ArticleCancer science2005
Whole-genome analyses of loss of heterozygosity and methylation analysis of four tumor-suppressor genes in N-methyl-N'-nitro-N-nitrosoguanidine-induced rat stomach carcinomas.
Article in Cancer science, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Mechanisms and applications of N-Methyl-N'-nitro-N-nitrosoguanidine in animal tumor models: current situation and challenges.Frontiers in oncology · 2025Review
- Human gastric cancer risk screening: From rat pepsinogen studies to the ABC method.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2021Article
- Global DNA Hypomethylation andTurkish journal of pharmaceutical sciences · 2020Article
- Pepsinogen C expression, regulation and its relationship with cancer.Cancer cell international · 2017Review
- Identification of a DNA methylation marker that detects the presence of lymph node metastases of gastric cancers.Oncology letters · 2012Article
- Article
- Initiation of trophectoderm lineage specification in mouse embryos is independent of Cdx2.Development (Cambridge, England) · 2010Article
- Lack of association between CpG island methylator phenotype in human gastric cancers and methylation in their background non-cancerous gastric mucosae.Cancer science · 2007Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced rat stomach carcinomas are considered to be a good model for differentiated-type human stomach carcinomas. However, as for their molecular basis, only infrequent mutations of Catnb (beta-catenin) and Trp53 (p53) have been observed. Here, we carried out a whole-genome analysis of loss of heterozygosity (LOH) using 21 stomach carcinomas induced by MNNG in F(1) hybrids of ACI and BUF rats, and also analyzed promoter methylation of four tumor-suppressor genes. LOH analysis was performed using 130 polymorphic markers covering rat chromosomes 1-20 with an average interval of 20 Mbp. Despite adapting conditions so that LOH could be detected with up to a 50% contamination of stromal cells, no LOH was detected at any loci. CpG islands in putative promoter regions of four tumor-suppressor genes, Cdh1 (E-cadherin), Cdkn2a (p16), Mlh1, and Rassf1a, were analyzed by methylation-specific polymerase chain reaction (PCR). However, no methylation was detected. In contrast, the promoter region of Pgc (pepsinogen C), which lacks a CpG island, was methylated in all 21-cancer samples. These results indicated that LOH spanning a chromosomal region larger than 30-40 Mbp or silencing of Cdh1, Cdkn2a, Mlh1, and Rassf1a, was not involved in MNNG-induced rat stomach carcinomas. The search for other genes involved in these carcinomas needs to be continued.
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