In late-line treatment for advanced gastric cancer (AGC), evidence supporting the use of irinotecan in older patients remains limited. We conducted a post-hoc age-subgroup analysis of the phase III RINDBeRG study, which randomized AGC patients previously treated with ramucirumab-based chemotherapy to receive ramucirumab plus irinotecan (RAM + IRI) or irinotecan alone (IRI).

Peritoneal metastasis (PM) is a major contributor to poor prognosis in advanced gastric cancer (GC), yet its molecular mechanisms remain insufficiently understood. The results of bioinformatic analysis and clinical sample validation reveal that LncRNA MZF1-AS1 is significantly upregulated in GC tissues, particularly in peritoneal metastases, and is associated with worse overall and post-progression survival. MZF1-AS1 enhances malignant phenotypes and PM of GC cells in vitro and in vivo. Mechanistically, RAB13 is demonstrated as a functional effector of MZF1-AS1 via RNA-seq. MZF1-AS1 enhances RAB13 expression by promoting its mRNA stability, thereby facilitating GC cell proliferation, EMT, migration, invasion, and stemness. Further, RNA pulldown and Mass Spectrometry reveal that MZF1-AS1 directly binds to NSUN2. MZF1-AS1 strengthens the interaction between NSUN2 and RAB13 mRNA, promoting NSUN2-mediated m5C modification and stabilizing RAB13 mRNA. Our findings uncover a novel epi-transcriptomic mechanism by which MZF1-AS1 promotes GC progression via NSUN2-dependent m5C methylation of RAB13 mRNA, offering new insights into PM pathogenesis and highlighting potential therapeutic targets for advanced GC.

Valvuloplastic esophagogastrostomy by a double flap technique has promise for preventing reflux after proximal gastrectomy. However, a short esophageal remnant sometimes strongly complicates the transhiatal procedure for alimentary tract reconstruction. We therefore developed secure robotic techniques for right transthoracic esophagogastrostomy by a double flap technique. To accomplish valvuloplastic esophagogastrostomy by this double flap technique in the right thorax of patients in the prone position, the esophagus and stomach were partially fixed before rotating these two organs to expose the anterior gastric wall side for anastomosis because it was invisible in the right thorax. However, this rotation process was complicated. Doubting that the required anastomosis that was conventionally created in the layout of the ventral esophagus and dorsal stomach in valvuloplastic esophagogastrostomy by a double flap technique protected against reflux, we have considered that, if the anastomosis is created at the posterior gastric wall, it may not be necessary to rotate the remnant esophagus and stomach. We herein describe a modified robotic procedure for right transthoracic valvuloplastic esophagogastrostomy incorporating a double flap technique. In this procedure, the anastomosis is created at the posterior remnant gastric wall under a natural operative view without re-arranging the anastomotic organs. This modified technique simplifies right transthoracic valvuloplastic esophagogastrostomy by a double flap technique without adversely influencing anti-acid reflux mechanisms.

Immune checkpoint inhibitors (ICI) are pivotal in cancer treatment. However, not all patients are responsive to current ICI therapies, and new targets are needed. Thus, the HLA-G/ILT2 pathway emerges as one such potential ICI. The present study aimed to analyze the implications of this pathway in cytotoxic T cells from patients with gastric adenocarcinoma.

We aimed to reveal the outcomes of endoscopic resection (ER) for locally recurrent early gastric cancer (LRGC) after ER using the data obtained in a Japanese multicenter prospective cohort study of ER for early gastric cancer (EGC) using Web registry (J-WEB/EGC).

The role of histone lysine lactylation (Kla) in gastric cancer mesenchymal stromal cells (GCMSCs) remains elusive. This study aimed to investigate the potential lactyltransferase and the influence of histone Kla in GCMSCs.

Telesurgery is gaining traction across surgical specialties. However, its use in radical gastrectomy for gastric cancer remains limited. This study evaluated the safety and feasibility of fifth-generation (5G) robot-assisted remote radical gastrectomy using the Toumai Endoscopic Surgery Robotic System.

Prognostic factors for conversion surgery in patients with metastatic gastric cancer remain unclear. This study aimed to identify the prognostic factors associated with conversion surgery, and evaluate the safety and survival outcomes of conversion surgery using data from Japanese patients enrolled in the CONVO-GC-1 study.

