The Chronic Inflammation Hypothesis suggests that persistent inflammation contributes to the development and progression of various chronic diseases, including cancer, diabetes, and cardiovascular disorders.
The Chronic Inflammation Hypothesis
The Chronic Inflammation Hypothesis suggests that persistent inflammation contributes to the development and progression of various chronic diseases, including cancer, diabetes, and cardiovascular disorders.
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Karen Pendergrass
The chronic inflammation model of carcinogenesis posits that sustained exposure to external or internal factors that activate the immune system, along with the presence of persistent immune cells, can lead to damage to the surrounding epithelial cells. This damage may occur through various mechanisms, including releasing reactive oxygen species (ROS) or producing cytokines that stimulate cell proliferation.
In this model, chronic inflammation plays a pivotal role in initiating and promoting the development of cancer. The continuous activation of the immune system can create a microenvironment within the affected tissue that is conducive to the accumulation of genetic mutations and DNA damage. ROS, which are highly reactive molecules, can directly harm DNA, leading to genetic alterations that can drive carcinogenesis.
Furthermore, the pro-inflammatory cytokines produced by immune cells can stimulate the proliferation of damaged or mutated cells, thereby contributing to the expansion of abnormal cell populations. Over time, these changes can increase the likelihood of oncogenic events and the progression towards cancer.
It is important to note that the chronic inflammation model highlights the intricate interplay between the immune system, tissue damage, and genomic instability in the context of cancer development. Understanding these mechanisms is crucial for designing targeted therapeutic interventions and preventive strategies aimed at reducing cancer risk associated with chronic inflammatory conditions.