Comparison of clinical outcomes and prognosis between surgery and endoscopic submucosal dissection in patients with synchronous multifocal early gastric cancer.

BACKGROUND: Synchronous multiple early gastric cancer (SMEGC) refers to the simultaneous occurrence of two or more malignant cancer lesions in the stomach. For patients with multiple early gastric carcinomas, the choice of appropriate treatment remains controversial. This study is dedicated to comparing the clinical outcomes and prognosis of patients with SMEGC who underwent endoscopic submucosal dissection (ESD) or gastrectomy. METHODS: A total of 180 patients with more than one malignant cancer lesion in the stomach who had received gastrectomy or ESD between 2012 and 2021 were retrospectively evaluated to determine their clinical outcomes and prognosis. Univariate and multivariate logistic regression were utilized to identify risk factors for tumor recurrence. RESULTS: Over the 57.5 months median follow-up period for the 140 enrolled cases, tumor recurrence occurred in 8 (12%) in the ESD group but only 1 (1%) in the surgery group. Relapse-free survival (RFS) was higher in the surgery group (p = 0.023) in all cases; however, there was no significant difference in Overall survival (OS, p = 0.772). Complications were significantly higher in the surgery group than in the ESD group, but fewer in the radical distal gastrectomy group. Multivariate regression analysis revealed that ESD(p = 0.034), the main lesion size > 2 cm(p = 0.019), and undifferentiated tumor(p = 0.022) were independent risk factors for tumor recurrence. CONCLUSIONS: For the treatment of simultaneous multifocal early gastric cancer, ESD has a good short-term effect and higher quality of life. However, ESD has a higher risk of recurrence than surgery. And we found that the partial gastrectomy appears to be considered as adequate treatment for some SMEGC patients.

Genome-wide screening for differentially methylated long noncoding RNAs identifies LIFR-AS1 as an epigenetically regulated lncRNA that inhibits the progression of colorectal cancer.

BACKGROUND: Aberrant DNA methylation is an epigenetic marker that has been linked to the pathogenesis of colorectal cancer (CRC). Long noncoding RNAs (lncRNAs) have been increasingly identified to be associated with tumorigenic processes of CRC. Identifying epigenetically dysregulated lncRNAs and characterizing their effects during carcinogenesis are focuses of cancer research. METHODS: Differentially methylated loci and expressed lncRNAs were identified by integrating DNA methylome and transcriptome analyses using The Cancer Genome Atlas database. Bisulfite sequencing PCR (BSP) was performed to analyze LIFR-AS1 promoter methylation status. The functional roles of LIFR-AS1 in CRC were determined by in vitro and in vivo experiments. RESULTS: We identified a novel hypermethylated lncRNA, LIFR-AS1, that was downregulated and associated with tumorigenesis, metastasis, and poor prognosis in CRC. High methylation burden of LIFR-AS1 indicated a poor survival of CRC patients. Promoter hypermethylation of LIFR-AS1 in tumor tissues was confirmed by BSP. Functional assays revealed that LIFR-AS1 could competitively bind to hsa-miR-29b-3p, and repressed colon cancer cell proliferation, colony formation and invasion. LIFR-AS1 also inhibited tumor growth in a mouse xenograft model of CRC. CONCLUSIONS: Our results showed that the identified DNA methylation-dysregulated lncRNAs may be potential biomarkers and highlighted a role for LIFR-AS1 as a tumor suppressor in CRC.