ArticleThe Journal of molecular diagnostics : JMD2007
Improved detection of KIT exon 11 duplications in formalin-fixed, paraffin-embedded gastrointestinal stromal tumors.
Article in The Journal of molecular diagnostics : JMD, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 12 citations in OpenAlex.
- Mutational spectrum and classification of novel mutations in patients with metastatic gastrointestinal stromal tumours.International journal of oncology · 2020Article
- Tyrosine-kinase mutations in c-KIT and PDGFR-alpha genes of imatinib naïve adult patients with gastrointestinal stromal tumours (GISTs) of the stomach and small intestine: relation to tumour-biological risk-profile and long-term outcome.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2012Article
- A quality control program for mutation detection in KIT and PDGFRA in gastrointestinal stromal tumours.Journal of gastroenterology · 2011Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastrointestinal stromal tumors (GISTs) are the most common gastrointestinal mesenchymal tumors driven by KIT or PDGFRA mutations. A majority of these mutations affect KIT exon 11 and represent deletions or point mutations, but insertions and duplications have also been reported. The latter have been found exclusively in the 3' part of KIT exon 11. Reported frequency of duplications varies, and a higher frequency has been reported in studies based on frozen tissue. Recently, we have hypothesized that in some cases, the duplications might remain undetected in formalin-fixed, paraffin-embedded GISTs because of the preferential polymerase chain reaction (PCR) amplification of wild-type KIT over the mutant allele. In this study, 16 GISTs initially diagnosed as a wild-type KIT were evaluated using PCR assay amplifying only the 3' part of KIT exon 11, the region commonly affected by duplications. Denaturing high-pressure liquid chromatography and direct sequencing analyses revealed duplications in 4 (25%) of 16 analyzed cases. Use of the PCR assay amplifying the specific region affected by duplications and yielding 129 bp in wild-type KIT can substantially improve the detection of these mutations in formalin-fixed, paraffin-embedded GISTs.
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