Department of Gastroenterology, First Affiliated Hospital of Shantou University Medical College, Shantou, 515041, Guangdong Province, China.
Intern Emerg Med. 2023 Aug;18(5):1303-1316. doi: 10.1007/s11739-023-03281-0. Epub 2023 May 3.
This is a literature review describes Crohn's disease (CD) concomitant with breast cancer and summarizes possible common pathogenic mechanisms shared by the two diseases involving the IL-17 and NF-κB signaling pathways. Inflammatory cytokines including TNF-α and Th17 cells in CD patients can induce activation of the ERK1/2, NF-κB and Bcl-2 pathways. Hub genes are involved in the generation of cancer stem cells (CSCs) and are related to inflammatory mediators, including CXCL8, IL1-β and PTGS2, which promote inflammation and breast cancer growth, metastasis, and development. CD activity is highly associated with altered intestinal microbiota processes, including secretion of complex glucose polysaccharides by Ruminococcus gnavus colonies; furthermore, γ-proteobacteria and Clostridium are associated with CD recurrence and active CD, while Ruminococcaceae, Faecococcus and Vibrio desulfuris are associated with CD remission. Intestinal microbiota disorder promotes breast cancer occurrence and development. Bacteroides fragilis can produce toxins that induce breast epithelial hyperplasia and breast cancer growth and metastasis. Gut microbiota regulation can also improve chemotherapy and immunotherapy efficacy in breast cancer treatment. Intestinal inflammation can affects the brain through the brain-gut axis, which activates the hypothalamic‒pituitary‒adrenal (HPA) axis to induce anxiety and depression in patients; these effects can inhibit the antitumor immune responses of the immune system and promote breast cancer occurrence in patients with CD. There are few studies on the treatment of patients with CD concomitant with breast cancer, but published studies show three main strategies: new biological agents combined with breast cancer treatment methods, intestinal fecal bacteria transplantation, and dietary treatment.
这是一篇文献综述，描述了克罗恩病（CD）与乳腺癌并存，并总结了两种疾病可能存在的共同发病机制，涉及 IL-17 和 NF-κB 信号通路。CD 患者中的炎症细胞因子，包括 TNF-α 和 Th17 细胞，可以诱导 ERK1/2、NF-κB 和 Bcl-2 途径的激活。枢纽基因参与癌症干细胞（CSC）的产生，与炎症介质有关，包括 CXCL8、IL1-β 和 PTGS2，它们促进炎症和乳腺癌的生长、转移和发展。CD 的活动与改变的肠道微生物群过程高度相关，包括 Ruminococcus gnavus 菌落分泌复杂的葡萄糖多糖；此外，γ-变形菌和梭状芽孢杆菌与 CD 的复发和活动性 CD 相关，而 Ruminococcaceae、Faecococcus 和 Vibrio desulfuris 与 CD 的缓解相关。肠道微生物群失调促进乳腺癌的发生和发展。脆弱拟杆菌可以产生毒素，诱导乳腺上皮细胞增生和乳腺癌的生长和转移。肠道微生物群的调节也可以提高乳腺癌治疗中的化疗和免疫治疗效果。肠道炎症可以通过肠-脑轴影响大脑，激活下丘脑-垂体-肾上腺（HPA）轴，导致患者出现焦虑和抑郁；这些影响会抑制免疫系统的抗肿瘤免疫反应，促进 CD 患者乳腺癌的发生。关于同时患有 CD 和乳腺癌的患者的治疗研究较少，但已发表的研究表明有三种主要策略：新型生物制剂联合乳腺癌治疗方法、肠道粪便细菌移植和饮食治疗。
