ArticleCancer medicine2018
Correlation between negative expression of pepsinogen C and a series of phenotypic markers of gastric cancer in different gastric diseases.
Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 9 citations in OpenAlex.
- Chinese integrated guideline on the management of gastric precancerous conditions and lesions.Chinese medicine · 2022Review
- Identification of cuprotosis-mediated subtypes, the development of a prognosis model, and influence immune microenvironment in hepatocellular carcinoma.Frontiers in oncology · 2022Article
- Pepsinogen and Serum IgG Detection Is a Valuable Diagnostic Method forDiagnostics (Basel, Switzerland) · 2021Article
- Identification of PGC-related ncRNAs and their relationship with the clinicopathological features of Gastric Cancer.Journal of Cancer · 2021Article
- The panoramic picture of pepsinogen gene family with pan-cancer.Cancer medicine · 2020Article
- PGC-MG7 combination could be used as a follow-up panel for monitoring dynamical progression of gastric precancerous diseases.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2020Article
- Correlation between negative expression of pepsinogen C and a series of phenotypic markers of gastric cancer in different gastric diseases.Cancer medicine · 2018Article
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7 authors at 1 institution in 1 country.
Funding
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Abstract
Gastric tumorigenesis is a multistep process initiated by chronic superficial gastritis (SG), followed by atrophic gastritis (AG), then intestinal metaplasia (IM), and finally by dysplasia and adenocarcinoma according to the Correa model. Pepsinogen C (PGC) decreases gradually during progression of cancer, which makes PGC an ideal negative marker for GC. To explore the correlation between PGC and other positive tumor markers in different gastric diseases, we observed the expression of PGC, MG7-Ag, MMP9, NM23, Ki-67, and E-cadherin by immunohistochemistry, quantitative RT-PCR, and immunoblot analysis. Our results showed that in SG, PGC was highly expressed while malignant phenotype markers were rarely expressed. In contrast with SG, malignant phenotype markers were highly expressed while the positive rate of PGC reached only 1.44% in GC. So there was no coexpression of PGC and malignant phenotype markers in SG or GC tissues. Only in the AG group, which is well-known to be gastric precancerous disease, coexpression of PGC and malignant phenotype markers was detected. Our results suggested that the expression of PGC in AG was negatively correlated with that of MG7-Ag and MMP9. Of all AG, those with low expression of PGC and high expression of MG7-Ag and MMP9 may possess a greater potential of malignant transformation. Combined detection of negative marker PGC and positive markers MG7-Ag and MMP9 could be used as a potential follow-up panel for monitoring dynamical progression of AG and improving the detection efficiency of high-risk individuals of gastric cancer, and then taking necessary interventions on the target population.
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