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Tumor promotion by tumor-associated macrophages.
- Source :
-
Advances in experimental medicine and biology [Adv Exp Med Biol] 2007; Vol. 604, pp. 67-86. - Publication Year :
- 2007
-
Abstract
- Recent years have seen a renaissance of the inflammation-cancer connection stemming from different lines of work and leading to a generally accepted paradigm (Balkwill and Mantovani 2001; Mantovani et al. 2002; Coussens and Werb 2002; Balkwill et al. 2005). An inflammatory component is present in the microenvironment of most neoplastic tissues, including those not causally related to an obvious inflammatory process Cancer-associated inflammation includes: the infiltration of white blood cells, prominently phagocytic cells called macrophages (TAM) (Paik et al. 2004); the presence of polipeptide messengers of inflammation (cytokines such as tumor necrosis factor (TNF) or interleukin-1 (IL-1), chemokines such as CCL2); the occurrence of tissue remodelling and angiogenesis. Chemokines have emerged as a key component of the tumor microenvironment which shape leukocyte recruitment and function (Pollard 2004). Strong direct evidence suggests that cancer associated inflammation promotes tumor growth and progression. Therapeutic targeting of cancer promoting inflammatory reactions is in its infancy, and its development is crucially dependent on defining the underlying cellular and molecular mechanisms in relevant systems.
- Subjects :
- Animals
Chemokine CCL2 metabolism
Chemokines metabolism
Cytokines metabolism
Disease Progression
Humans
Inflammation
Interleukin-1 metabolism
Macrophage Activation
Models, Biological
Neoplasms immunology
Neoplasms pathology
Phagocytosis
Tumor Necrosis Factor-alpha metabolism
Macrophages metabolism
Neoplasms metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0065-2598
- Volume :
- 604
- Database :
- MEDLINE
- Journal :
- Advances in experimental medicine and biology
- Publication Type :
- Academic Journal
- Accession number :
- 17695721
- Full Text :
- https://doi.org/10.1007/978-0-387-69116-9_5