Dicarbonyl Electrophiles Mediate Inflammation-Induced Gastrointestinal Carcinogenesis

Inflammation and stem cells in gastrointestinal carcinogenesis.

Chronic inflammation-induced carcinogenesis is a commonly accepted entity and is frequently seen within the gastrointestinal tract, although the underlying mechanisms remain unclear. Alterations in specific oncogenes and tumor suppressor genes are known to be responsible for malignant transformation. Nevertheless, the inflammatory microenvironment classically affects tumor promotion in its role...

Link between chronic inflammation and human papillomavirus-induced carcinogenesis (Review)

Inflammation is a defense strategy against invading agents and harmful molecules that is activated immediately following a stimulus, and involves the release of cytokines and chemokines, which activate the innate immune response. These mediators act together to increase blood flow and vascular permeability, facilitating recruitment of effector cells to the site of injury. Following resolution o...

Inflammation and Carcinogenesis

We consider that inflammatory substances play an important role in the carcinogenesis process. In the process, cytokines and growth factor secreted by cells can actively recruit immune cells in the carcinogenesis microenvironment, further, promote carcinogenesis progression. The carcinogenesis microenvironment even subverted the immune system, moreover, enhanced the carcinogenesis through immun...

Inflammation-Induced Fetal Demise in Uterine NK Cells Mediate

Does endoplasmic reticulum stress mediate endothelin-1-induced renal inflammation?

Endothelin-1 (ET-1) is the most potent vasoconstrictor peptide known. It exerts its actions through two pharmacologically different receptors: ETA and ETB receptors. In the renal vasculature, there is a majority of ETB receptors in the efferent arteriole, whereas a greater amount of ETA receptors are located in the afferent arteriole. The nephron is rich in ETB receptors, especially in the thic...