Its expression corresponded to B lymphocyte, T lymphocyte, and macrophage infiltration, and was found to correlate with the overall presence of inflammatory cell components ( 16). MIP-1β expression was also higher in high-grade breast carcinomas compared to low-grade tumors.
#Brain out lv 73 Activator
Surprisingly, the expression level of IL-8, an important regulator of neutrophil activation and chemotaxis, and an activator of NF-kB, negatively corresponded with estrogen receptor status the mediator was also more abundant in high-grade tumors than low-grade tumors, and was increased in tumors that exhibited high macrophage content and increased vascularization. In a study conducted by Chavey et al, a number of cytokines, including IL-6, IL-8, G-CSF (granulocyte colony stimulating factor), IFN-γ (interferon-γ), and MIP-1β (macrophage inflammatory protein- 1β), were found to be more abundant in breast carcinoma than in normal breast tissue ( 16). These molecular mediators and their respective receptors have a significant impact on angiogenesis, cell migration, and metastasis ( 14, 15). For example, numerous cancer cells express cytokines and chemokines and their receptors. As a tumor develops, it expresses phenotypes similar to inflammatory cells ( 13). There is extensive data demonstrating that inflammation plays a role in the establishment, progression, and/or aggressiveness of various malignancies. Thus, inflammation may provide both the key mutations and the proper environment to foster tumor growth. Together, these processes provide a favorable microenvironment for the exponential growth of malignant cells. During chronic inflammation, pro-inflammatory molecules, such as cytokines, inducible nitric oxide synthase (iNOS), reactive oxygen species (ROS), and NF-kB are upregulated ( 12). All of these processes have been implicated in the initiation and progression of cancers. Increased genomic damage, increased DNA synthesis, cellular proliferation, disruption of DNA repair pathways, inhibition of apoptosis, and the promotion of angiogenesis and invasion are also associated with chronic inflammation ( 11). That inflammation may lead to the initiation of cancer is reasonable considering that chronic inflammation is characterized by infiltration of mononuclear immune cells (including macrophages, lymphocytes, and plasma cells), tissue destruction, fibrosis, and increased angiogenesis ( 9, 10). Thus, the presence of inflammation appears to induce or facilitate carcinogenesis. Exemplary studies have indicated that there is an approximately 14% increase in prostate cancer risk due to prostatitis (( 1- 3), a 25% increase in colorectal cancer risk due to ulcerative colitis ( 4, 5), and a 10-20-fold increase in the risk of pancreatic cancer for patients who have experienced pancreatitis ( 6- 8). It has long been recognized that infections and inflammation are related to cancer, and strong correlations between the presence of inflammation and the development of pre-cancerous lesions at various anatomic sites have been established.