The Complex Network between Inflammation and Colorectal Cancer: A Systematic Review of the Literature

SIMPLE SUMMARY: Colorectal cancer is one of the most diffuse malignant pathologies, and many factors are involved in its genesis. Among these factors, inflammation plays an important role. Many molecules are involved in inflammation processes and are linked in different pathways, either in the sense of pro-tumorigenesis or anti-tumorigenic action. This review was conducted with the aim to review in a single paper the majority of actual knowledge in the literature and to comprehend inflammation patterns for better clinical and surgical management of patients. ABSTRACT: Background: colorectal cancer (CRC) has a multifactorial etiology which comprises microbiota, genetic predisposition, diet, environmental factors, and last but not least, a substantial contribution by inflammation. The aim of this study is to conduct a systematic review of the literature regarding the strong link between inflammation and colorectal cancer. Methods: A systematic review of the literature on PubMed (Medline), Scopus, Cochrane and EMBase databases was performed, following the PRISMA 2020 guidelines. Each paper was reviewed by two groups of researchers in a single-blind format by using a pre-planned Microsoft(©) Excel(®) grid. Results: Using automated research filters, 14,566 studies were included, but 1% was found significant by the reviewers. Seventy pathways of inflammation were described in the sequence of inflammation-carcinogenesis, and anti-tumorigenic molecules were also found. Conclusion: several studies suggest a strong role of inflammation in the tumorigenesis of colorectal cancer through different pathways: this may have a diagnostic and clinical role and also therapeutic purpose in preventing carcinogenesis by treating inflammation. In vitro tests support this theory, even if many other clinical trials are necessary. The present paper was registered in the OpenScience Framework registry (Identifier: DOI 10.17605/OSF.IO/2KG7T).