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Article summary:

1. Chronic inflammation is strongly linked to the development of colon cancer, and studying the mechanisms by which chronic inflammation promotes colonic tumorigenesis could provide insights into the pathogenesis of sporadic colorectal tumorigenesis.

2. Polyunsaturated fatty acid (PUFA) oxidative metabolism is enzymatically regulated in cells via several groups of enzymes, including lipoxygenases (LOXs), which play a crucial role in regulating inflammation and its resolution.

3. ALOX15 (human 15-lipoxygenase-1; mouse 12/15-lipoxygenase) plays an important role in the formation of key lipid mediators to terminate inflammation, and its downregulation during tumorigenesis likely enhances the link between colitis and colorectal tumorigenesis. ALOX15 also suppresses signaling pathways that promote colitis-associated colonic tumorigenesis, such as TNF-α, IL-1β/NF-κB, and IL-6/STAT3.

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