Diffuse Gastric Cancer: A Summary of Analogous Contributing Factors for Its Molecular Pathogenicity

Ansari, Shamshul; Gantuya, Boldbaatar; Tuan, Vo Phuoc; Yamaoka, Yoshio

doi:10.3390/ijms19082424

Cited by 69 publications

(68 citation statements)

References 157 publications

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“…In the present study, no difference in miRNA expression was found within intestinal and diffuse type tumors except for miR-26a. Although intestinal type and diffuse type are thought to be caused by distinct mechanisms 31,32 , H. pylori infection is related to gastric carcinogenesis in both Lauren types 33 , and H. pylori infection is known to be associated with miRNA expression patterns 3,20,21,34 . Given these observations, we hypothesize that H. www.nature.com/scientificreports www.nature.com/scientificreports/ pylori and miRNA expression may be associated with field cancerization regardless of Lauren's classification.…”

Section: Discussionmentioning

confidence: 99%

Dysregulated miRNA in a cancer-prone environment: A study of gastric non-neoplastic mucosa

Kim

Jang

Heo

et al. 2020

Sci Rep

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Understanding cancer-prone environments is important to efficiently detect and prevent cancers. The associations between miRNA and cancer-prone environments are still largely unknown in gastric cancer (GC). Six miRNAs that are differentially expressed during gastric carcinogenesis were selected, and quantitative real-time pcR was performed in an independent training set (fresh non-tumor and tumor samples from 18 GC patients) and validation sets (set 1 with formalin-fixed paraffin-embedded non-tumor and tumor samples from 19 solitary GC and set 2 with 37 multiple GC patients). The results were compared with those of 37 gastric mucosa from 20 healthy volunteers. The expression levels of miR-26a, miR-375, and miR-1260 in gastric mucosa from healthy volunteers were statistically higher than that of non-tumorous gastric mucosa located 3 cm apart from the GC in the training set (miR-26a, P < 0.0001; miR-375, P = 0.0049; miR-1260, P = 0.0172), validation set 1 (miR-26a and miR-375, P < 0.0001; miR-1260, P = 0.0008), and validation set 2 (miR-26a, miR-375, and miR-1260, P < 0.0001). And a combination of miR-26a and miR-1260 showed the highest area under the curve value of 0.89. miRNAs are differentially expressed in non-neoplastic gastric mucosa and can be used as a biomarker to predict cancer-prone environments.

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Section: Discussionmentioning

confidence: 99%

Dysregulated miRNA in a cancer-prone environment: A study of gastric non-neoplastic mucosa

Kim

Jang

Heo

et al. 2020

Sci Rep

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“…This disproportion may be primarily genetically determined, specifically alterations in the CDH1 gene, which predispose individuals to GC at a young age with a diffuse phenotype. Diffuse-type GC lacks intercellular adhesion, which is often observed with diffuse invasion growth patterns throughout the stroma, characterized by rapid disease progression, being highly metastatic [68].…”

Section: More Aggressive Tumormentioning

confidence: 99%

Gastric Cancer in Young Adults: A Different Clinical Entity from Carcinogenesis to Prognosis

2020

Gastroenterology Research and Practice

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Approximately 5.0% of gastric cancer (GC) patients are diagnosed before the age of 40 and are not candidates for screening programs in most countries and regions. The incidence of gastric cancer in young adults (GCYA) has declined over time in most countries except in the United States. Genetic alterations, environmental factors, and lifestyle may predispose some young adults to GC. According to molecular classifications, the cancer of most GCYA patients belongs to the genomically stable or microsatellite stable/epithelial-mesenchymal transition subtype, with the common genetic aberrations being mutations in CDH1. What characterizes GCYA are a higher prevalence in females, more aggressive tumor behaviors, diagnosis at advanced stages, fewer comorbidities and being better treatment candidates, and a similar or better survival outcome when compared with older patients. Considering the greater loss of life-years in younger patients, lowering the incidence of GC and diagnosing at a relatively early stage are the two most effective ways to decrease GC mortality. To achieve these goals, the low awareness of GCYA among general people, policy-makers, clinicians, and researchers should be changed.

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“…Furthermore, intestinal metaplasia and intestinal-type gastric cancer also showed a relatively high frequency of alteration of the CDH1 gene [42]. Accordingly, mutational alterations of p53 and other factors may be associated with diffuse-type gastric cancer, as well as dysregulation of E-cadherin [37]. strong tendency of a lower location in Barrett-type adenocarcinoma.…”

Section: Chronic Active Gastritis-atrophic Gastritis (Mucosal Remodelmentioning

confidence: 97%

“…E-cadherin is important in maintaining cell-cell adhesion, cell survival and cell migration for tissue morphogeneis and homeostasis. Non-phosphorylated CagA of H. pylori binds E-cadherin or causes mutational alterations in p53 and hyper-methylation of the E-cadherin (CDH1) gene, resulting in the dissociation of the E-cadherin-β-catenin complex or the impairment of E-cadherin synthesis [37]. In diffuse-type gastric cancers, mutations in or hyper-methylation of the CDH1 gene is frequently found, suggesting disruption of E-cadherin function [38][39][40].…”

Section: Chronic Active Gastritis-atrophic Gastritis (Mucosal Remodelmentioning

confidence: 99%

Proposal for an Organ-Specific Chronic Inflammation–Remodeling–Carcinoma Sequence

Okayasu

Ichinoe

Yoshida

2019

Gastrointestinal Disorders

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An organ-specific chronic inflammation-remodeling-carcinoma sequence has been proposed, mainly for the alimentary tract. As representative diseases, gastroesophageal reflux disease, chronic gastritis and inflammatory bowel disease (ulcerative colitis and Crohn's disease of the colitis type) were adopted for this discussion. Tissue remodeling is such an important part of tumorigenesis in this sequence that an organ-specific chronic inflammation-remodeling-carcinoma sequence has been proposed in detail. Chronic inflammation accelerates the cycle of tissue injury and regeneration; in other words, cell necrosis (or apoptosis) and proliferation result in tissue remodeling in long-standing cases of inflammation. Remodeling encompasses epithelial cell metaplasia and stromal fibrosis, and modifies epithelial-stromal cell interactions. Further, the accumulation of genetic, epigenetic and molecular changes-as well as morphologic disorganization-also occurs during tissue remodeling. The expression of mucosal tissue adapted to chronic inflammatory injury is thought to occur at an early stage. Subsequently, dysplasia and carcinoma develop on a background of remodeling due to continuous, active inflammation. Accordingly, organ-specific chronic inflammation should be ameliorated or well controlled with appropriate monitoring if complete healing is unachievable.

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Diffuse Gastric Cancer: A Summary of Analogous Contributing Factors for Its Molecular Pathogenicity

Cited by 69 publications

References 157 publications

Dysregulated miRNA in a cancer-prone environment: A study of gastric non-neoplastic mucosa

Dysregulated miRNA in a cancer-prone environment: A study of gastric non-neoplastic mucosa

Gastric Cancer in Young Adults: A Different Clinical Entity from Carcinogenesis to Prognosis

Proposal for an Organ-Specific Chronic Inflammation–Remodeling–Carcinoma Sequence

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