Pierce Ellen S
Spokane Valley, Washington, USA.
Infect Agent Cancer. 2018 Jan 4;13:1. doi: 10.1186/s13027-017-0172-3. eCollection 2018.
Infectious agents are known causes of human cancers. and cause a percentage of colorectal cancers in countries where the respective species are prevalent. Colorectal cancer is a complication of ulcerative colitis and colonic Crohn's disease, the two main forms of idiopathic inflammatory bowel disease (IIBD). subspecies (MAP), the cause of a chronic intestinal disease in domestic and wild ruminants, is one suspected cause of IIBD. MAP may therefore be involved in the pathogenesis of IIBD-associated colorectal cancer as well as colorectal cancer in individuals without IIBD (sporadic colorectal cancer) in countries where MAP infection of domestic livestock is prevalent and MAP's presence in soil and water is extensive. MAP organisms have been identified in the intestines of patients with sporadic colorectal cancer and IIBD when high magnification, oil immersion light microscopy (×1000 total magnification rather than the usual ×400 total magnification) is used. Research has demonstrated MAP's ability to invade intestinal goblet cells and cause acute and chronic goblet cell hyperplasia. Goblet cell hyperplasia is the little-recognized initial pathologic lesion of sporadic colorectal cancer, referred to as transitional mucosa, aberrant crypt foci, goblet cell hyperplastic polyps or transitional polyps. It is the even lesser-recognized initial pathologic feature of IIBD, referred to as hypermucinous mucosa, hyperplastic-like mucosal change, serrated epithelial changes, flat serrated changes, goblet cell rich mucosa or epithelial hyperplasia. Goblet cell hyperplasia is the precursor lesion of adenomas and dysplasia in the classical colorectal cancer pathway, of sessile serrated adenomas and serrated dysplasia in the serrated colorectal cancer pathway, and of flat and elevated dysplasia and dysplasia-associated lesions or masses in IIBD-associated intestinal cancers. MAP's invasion of intestinal goblet cells may result in the initial pathologic lesion of IIBD and sporadic colorectal cancer. MAP's persistence in infected intestines may result in the eventual development of both IIBD-associated and sporadic colorectal cancer.
感染因子是人类癌症的已知病因,在相应物种流行的国家中,会导致一定比例的结直肠癌。结直肠癌是溃疡性结肠炎和结肠克罗恩病(特发性炎症性肠病(IIBD)的两种主要形式)的并发症。副结核分枝杆菌(MAP)是家养和野生反刍动物慢性肠道疾病的病因,是IIBD的一个疑似病因。因此,在国内家畜感染MAP普遍且土壤和水中MAP广泛存在的国家,MAP可能参与IIBD相关结直肠癌以及无IIBD个体(散发性结直肠癌)的发病机制。当使用高倍油浸光学显微镜(总放大倍数为×1000,而不是通常的×400)时,已在散发性结直肠癌和IIBD患者的肠道中鉴定出MAP微生物。研究表明,MAP有能力侵入肠道杯状细胞并导致急性和慢性杯状细胞增生。杯状细胞增生是散发性结直肠癌鲜为人知的初始病理病变,称为移行黏膜、异常隐窝灶、杯状细胞增生性息肉或移行息肉。它也是IIBD鲜为人知的初始病理特征,称为高黏液性黏膜、增生样黏膜改变、锯齿状上皮改变、扁平锯齿状改变、富含杯状细胞的黏膜或上皮增生。杯状细胞增生是经典结直肠癌途径中腺瘤和发育异常的前体病变,是锯齿状结直肠癌途径中无蒂锯齿状腺瘤和锯齿状发育异常的前体病变,也是IIBD相关肠道癌中扁平及隆起性发育异常和发育异常相关病变或肿块的前体病变。MAP侵入肠道杯状细胞可能导致IIBD和散发性结直肠癌的初始病理病变。MAP在受感染肠道中的持续存在可能导致IIBD相关和散发性结直肠癌的最终发展。