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Review
. 2016 Jan 21;22(3):1160-71.
doi: 10.3748/wjg.v22.i3.1160.

Personalized medicine in gastric cancer: Where are we and where are we going?

Alexandre A Jácome  1 , Anelisa K Coutinho  1 , Enaldo M Lima  1 , Aline C Andrade  1 , José Sebastião Dos Santos  1
Affiliations
Review

Personalized medicine in gastric cancer: Where are we and where are we going?

Alexandre A Jácome et al. World J Gastroenterol. .

Abstract

Despite improvements in adjuvant therapies for gastric cancer in recent years, the disease is characterized by high recurrence rates and a dismal prognosis. The major improvement in the treatment of recurrent or metastatic gastric cancer in recent years has been the incorporation of trastuzumab, a monoclonal antibody that inhibits human epidermal growth factor receptor 2 (HER2) heterodimerization, after the demonstrated predictive value of the overexpression and/or amplification of this receptor. Beyond HER2, other genetic abnormalities have been identified, and these mutations may be targetable by tyrosine kinase inhibitors or monoclonal antibodies. The demonstration of four distinct molecular subtypes of gastric cancer by the Cancer Genome Atlas study highlight the enormous heterogeneity of the disease and its complex interplay between genetic and epigenetic alterations and provide a roadmap to implement genome-guided personalized therapy in gastric cancer. In the present review, we aim to discuss, from a clinical point of view, the genomic landscape of gastric cancer described in recent studies, the therapeutic insights derived from these findings, and the clinical trials that have been conducted and those in progress that take into account tailored therapies for gastric cancer.

Keywords: Biological markers; Individualized medicine; Molecular targeted therapy; Stomach neoplasms; Transcriptome.

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Figures

Figure 1
Figure 1
Proportion of genetic abnormalities in gastric cancer. PIK3CA/AKT: Phosphatidylinositol 3-kinase CA/AKT; HER2: Human epidermal growth factor receptor 2; HER3: Human epidermal growth factor receptor 3; FGFR2: Fibroblast growth factor receptor 2; KRAS: Kirsten rat sarcoma oncogene; MET: Mesenchymal-epithelial transition; JAK2: Janus kinase 2; PD-1/PD-L1: Programmed cell death-1/ Programmed cell death-ligand 1.
Figure 2
Figure 2
Proportion of genetic abnormalities in distinct gastric cancer subtypes. EBV: Epstein-Barr-positive; MSI: Microsatellite-instability; GS: Genomically stable; CIN: Chromosomal instability; PIK3CA/AKT: Phosphatidylinositol 3-kinase CA/AKT; HER2: Human epidermal growth factor receptor 2; HER3: Human epidermal growth factor receptor 3; FGFR2: Fibroblast growth factor receptor 2; KRAS: Kirsten rat sarcoma oncogene; MET: Mesenchymal-epithelial transition; JAK2: Janus kinase 2; PD-1/PD-L1: Programmed cell death-1/programmed cell death-ligand 1.
See this image and copyright information in PMC

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