CANCER-RELATED INFLAMMATION

Cancer-Related Inflammation

CANCER-RELATED INFLAMMATION

Introduction

Inflammation activates the innate immune systems, but can also induce adverse effects in the host. Acute inflammation is the natural defense system that activates the mechanisms of acquired immunity, however, when inflammation becomes chronic is associated with increased risk of many diseases, including cancer, diabetes, lung disease and cardiovascular disease and neurological. While under normal conditions is a self-limited, persistent inflammatory stimulus or an imbalance between proinflammatory and anti-inflammatory mechanisms may participate in the chronicity. In chronic inflammation undertake the production of inflammatory mediators and the elimination of cells involved in the process. (Jack, 2008, 213-218)

Acute inflammation is a series of events, usually sequential. Firstly, there is recruitment of polymorphonuclear cells and then infiltration of the inflamed region with monocytes, which in tissue macrophages become local. During acute inflammation, cells release large amounts of inflammatory mediators, including cytokines, eicosanoids and proteases, which are associated with increased cell recruitment and cell activation. The activation of genes involved usually due to the presence of the NFKB transcription factor, a factor that is activated in many tumors. (Serrano, 2008, 33-44)

The increased risk of developing cancer in chronic inflammatory conditions is well characterized. And ulcerative colitis, associated with the occurrence of colon adenocarcinomas, is treated with anti-inflammatory drugs. An animal model of mice whose gene has been invalidated IKKß helped to highlight the contribution of the pathway NF-kB in carcinogenesis. The inflammatory response is exacerbated in animals-IKKß and is associated with apoptosis increased. NF-kBis activated by inflammatory cytokines and is responsible for anti-apoptotic signals. (Carol, 2007, pp. 270)

To separate the two functions, animals with a deficiency of IKKß in myeloid lineage only / monocyte were generated. Reduced incidence of cancers has been observed, correlated with a decrease in intestinal proliferation. In conclusion, NF-kB promotes intestinal carcinogenesis in two ways:  Protection of apoptosis in response to inflammation  stimulation of intestinal proliferation in response to cytokines produced by macrophages.

Numerous indications suggest a connection between chronic inflammation and cancer, for example, inflammation or persistent infection can cause DNA damage. For its part, tumor cells can produce pro-inflammatory factors that stimulate inflammation chronic. (Mikkelsen, 2009, 1600-11)

Although the mechanisms that trigger inflammation are known quite accurately, much less is known about those involved in the resolution of the process. Even so, there is evidence that certain cytokines, including interleukin (IL) -10 and transforming growth factor beta, the lipotoxinas and prostaglandins are crucial as they are involved in apoptosis of leukocytes and the elimination of activated tissue macrophages. The migration of antigen presenting cells is an essential step for activation of T and B lymphocytes in lymph nodes. Myelopoiesis and hematopoiesis may be committed during inflammation. In the progression of certain tumors is found a high number of myeloid suppressor cells that inhibit normal anti-tumor immune mechanisms. (McKay, 2009, 4-6)

Discussion And Analysis

This neoplasia occurs spontaneously in BALB / c, tumor progression is associated with various paraneoplastic symptoms similar to those seen in humans with non-small cell lung adenocarcinomas, and the most common are leukocytosis, hypercalcemia and cachexia. The cell line derived from this tumor-LP07-has the same features as the primary tumor cells which secrete IL-6, colony stimulating factor and granulocyte macrophage-related protein ...