ABSTRACT
Introduction
Gastric cancer (GC) is the fifth most common malignancy in the world and accounts for 7.7% of all cancer-related deaths. Early diagnosis of GC is critical in terms of prognosis, and aberrations at the molecular level, especially epigenetic alterations, manifest much earlier than histological findings. In recent years, there has been a great deal of research on the epigenomic profile of GC, and epigenetic alterations seem to play a more important role than genetic factors. With the introduction of epigenetic drugs into clinical use in the last decade, the importance of the epigenetic background of GC has increased considerably.
Areas Covered
In this review, we summarize the role of methylation changes, histone modifications, and non-coding RNAs in the pathogenesis of GC and how these signatures can be used as diagnostic and therapeutic targets in clinical management.
Expert Opinion
Epigenetic alterations take place before most genetic aberrations observed in GC and may have an initiating role in the pathogenesis of GC. They can be used as biomarkers in risk calculation, early diagnosis, and evaluation of prognosis of GC, as well as treatment targets.
Article highlights
Gastric cancer (GC) is the fifth most common malignancy in the world and accounts for 7.7% of all cancer-related deaths.
Early diagnosis of GC is critical for the surgical option and the discovery of molecular markers that can be used for this purpose has accelerated in recent years.
Epigenetic alterations occur in excessive amounts and more frequently than genetic aberrations in GC.
Some epigenetic alterations are observed even before the GC can be detected histopathologically.
Specific epigenetic alterations are highly unique to different pathological and molecular classes of GC.
These epigenetic markers can be used as targets in the early diagnosis and treatment of GC.
Declaration of interest
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
Reviewers disclosure
Peer reviewers on this manuscript have no relevant financial relationships or otherwise to disclose.
Availability of supporting data
All data needed to evaluate the conclusions in the paper are present in the paper.