Por favor, use este identificador para citar o enlazar este Item:http://hdl.handle.net/20.500.12105/6594
Título
Macrophages, inflammation, and tumor suppressors: ARF, a new player in the game
Autor(es)
Fecha de publicación
2012
Cita
Mediators Inflamm. 2012; Article ID:568783.
Idioma
Inglés
Tipo de documento
journal article
Resumen
The interaction between tumor progression and innate immune system has been well established in the last years. Indeed, several lines of clinical evidence indicate that immune cells such as tumor-associated macrophages (TAMs) interact with tumor cells, favoring growth, angiogenesis, and metastasis of a variety of cancers. In most tumors, TAMs show properties of an alternative polarization phenotype (M2) characterized by the expression of a series of chemokines, cytokines, and proteases that promote immunosuppression, tumor proliferation, and spreading of the cancer cells. Tumor suppressor genes have been traditionally linked to the regulation of cancer progression; however, a growing body of evidence indicates that these genes also play essential roles in the regulation of innate immunity pathways through molecular mechanisms that are still poorly understood. In this paper, we provide an overview of the immunobiology of TAMs as well as what is known about tumor suppressors in the context of immune responses. Recent advances regarding the role of the tumor suppressor ARF as a regulator of inflammation and macrophage polarization are also reviewed.
MESH
Animals | Cyclin-Dependent Kinase Inhibitor p16 | Humans | Immune Tolerance | Inflammation Mediators | Macrophages | Neoplasms | Neovascularization, Pathologic | Tumor Microenvironment | Tumor Suppressor Protein p14ARF | Tumor Suppressor Proteins
Versión en línea
DOI
Aparece en las colecciones