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Gastric cancer (GC) is one of the leading types of cancer worldwide, particularly in East Asian populations. Helicobacter pylori (HP) infection has been established as a major risk factor for GC. Although more than 50% of the world population is infected with this bacterium, less than 2% develop GC. Therefore, further risk factors (such as host genetic polymorphisms and lifestyle, as well as environmental and epigenetic factors) may also play a role in its occurrence. The correlation between HP infection and GC represents a typical model of a multi‑step process, characterized by some pre-neoplastic lesions with a high risk of progression (atrophic gastritis, intestinal metaplasia and dysplasia). In addition, HP also plays an oncogenic role in the development of mucosa‑associated lymphoid tissue (MALT) lymphoma, that accounts for approximately 3% of all gastric tumors. Hyperplastic polyps often arise in patients with atrophic gastric mucosa and HP‑associated gastritis (25% of cases); however, their malignant transformation is rare (<3% of cases). A number of trials have demonstrated the possibility of cancer prevention through HP screening and eradication, particularly in high‑risk populations, whereas it may not be cost‑effective in areas of low risk. In this review, we discuss i) the complex pathogenetic mechanisms of gastric carcinogenesis in which HP is involved; ii) the main approaches to the diagnosis, prevention, surveillance and treatment of pre-malignant lesions associated with HP infection; iii) the most effective way to detect GC in its earlier stages; and iv) the most important contribution to reducing the burden of GC.

ABSTRACT

Colorectal cancer (CRC) is a common and often lethal tumor. Over the last 25 years, remarkable progress has been made in understanding its biological and molecular features and in elucidating the steps involved in colon carcinogenesis. This, in turn, has led to a more rational and effective clinical approach to the treatment of CRC. While colorectal adenoma is the most frequent precancerous lesion, other potentially premalignant conditions, including chronic inflammatory bowel diseases and hereditary syndromes, such as familial adenomatous polyposis, Peutz-Jeghers syndrome and juvenile polyposis, involve different sites of the gastrointestinal tract with an overall incidence of less than 5%. In all such cases, disease recognition at an early stage is essential to devise suitable preventive cancer strategies. These topics are addressed in this review, along with the most important epidemiological, pathogenetic and clinical features that lead to malignant transformation. Novel biomarkers for early cancer prediction, detection, prognostic evolution, and the response to treatment are critically assessed as well. Continued improvements in our knowledge of the molecular basis of CRC and the transfer of this information into daily clinical practice will reduce the burden of this disease.

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