To develop and validate a nomogram for predicting lymph node metastasis in early gastric cancer according to the characteristics of the tumor microenvironment to optimize treatment strategies.

This research examines how NF-κB Interacting LncRNA (NKILA) and its functional variant rs2273534 influence gastric cancer (GC) risk, development, and prognosis, along with the molecular pathways involved.

The INTEGRATE trials evaluated regorafenib in advanced gastric and esophagogastric junction cancer (AGOC), a poor prognosis population. In INTEGRATE 1 (I1, phase 2), regorafenib improved progression-free survival (PFS) without a clear excess decline in health-related quality of life (HRQoL). INTEGRATE 2a (I2a, phase 3) demonstrated an overall survival (OS) benefit, alone and in a pre-specified pooled analysis with I1.

This study aimed to evaluate the impact of drain placement on the incidence of postoperative complications in patients undergoing gastrectomy.

Peritoneal dissemination is a major cause of poor prognosis in gastric cancer (GC). Although conventional peritoneal lavage cytology (CY) is used to detect micrometastatic peritoneal spread, its sensitivity is limited. This study aimed to evaluate the clinical utility of droplet digital methylation-specific PCR (ddMSP) targeting cancer-specific methylation for DNA-based detection of peritoneal dissemination.

Extrachromosomal DNA (ecDNA), a form of circular DNA located outside chromosomes, is a common driver of oncogene amplification. Recent pan-cancer studies have associated ecDNA with cancer progression and poor prognosis. Moreover, its relationship with specific genomic features is becoming increasingly evident. However, the clinicopathological characteristics and underlying genomic mechanisms of ecDNA in gastric cancer remain poorly understood.

Claudin-3, Claudin-4, and Claudin-7 are expressed on the surface of epithelial cells. Their absence in neoplastic cells of epithelial origin is an aggressiveness marker in different cancers. The NF-YA gene codes for the Nuclear-Transcription-Factor-Y-Subunit-A, which is overexpressed in various tumors. In tumors, the relative ratio of the two major NF-YA alternative splicing isoforms, NF-YA long and NF-YA short, is associated with a mesenchymal phenotype and a poor prognosis. Based on a high NF-YA long/NF-YA short ratio, we generated a 158-gene signature that is common to Claudin Breast Carcinomas (BRCA) and Stomach Adenocarcinomas (STAD).

Undifferentiated-type gastric cancer (UGC) is more pathologically aggressive and progresses faster than differentiated-type gastric cancer (DGC). However, the impact of Helicobacter pylori (Hp) status on survival outcomes and clinicopathological features of UGC remains unclear.

Palliative resection for metastatic gastric cancer is not recommended in current practice guidelines; however, it is frequently performed based on clinical considerations. Prospective trials face challenges, necessitating large-scale retrospective analyses to provide clinical evidence.

Helicobacter (H.) pylori is the major risk factor of gastric cancer (GC). We aimed to estimate the population attributable fraction (PAF) of GC and the number of new GC cases and deaths for GC attributable to H. pylori in different countries worldwide in 2022.

Corpus atrophic gastritis (CAG) requires endoscopic-histological surveillance due to the risk of developing gastric neoplastic lesions (GNL). This study aimed to identify variables associated with GNL development at long-term follow-up using a Fisher score-based feature-ranking-approach coupled with a One-Class Support-Vector-Machine (SVM) model.

Helicobacter pylori (H. pylori) infection is a recognized risk factor for gastric cancer (GC), which is the leading cause of cancer-related deaths worldwide. As a Class I carcinogen, H. pylori plays a central role in the occurrence and development of GC. Recent studies have highlighted the critical role of metabolic reprogramming inthe gastric cancer, and H. pylori infection has been shown to significantly alter metabolic pathways in gastric cancer. This review explores the mechanisms by which H. pylori infection drives metabolic changes in GC, particularly in glycolysis, lipid metabolism, and amino acid metabolism. By altering these metabolisms, H. pylori enhances the survival, proliferation, and metastasis of tumor cells, and also promotes immune evasion. Therefore, understanding the ways in which H. pylori-induced metabolic reprogramming of GC cells is essential for identifying new therapeutic targets. By summarizing the latest research progress of these metabolic pathways, new strategies and directions can be provided for gastric cancer treatment.