gratchev
Jahr:2016
Umfang:6 S.
Fussnoten:Gesehen am 22.10.2019
Titel Quelle:Enthalten in: Analytical cellular pathology
Ort Quelle:New York : Hindawi Publishing Corporation, 2010
Jahr Quelle:2016
Band/Heft Quelle:(2016) Artikel-Nummer 9307549, 6 Seiten
ISSN Quelle:2210-7185
Abstract:Tumor associated macrophages (TAMs) are an important element of tumor stroma. They originate from blood monocytes attracted by chemokines and cytokines produced by tumor cells and, being instructed by tumor microenvironment, develop into potent tumor-supporting cell population. TAMs were demonstrated to directly stimulate tumor cell proliferation and to promote angiogenesis. Further TAMs provide for efficient immune escape by producing immunosuppressive cytokines and facilitate tumor dissemination by producing extracellular matrix remodeling enzymes. In renal cell carcinoma (RCC), numerous studies were performed for elucidation of the role of TAM in tumor progression. Using pan-macrophages marker CD68 and type 2 macrophage (M2) markers CD163 and CD206, it was demonstrated that increased density of TAMs is associated with poor survival of patients. Although most of the studies are focused on M2 population in RCC, several markers rather typical for type 1 macrophages (M1) were also characterized. Macrophages isolated from RCC tumors were shown to produce proinflammatory cytokines TNF, IL-, IL-6, and CCL2. It can be concluded that RCC is an excellent example of a tumor with hybrid phenotype of TAMs that share both M1 and M2 properties. Moreover, TAMs seem to be an attractive therapeutic target as well. Further investigations are needed for identification of RCC-specific TAM markers with high predictive capacity and/or suitable for therapeutic targeting.
DOI:doi:10.1155/2016/9307549
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1155/2016/9307549
 Verlag: https://www.hindawi.com/journals/acp/2016/9307549/
 DOI: https://doi.org/10.1155/2016/9307549
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1679361775
Verknüpfungen:→ Zeitschrift

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