Abstract
Gastric carcinoma (GC) represents one of the most common and most lethal malignancies worldwide. The histopathological characterization of GC precursor lesions has provided great knowledge about gastric carcinogenesis, with the consequent introduction of effective strategies of primary and secondary prevention. In recent years, a large amount of data about the molecular events in GC development is emerging, flanking the histomorphological descriptions. In this review, we describe the landscape of molecular alterations in gastric pre-invasive lesions with a glance at their potential use in the diagnostic and therapeutic decision-making process.
Highlights
Intestinal-type gastric adenoma differs from gastric dysplasia because of its polypoid nature. It may develop in the context of diffuse atrophic gastritis; its genetic landscape is similar to what has been described for the multistep carcinogenetic process and somewhat analogous to what has been observed in colorectal adenomas
The discovery of the role of Helicobacter pylori (Hp) in Gastric carcinoma (GC) has allowed the medical community to understand the importance of Hp eradication, with great benefits in terms of GC incidence and mortality reduction
It is tempting to say that understanding the molecular landscape of pre-invasive gastric lesions could lead to the milestone discovery in GC prevention
Summary
According to the latest GLOBOCAN analysis [1], gastric cancer (GC) is the fifth most diagnosed carcinoma in both males and females, with more than 1 million new diagnoses in 2018. With about 800,000 deaths in 2018, GC represents the third leading cause of cancer-related death worldwide. Both GC incidence and mortality present substantial differences among countries, with low/middle income areas accounting for more than 70% of cases. GC is a multifactorial disease and both genetic and environmental factors are involved in gastric carcinogenesis. Inherited GC risk factors are best exemplified by hereditary syndromes with mutations in genes involved in molecular pathways of gastric carcinogenesis. Hereditary GCs, related to both cancer susceptibility syndromes and/or other genetic causes, account approximately for 1–3% of cases, and a detailed discussion of these conditions is far beyond the aim of this review [10,11]. GC-related precancerous conditions are chronic atrophic/metaplastic gastritis (AG), pernicious anemia, peptic ulcer disease, previous gastric surgery and Ménétrier’s disease [4,9]
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