Please use this identifier to cite or link to this item:
|Title:||Erratum to: Mutational landscape of mucinous ovarian carcinoma and its neoplastic precursors.|
|Other Authors:||Ryland, Georgina|
Australian Ovarian Cancer Study Group
|Keywords:||Mucinous Ovarian Tumors|
Ovarian Surface Epithelium
Epithelial Ovarian Tumors
Epworth Research Institute, Epworth HealthCare, Richmond, Victoria Australia.
Obstetrics and Gynaecology Clinical Institute, Epworth HealthCare, Victoria, Australia
|Citation:||Genome Med. 2017 Jan 12;9(1):1.|
|Abstract:||ERRATUM TO: Mutational landscape of mucinous ovarian carcinoma and its neoplastic precursors. BACKGROUND: Mucinous ovarian tumors are an unusual group of rare neoplasms with an apparently clear progression from benign to borderline to carcinoma, yet with a controversial cell of origin in the ovarian surface epithelium. They are thought to be molecularly distinct from other ovarian tumors but there have been no exome-level sequencing studies performed to date. METHODS: To understand the genetic etiology of mucinous ovarian tumors and assess the presence of novel therapeutic targets or pathways, we undertook exome sequencing of 24 tumors encompassing benign (5), borderline (8) and carcinoma (11) histologies and also assessed a validation cohort of 58 tumors for specific gene regions including exons 4-9 of TP53. RESULTS: The predominant mutational signature was of C>T transitions in a NpCpG context, indicative of deamination of methyl-cytosines. As well as mutations in known drivers (KRAS, BRAF and CDKN2A), we identified a high percentage of carcinomas with TP53 mutations (52 %), and recurrent mutations in RNF43, ELF3, GNAS, ERBB3 and KLF5. CONCLUSIONS: The diversity of mutational targets suggests multiple routes to tumorigenesis in this heterogeneous group of tumors that is generally distinct from other ovarian subtypes.|
|Description:||ERRATUM: There is an error in Additional file 2 for this article . When opening Additional file 2, this links to the incorrect file. NOTES: The online version of the original article can be found at http://dx.doi.org/10.1186/s13073-015-0210-y. ADDITIONAL FILES: Additional file 2: Figure S1. Nucleotide substitution frequency and context. Figure S2. RRAS2 somatic mutation. Figure S3. Genetic comparison between mucinous ovarian tumors and mucinous cancers from other anatomical sites. Figure S4. ELF3 somatic mutations. Figure S5. H&E stained sections of frozen tissues used for exome discovery cohort.|
|Journal Title:||Genome Medicine|
|Affiliated Organisations:||Cancer Genetics Laboratory, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.|
Bioinformatics Core Facility, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.
Department of Anatomical Pathology, Royal Melbourne Hospital, Parkville, VIC, Australia
Department of Pathology, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.
Centre for Cancer Research, MIMR-PHI Institute of Medical Research, Clayton, VIC, Australia.
Department of Molecular and Translational Sciences, Monash University, Clayton, VIC, Australia.
Cancer Genetics and Genomics Laboratory, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.
Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville, VIC, Australia.
Department of Biochemistry and Molecular Biology, University of Melbourne, Parkville, VIC, Australia.
Department of Pathology, University of Melbourne, Parkville, VIC, Australia.
|Type of Clinical Study or Trial:||Cohort Study|
|Appears in Collections:||Cancer Services|
Obstetrics & Gynaecology
Items in Epworth are protected by copyright, with all rights reserved, unless otherwise indicated.