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Macrophages Instruct Aberrant Glycosylation in Colon Cancer by Chemokine and Cytokine Signals

机译:巨噬细胞通过趋化因子和细胞因子信号指示结肠癌中的异常糖基化

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摘要

Myeloid cells can alter diverse molecular and metabolic pathways in cancer cells, contributing to their survival, migration, and resistance to chemotherapy and immune attack. The results by Kvorjak and colleagues unveil a novel circuit whereby altered glycosylation in epithelial cells promotes the pathogenesis of ulcerative colitis and colitisassociated colon cancer, via the production of IL13 and CCL17 by M2-polarized macrophages.
机译:骨髓细胞可以改变癌细胞中不同的分子和代谢途径,有助于它们的存活,迁移和抗化疗和免疫发作。 Kvorjak和同事的结果揭示了一种新的电路,由此通过M2-偏振巨噬细胞的产生IL13和CCl17,上皮细胞中糖溶解和结肠炎和结肠炎的发病机制。

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