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Targeted next-generation sequencing of 22 mismatch repair genes identifies Lynch syndrome families.
Talseth-Palmer, Bente A; Bauer, Denis C; Sjursen, Wenche; Evans, Tiffany J; McPhillips, Mary; Proietto, Anthony; Otton, Geoffrey; Spigelman, Allan D; Scott, Rodney J.
Affiliation
  • Talseth-Palmer BA; School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Newcastle, New South Wales, Australia.
  • Bauer DC; Centre for Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia.
  • Sjursen W; CSIRO Digital Productivity, Sydney, New South Wales, Australia.
  • Evans TJ; Department of Laboratory Medicine Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
  • McPhillips M; Department of Pathology and Medical Genetics, St Olavs University Hospital, Trondheim, Norway.
  • Proietto A; School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle, Newcastle, New South Wales, Australia.
  • Otton G; Centre for Information-Based Medicine, Hunter Medical Research Institute, Newcastle, New South Wales, Australia.
  • Spigelman AD; Hunter Area Pathology Service, Pathology North, Hunter New England Area Health, Newcastle, New South Wales, Australia.
  • Scott RJ; Hunter Centre for Gynaecological Cancer, Hunter New England Area Health, Newcastle, New South Wales, Australia.
Cancer Med ; 5(5): 929-41, 2016 05.
Article de En | MEDLINE | ID: mdl-26811195
Causative germline mutations in mismatch repair (MMR) genes can only be identified in ~50% of families with a clinical diagnosis of the inherited colorectal cancer (CRC) syndrome hereditary nonpolyposis colorectal cancer (HNPCC)/Lynch syndrome (LS). Identification of these patients are critical as they are at substantially increased risk of developing multiple primary tumors, mainly colorectal and endometrial cancer (EC), occurring at a young age. This demonstrates the need to develop new and/or more thorough mutation detection approaches. Next-generation sequencing (NGS) was used to screen 22 genes involved in the DNA MMR pathway in constitutional DNA from 14 HNPCC and 12 sporadic EC patients, plus 2 positive controls. Several softwares were used for analysis and functional annotation. We identified 5 exonic indel variants, 42 exonic nonsynonymous single-nucleotide variants (SNVs) and 1 intronic variant of significance. Three of these variants were class 5 (pathogenic) or class 4 (likely pathogenic), 5 were class 3 (uncertain clinical relevance) and 40 were classified as variants of unknown clinical significance. In conclusion, we have identified two LS families from the sporadic EC patients, one without a family history of cancer, supporting the notion for universal MMR screening of EC patients. In addition, we have detected three novel class 3 variants in EC cases. We have, in addition discovered a polygenic interaction which is the most likely cause of cancer development in a HNPCC patient that could explain previous inconsistent results reported on an intronic EXO1 variant.
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Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Tumeurs colorectales héréditaires sans polypose / Réparation de mésappariement de l'ADN Type d'étude: Diagnostic_studies / Prognostic_studies / Screening_studies Limites: Adult / Aged / Female / Humans / Middle aged Langue: En Journal: Cancer Med Année: 2016 Type de document: Article Pays d'affiliation: Australie Pays de publication: États-Unis d'Amérique

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Tumeurs colorectales héréditaires sans polypose / Réparation de mésappariement de l'ADN Type d'étude: Diagnostic_studies / Prognostic_studies / Screening_studies Limites: Adult / Aged / Female / Humans / Middle aged Langue: En Journal: Cancer Med Année: 2016 Type de document: Article Pays d'affiliation: Australie Pays de publication: États-Unis d'Amérique