Molecular classification and prediction in gastric cancer

Abstract

Gastric cancer, a highly heterogeneous disease, is the second leading cause of cancer death and the fourth most common cancer globally, with East Asia accounting for more than half of cases annually. Alongside TNM staging, gastric cancer clinic has two well-recognized classification systems, the Lauren classification that subdivides gastric adenocarcinoma into intestinal and diffuse types and the alternative World Health Organization system that divides gastric cancer into papillary, tubular, mucinous (colloid), and poorly cohesive carcinomas. Both classification systems enable a better understanding of the histogenesis and the biology of gastric cancer yet have a limited clinical utility in guiding patient therapy due to the molecular heterogeneity of gastric cancer. Unprecedented whole-genome-scale data have been catalyzing and advancing the molecular subtyping approach. Here we cataloged and compared those published gene expression profiling signatures in gastric cancer. We summarized recent integrated genomic characterization of gastric cancer based on additional data of somatic mutation, chromosomal instability, EBV virus infection, and DNA methylation. We identified the consensus patterns across these signatures and identified the underlying molecular pathways and biological functions. The identification of molecular subtyping of gastric adenocarcinoma and the development of integrated genomics approaches for clinical applications such as prediction of clinical intervening emerge as an essential phase toward personalized medicine in treating gastric cancer.

QKI5-mediated alternative splicing of the histone variant macroH2A1 regulates gastric carcinogenesis

“…In spite of the progress in chemotherapy, radiotherapy, and surgical techniques for GC in recent years, the survival rate of GC patients remains unsatisfactory [36–38]. Although many oncogenes or tumor suppressors have been identified as key regulators in GC tumorigenesis, almost no commonly accepted biomarkers or therapy targets have been established to facilitate the comprehensive management of patients [39, 40]. Therefore, the identification of the novel regulators for GC and a detailed understanding of the molecular mechanisms underlying gastric carcinogenesis will be of great importance to help our understanding of GC.…”

TGR5, Not Only a Metabolic Regulator

“…Gastric carcinogenesis is a complex process and easily causes death (Lin et al, 2015). There are few reports about TGR5 and cancer.…”

Chromoendoscopy in combination with random biopsies does not improve detection of gastric cancer foci in CDH1 mutation positive patients

“…In this context, sensitive identification of foci that are beginning to progress or which display specific gene expression signatures 32 33 34 35 36 37 suggesting a high likelihood of progression would be of great diagnostic benefit. Future studies are needed to clarify whether novel endoscopic methods such as confocal endomicroscopy 38 in combination with molecular analysis of targeted biopsies 39 may be helpful to achieve this goal.…”