Dysregulation of CDX1, CDX2 and SOX2 in patients with gastric cancer also affects the non-malignant mucosa

Bornschein, Jan; Tóth, Kinga; Selgrad, Michael; Kuester, Doerthe; Wex, Thomas; Molnár, Béla; Tulassay, Zsolt; Malfertheiner, Peter

doi:10.1136/jclinpath-2013-201448

Cited by 22 publications

(15 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CDX2 has a tumour suppressor role and is known to regulate intestinal differentiation . Induction of CDX2 appears to be an early event in the progression of gastric cancer of the intestinal and diffuse type, and thus CDX2 negativity in our cases suggests that these lesions probably develop along a different pathway of tumorigenesis.…”

Section: Discussionmentioning

confidence: 76%

Chief cell‐predominant gastric polyps: a series of 12 cases with literature review

Chan

Brown

Kyle³

et al. 2015

Histopathology

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 76%

Chief cell‐predominant gastric polyps: a series of 12 cases with literature review

Chan

Brown

Kyle³

et al. 2015

Histopathology

View full text Add to dashboard Cite

show abstract

“…Under normal conditions, the expression of CDX2 was detected in IM but was absent in normal gastric cells [48]. In previous studies, researchers showed that the up-regulation of CDX2 expression during IM is important in the determination of the incomplete type of IM (type IIb, III) and early-stage GC, which had also been demonstrated in animals [49–52]. However, the regulation of CDX2 in GIM remains largely unknown.…”

Section: Discussionmentioning

confidence: 99%

hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway

et al. 2017

View full text Add to dashboard Cite

BackgroundhTERT has been reported involved in the proliferation and metastasis of gastric cancer, but the role of hTERT in gastric intestinal metaplasia, a premalignant lesion of the gastric mucosa was unknown. The aim of the present study was to investigate the role of hTERT in GIM and the effect of hTERT on CDX2 expression in gastric cells.ResultsExperiments showed that expression of hTERT was significantly higher in GIM than in normal gastric mucosa. Moreover, hTERT increased the KLF4 level via NF-κB during GIM. Furthermore, KLF4 is involved in the up-regulation of CDX2 induced by hTERT, and hTERT can interact with p50, thereby increasing the level of CDX2.Materials and MethodsImmunohistochemistry was used to detect the expression of hTERT in gastric intestinal metaplasia tissue. Then, effect of hTERT on the expression of CDX2 was detected by qRT-PCR, WB and dual luciferase experiment. The role of p65 and p50 in the regulation of CDX2 were further detected by WB, CO-IP and ChIP.ConclusionsWe may conclude that hTERT promotes GIM by up-regulating CDX2 via NF-κB signaling pathway.

show abstract

“…It is caused naturally by the remnant stomach, which is preserved after ER. In addition, the surrounding non-tumorous mucosa may be at high risk of developing metachronous gastric lesions because it used to share the environment with gastric cancer [ 28 ]. Therefore, eradication of H .…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Eradication on the Prevention of Metachronous Lesions after Endoscopic Resection of Gastric Neoplasm: A Meta-Analysis

et al. 2015

View full text Add to dashboard Cite

BackgroundThere is controversy about the effect of Helicobacter pylori (H. pylori) eradication on the prevention of metachronous gastric cancer after endoscopic resection (ER).AimsThe aim of this study was to systematically evaluate the effect of H. pylori eradication on the prevention of metachronous gastric lesions after ER of gastric neoplasms.MethodsWe performed a systematic search of PubMed, EMBASE, the Cochrane Library, and MEDLINE that encompassed studies through April 2014. Our meta-analysis consisted of 10 studies, which included 5881 patients who underwent ER of gastric neoplasms.ResultsWhen we compared the incidence of metachronous lesions between H. pylori-eradicated and non-eradicated groups, H. pylori eradication significantly lowered the risk of metachronous lesions after ER of gastric neoplasms (five studies, OR = 0.392, 95% CI 0.259 – 0.593, P < 0.001). When we compared H. pylori-eradicated and persistent groups, again, H. pylori eradication significantly lowered the incidence of metachronous lesions after ER of gastric neoplasms (six studies, OR = 0.468, 95% CI 0.326 – 0.673, P < 0.001). There was no obvious heterogeneity across the analyzed studies.ConclusionsThis meta-analysis suggests a preventive role for H. pylori eradication for metachronous gastric lesions after ER of gastric neoplasms. Thus, H. pylori eradication should be considered if H. pylori infection is confirmed during ER.

show abstract

Dysregulation of CDX1, CDX2 and SOX2 in patients with gastric cancer also affects the non-malignant mucosa

Cited by 22 publications

References 13 publications

Chief cell‐predominant gastric polyps: a series of 12 cases with literature review

Chief cell‐predominant gastric polyps: a series of 12 cases with literature review

hTERT promotes gastric intestinal metaplasia by upregulating CDX2 via NF-κB signaling pathway

Helicobacter pylori Eradication on the Prevention of Metachronous Lesions after Endoscopic Resection of Gastric Neoplasm: A Meta-Analysis

Contact Info

Product

Resources

About