ArticleClinical and experimental medicine2013
hTERT and TP53 deregulation in intestinal-type gastric carcinogenesis in non-human primates.
Article in Clinical and experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 8 citations in OpenAlex.
- Dietary phytochemicals as the potential protectors against carcinogenesis and their role in cancer chemoprevention.Clinical and experimental medicine · 2020Review
- CDKN1A histone acetylation and gene expression relationship in gastric adenocarcinomas.Clinical and experimental medicine · 2017Article
- Deregulation of MYC and TP53 through genetic and epigenetic alterations in gallbladder carcinomas.Clinical and experimental medicine · 2015Article
- Deregulated expression of Nucleophosmin 1 in gastric cancer and its clinicopathological implications.BMC gastroenterology · 2014Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the high incidence, the molecular events involved in intestinal-type gastric carcinogenesis remains unclear. We previously established an intestinal-type gastric carcinogenesis model in Cebus apella, a New World monkey. In the present study, we evaluated hTERT and TP53 mRNA expression, as well as their protein immunoreactivity, in normal mucosa, non-atrophic gastritis, atrophic gastritis, intestinal metaplasia, and intestinal-type gastric cancer samples of non-human primates treated with N-methyl-nitrosourea. In addition, we evaluated the number of TP53 copies in these samples. Although hTERT immunoreactivity was only detected in gastric cancer, a continuous increase of hTERT mRNA expression was observed from non-atrophic gastritis to gastric tumors. No sample presented p53 immunoreactivity. However, we also observed a continuous decrease of TP53 mRNA expression during the sequential steps of gastric carcinogenesis. Moreover, loss of TP53 copies was observed in intestinal metaplasia and gastric cancer samples. Our study highlights that hTERT and TP53 have a key role in intestinal-type gastric cancer initiation.
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