Published online Apr 15, 2021. doi: 10.4251/wjgo.v13.i4.265
Peer-review started: December 23, 2020
First decision: February 14, 2021
Revised: February 16, 2021
Accepted: March 22, 2021
Article in press: March 22, 2021
Published online: April 15, 2021
Remnant gastric cancer (RGC) is defined as a carcinoma arising in the stomach remnant after a previous gastrectomy. Despite the improvement in diagnosis and treatment, difficulties in predicting the prognosis and the best therapeutic approach in RGC patients are still challenges in clinical practice.
New classifications based on molecular subtypes have provided a promising prognostic tool and facilitate the development of targeted agents in clinical trials. However, gastric cancer (GC) profiles and the distribution of molecular subtypes have not been evaluated for RGC.
This study aimed to evaluate RGC according to molecular subtypes and determine whether the expression profile is different between RGC and primary GC (PGC).
RGC patients who underwent gastrectomy between 2009 and 2019 were assessed using a panel of immunohistochemistry (IHC) and in situ hybridization (ISH): Epstein-Barr virus (EBV) ISH, IHC for mismatch repair proteins (MutL homolog 1, MutS homolog 2, MutS homolog 6, and PMS1 homolog 2), p53 protein, and E-cadherin expression.
A total of 40 RGC patients were included, and 284 PGC served as a comparison group. EBV-positive tumors were higher in RGC compared to PGC (P = 0.039). The frequency of microsatellite instability, aberrant p53 immunostaining, and loss of E-cadherin expression were similar between RGC and PGC. Higher rates of simultaneous changes in two or more profiles were observed in RGC compared to PGC. According to the molecular classification, there was no significant difference in survival between the subtypes of RGC.
The presence of EBV-positive was significantly higher in patients with RGC compared to PGC. In addition, they also exhibited higher rates of co-altered expression profile profiles compared to PGC.
Our findings provide new data regarding the profiles of RGC according to the subtypes of molecular classification, reflecting potential differences from PGC that may assist in determining which markers could best define GC subtypes and stratify patients with RGC to the appropriate screening and treatment programs.