This study used an extremes-of-survivorship approach to identify an association between TP53 hotspot mutations co-occurring with loss of heterozygosity and unexpectedly poor survival in early gastric cancer.
Eighty-three percent of mutations in early gastric cancer and 52% of mutations in advanced gastric cancer showed G:C-to-A:T transition, almost exclusively at CpG dinucleotide mutational hot spots, indicating that the spectrum of p53 mutation was similar to that of colorectal cancer.
The Pro/Pro genotype of the p53 codon 72 polymorphism carries a higher risk for gastric cancer in general and is also associated with a much higher risk for EGC than AGC.
Seven HG-IEN lesions shared an identical mutational profile with the EGC from the same patient; 13 mutations observed in APC, ATM, FGFR3, PIK3CA, RB1, STK11, and TP53 genes were shared by both HG-IEN and ECG lesions.
These novel findings concerning MYC copy number alteration in early gastric cancer suggest that MYC alteration is observed in the beginning of gastric carcinogenesis and could be used as a therapeutic target.
These data confirmed miR-34brs4938723 polymorphism was also recognized as a biomarker to predict recurrence after ESD in EGC patients via analysis upon the recurrence-free rate among different genotypes of EGC patients.
In this report we describe the pregnancy outcomes in three CDH1 mutation positive women after PTG and in a CDH1 mutation negative woman after total gastrectomy for early gastric cancer.
We analyzed the Interleukin-10 (IL-10) single nucleotide polymorphism (SNP) and IgG subclass responses to the bacteria in patients with early gastric cancer and recurrent gastric cancer.
The results showed that PDGFRB was validated as a target of miR‑499a, and rs3746444 was identified as a potential biomarker to predict the recurrence of EGC following ESD.
Cell-cycle regulation may play a role in gastric cancer initiation and development and the CCND1A870G genotype maybe a useful biomarker for detection of early gastric cancer.
Our results support the molecular similarity between HG-IEN and EGC and suggest a relevant role for TP53 in the progression to the invasive phenotype and the use of immunohistochemistry as a surrogate to detect TP53 gene mutations.
We retrospectively stratified the risk of LNM according to the total number of four LNM risk factors (RFs) that resulted in non-curative resection for ESD in 861 EGC patients who underwent gastrectomy.
These estimates of LNM should be incorporated into decisions regarding further management of patients with EGC ≤ 3 cm who are found to have slight submucosal invasion (< 500 µm) in an ESD specimen.
Expressions of Ras Homolog Gene Family, Member A (RhoA) and Cyclooxygenase-2 (COX-2) Proteins in Early Gastric Cancer and Their Role in the Development of Gastric Cancer.