The prognostication of colorectal cancer (CRC) has traditionally relied on staging as defined by the Union for International Cancer Control (UICC) and American Joint Committee on Cancer (AJCC) TNM staging classifications. However, clinically, there appears to be differences in survival patterns independent of stage, suggesting a complex interaction of stage, pathological features, and biomarkers playing a role in guiding prognosis, risk stratification, and guiding neoadjuvant and adjuvant therapies. Histological features such as tumour budding, perineural invasion, apical lymph node involvement, lymph node yield, lymph node ratio, and molecular features such as MSI, KRAS, BRAF, and CDX2 may assist in prognostication and optimising adjuvant treatment. This study provides a comprehensive review of the pathological features and biomarkers that are important in the prognostication and treatment of CRC. We review the importance of pathological features and biomarkers that may be important in colorectal cancer based on the current evidence in the literature.

Helicobacter pylori is a class one carcinogen which causes chronic atrophic gastritis, gastric intestinal metaplasia, dysplasia and adenocarcinoma. The mechanisms by which H. pylori interacts with other risk and protective factors, particularly vitamin C in gastric carcinogenesis are complex. Gastric carcinogenesis includes metabolic, environmental, epigenetic, genomic, infective, inflammatory and oncogenic pathways. The molecular classification of gastric cancer subtypes has revolutionized the understanding of gastric carcinogenesis. This includes the tumour microenvironment, germline mutations, and the role of Helicobacter pylori bacteria, Epstein Barr virus and epigenetics in somatic mutations. There is evidence that ascorbic acid, phytochemicals and endogenous antioxidant systems can modify the risk of gastric cancer. Gastric juice ascorbate levels depend on dietary intake of ascorbic acid but can also be decreased by H. pylori infection, H. pylori CagA secretion, tobacco smoking, achlorhydria and chronic atrophic gastritis. Ascorbic acid may be protective against gastric cancer by its antioxidant effect in gastric cytoprotection, regenerating active vitamin E and glutathione, inhibiting endogenous N-nitrosation, reducing toxic effects of ingested nitrosodimethylamines and heterocyclic amines, and preventing H. pylori infection. The effectiveness of such cytoprotection is related to H. pylori strain virulence, particularly CagA expression. The role of vitamin C in epigenetic reprogramming in gastric cancer is still evolving. Other factors in conjunction with vitamin C also play a role in gastric carcinogenesis. Eradication of H. pylori may lead to recovery of vitamin C secretion by gastric epithelium and enable regression of premalignant gastric lesions, thereby interrupting the Correa cascade of gastric carcinogenesis.

There has been a resurgence of interest in the use of mechanical bowel preparation (MBP) and oral antibiotics (OAB) before elective colorectal surgery (CRS). This is a current and controversial topic, not owing to a lack of high-quality evidence but because studies on this topic have reported a diverse range of outcomes.

Colorectal cancer is the third most common cancer, with nearly 2 million cases worldwide and just under 1 million deaths in 2020. Several trials have demonstrated that aspirin has the potential to reduce the incidence and/or recurrence of colorectal cancer; however, the optimal aspirin dose is unclear. Relevant studies were identified by searching MEDLINE, Embase and the Cochrane Library from database inception to 2 February 2022. Data from RCTs in which the incidence of colorectal cancer in patients without active colorectal cancer assigned to aspirin versus control were included. Two investigators independently identified studies and abstracted data. Study quality was assessed using Cochrane Collaboration risk-of-bias 2 tool. The study was performed according to PRISMA guidelines. Aspirin dose was stratified into low (50–163 mg/day), mid (164–325 mg/day), and high (500–1200 mg/day). Thirteen articles representing 11 RCTs (92 550 participants) were included, with studies assessing aspirin as primary prophylaxis in general or high-risk populations, and as secondary prophylaxis for metachronous colorectal cancer. There was a statistically significant reduction in colorectal cancer incidence in the high-dose aspirin group compared with the group that received no aspirin or placebo (OR 0.69, 95 per cent credible interval 0.50 to 0.96; surface under the cumulative ranking 0.82). There was no statistically significant difference between mid- and low-dose aspirin versus no aspirin/placebo. In this network meta-analysis of RCTs, high-dose aspirin was associated with a reduction in colorectal cancer incidence. However, this was based on a limited number of trials. This study did not show a statistically significant risk reduction in colorectal cancer incidence with mid- or low-dose aspirin.