A plethora of experimental and epidemiological evidence supports a critical role for inflammation and adaptive immunity in the onset of cancer and in shaping its response to therapy. These data are particularly robust for gastrointestinal (GI) cancers, such as those affecting the GI tract, liver, and pancreas, on which this review is focused. We propose a unifying hypothesis according to which intestinal barrier disruption is the origin of tumor-promoting inflammation that acts in conjunction with tissue-specific cancer-initiating mutations. The gut microbiota and its products impact tissue-resident and recruited myeloid cells that promote tumorigenesis through secretion of growth- and survival-promoting cytokines that act on epithelial cells, as well as fibrogenic and immunosuppressive cytokines that interfere with the proper function of adaptive antitumor immunity. Understanding these relationships should improve our ability to prevent cancer development and stimulate the immune system to eliminate existing malignancies.

中文翻译：

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仁慈残忍：胃肠癌中的上皮细胞、微生物和免疫细胞相互作用。

大量的实验和流行病学证据支持炎症和适应性免疫在癌症发作和塑造其对治疗的反应中的关键作用。这些数据对于胃肠道 (GI) 癌症尤其可靠，例如影响胃肠道、肝脏和胰腺的癌症，本综述重点关注这些癌症。我们提出了一个统一的假设，根据该假设，肠道屏障破坏是促肿瘤炎症的起源，它与组织特异性癌症起始突变一起起作用。肠道微生物群及其产物影响组织驻留和募集的骨髓细胞，这些细胞通过分泌作用于上皮细胞的生长和存活促进细胞因子来促进肿瘤发生，以及干扰适应性抗肿瘤免疫正常功能的纤维化和免疫抑制细胞因子。了解这些关系应该可以提高我们预防癌症发展和刺激免疫系统消除现有恶性肿瘤的能力。