ArticleBritish journal of cancer1999
Chromosome band 16q24 is frequently deleted in human gastric cancer.
Article in British journal of cancer, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- CaAntibodies (Basel, Switzerland) · 2026Article
- T-cadherin as a potential novel regulator of intestinal inflammation and fibrosis.Frontiers in physiology · 2026Review
- Mechanosensitive Ion Channels and Their Role in Cancer Cells.Membranes · 2023Review
- CDK10 in Gastrointestinal Cancers: Dual Roles as a Tumor Suppressor and Oncogene.Frontiers in oncology · 2021Review
- The role of F-box only protein 31 in cancer.Oncology letters · 2018Review
- Upregulation of T-cadherin suppresses cell proliferation, migration and invasion of gastric cancerExperimental and therapeutic medicine · 2017Article
- Article
- Emerging Roles of ADAMTSs in Angiogenesis and Cancer.Cancers · 2012Article
- Article
- Article
- Suppression subtractive hybridization identifies distinctive expression markers for coronary and internal mammary arteries.Arteriosclerosis, thrombosis, and vascular biology · 2003Article
- Chromosomal alterations in paired gastric adenomas and carcinomas.The American journal of pathology · 2001Article
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have analysed the loss of heterozygosity (LOH) on chromosome bands 16q22-q24 in 24 primary gastric cancer tissues and found three regions of frequent allelic loss (16q22, 16q24.1-q24.3 and 16q24.3). The region for the most frequent allelic loss (63%) was in 16q24.1-q24.3. LOH of this region had no relationship with histological subtype, but a significant association between LOH and microscopic lymphangial invasion was observed. Although not significant, vascular and gastric wall invasions are also associated with LOH. The region includes the locus for the H-cadherin gene. Therefore we examined the genetic and epigenetic alterations of this gene. Markedly reduced expression was observed in gastric cancer cell lines compared with that of normal gastric mucosa. However, no mutation was found in this gene in any of the gastric cancer tissues or the gastric cancer cell lines. Furthermore, we analysed the methylation status of the 5'-flanking region of the gene, but no significant association was found. We suggest that some other tumour suppressor gene(s) in 16q24.1-q24.3 may be responsible for gastric carcinogenesis.
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