Non-specific inflammatory bowel disease and the risk of tumour growth

Abstract

Inflammatory bowel disease (IBD), which mainly includes ulcerative colitis (UC) and Crohn’s disease (Lesniowski-Crohn’s, ChL-C, CD), is a chronic and recurrent inflammatory condition of the gastrointestinal tract with multifactorial causes. Both types of IBD are characterized by chronic inflammation with periods of remission and exacerbation. An increasing number of studies have recently shown that chronic inflammation plays an important role in the carcinogenesis of colorectal cancer (CRC), generating suitable microenvironments for the formation and progression of the disease. The main factors are chronic inflammation and the scope and duration of the disease. The pro-inflammatory interleukins IL-13, IL-8 and TNF-α play an important role in tumorigenesis. It is further emphasized that reactive oxygen species (ROS) and reactive nitrogen species produced by inflammatory cells may interact with key genes involved in carcinogenic pathways such as TP53. Carcinogenesis in IBD involves proteins determined by the genes DLG5, OCTN and NOD2. Immunosuppressive drugs such as thiopurines and methotrexate may play a role in extra-intestinal tumour development by impairing the immune system and surveillance of tumour cells or by inducing DNA damage. Recognition of neoplastic changes associated with IBD is difficult due to the heterogeneity of the endoscopic image and variation in the diagnosis depending on the observer. Therefore surveillance of IBD patients by a multidisciplinary team is essential for early detection of the neoplastic process.