ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Three novel mutations of APC gene in Chinese patients with familial adenomatous polyposis.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Adenomatous Polyposis Coli Gene Mutations in 22 Chinese Pedigrees with Familial Adenomatous Polyposis.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Cyclin G2 suppresses Wnt/β-catenin signaling and inhibits gastric cancer cell growth and migration through Dapper1.Journal of experimental & clinical cancer research : CR · 2018Article
- Is APC hypermethylation a diagnostic biomarker for bladder cancer? A meta-analysis.OncoTargets and therapy · 2018Article
- c.1439delA frameshift deletion mutation in familial adenomatous polyposis.OncoTargets and therapy · 2018Article
- Novel APC gene mutations associated with protein alteration in diffuse type gastric cancer.BMC medical genetics · 2017Article
- A novel pathogenic splice acceptor site germline mutation in intron 14 of the APC gene in a Chinese family with familial adenomatous polyposis.Oncotarget · 2017Article
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Abstract
Familial adenomatous polyposis (FAP) is an autosomal dominant disorder characterized by the development of hundreds to thousands of colonic adenomas and an increased risk of colorectal cancer. Adenomatous polyposis coli (APC), encoding a large multidomain protein involved in antagonizing the Wnt signaling pathway, has been identified as the main causative gene responsible for FAP. In this study, we identified three novel mutations as well as two recurrent mutations in the APC in five Chinese FAP families by sequencing. Immunohistochemical analysis revealed that among these mutations, a nonsense mutation (c.2510C>G) and two small deletions (c.2016_2047del, c.3180_3184del) led to the truncation of the APC protein and the cytoplasmic and nuclear accumulation of β-catenin in the colorectal samples from affected individuals, respectively. Our study expands the database on mutations of APC and provides evidence to understand the function of APC in FAP.
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