Abstract
Targeting IL-11 signaling in colon cancer
Highlights
The development of Colorectal cancer (CRC), the fourth most common cause of malignancy worldwide, is driven by the sequential accumulation of genetic changes
Myeloid-cell specific Stat3 ablation triggered the development of enterocolitis, consistent with its identification as a ulcerative colitis (UC) susceptibility locus and molecularly reconciled with the failure for IL-10 to dampen the host’s ensuing immune response
IL-6 has been associated with many epithelial cancers, including those of the gastrointestinal tract, where elevated serum IL-6 often serves as an indicator of poor prognosis, we have recently found that IL-11 acts as a more potent driver for CAC and in mouse models of sporadic CRC [6]
Summary
The development of Colorectal cancer (CRC), the fourth most common cause of malignancy worldwide, is driven by the sequential accumulation of genetic changes. Myeloid and epithelial cell-specific ablation of NF-κB signaling reduced tumor development in CAC-challenged mice [4]. This implied a role for myeloid cell-derived cytokines produced by these sentinels in response to engagement of pathogen recognition receptors.
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