IMAGE: Bowel of a patient with ulcerative colitis, a chronic inflammatory bowel disease. In green: macrophage marker, in red: activated p38 protein, in blue: nucleus. view more
Credit: Author: Catrin Youssif, IRB Barcelona.
Scientists headed by ICREA researcher Angel R. Nebreda at the Institute for Research in Biomedicine (IRB Barcelona) report a new mechanism that contributes to the development of inflammation-associated colon cancer and points to new therapeutic targets. The study has been published in the journal EMBO Molecular Medicine.
More than a million people worldwide are diagnosed with colon cancer every year. Although many of these cases are spontaneous, chronic inflammation is one of the main causes underlying the development of this disease.
“Our study demonstrates that the capacity of myeloid cells to enhance tumorigenesis is determined by the protein p38. In particular, we have identified an important contribution of the hormone IGF-1, which is activated by p38 in myeloid cells”, explains Nebreda, head of the Cell Sigalling and Cell Cycle lab.
The research has been done using models of acute and chronic inflammation in genetically modified mice or in mice treated with pharmacological inhibitors.
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