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Title: Copy number analysis of ductal carcinoma in situ with and without recurrence.
Austin Authors: Gorringe, Kylie L;Hunter, Sally M;Pang, Jia-Min;Opeskin, Ken;Hill, Prue;Rowley, Simone M;Choong, David Y H;Thompson, Ella R;Dobrovic, Alexander ;Fox, Stephen B;Mann, G Bruce;Campbell, Ian G
Affiliation: The Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Victoria, Australia
Cancer Genetics Laboratory, Peter MacCullum Cancer Centre, East Melbourne, Victoria, Australia
Department of Pathology, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
Department of Surgery, University of Melbourne, Melbourne, Victoria, Australia
The Royal Melbourne and Royal Women's Hospitals, Parkville, Victoria, Australia
Department of Anatomical Pathology, St Vincent's Hospital, Fitzroy, Victoria, Australia
Department of Pathology, University of Melbourne, Melbourne, Victoria, Australia
Translational Genomics and Epigenomics Laboratory, Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia
School of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia
Issue Date: Sep-2015 2015-06-19
Publication information: Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 2015; 28(9): 1174-84
Abstract: Ductal carcinoma in situ (DCIS) is a non-obligate precursor of invasive breast cancer and a frequent mammographic finding requiring treatment. Up to 25% of DCIS can recur and half of recurrences are invasive, but there are no reliable biomarkers for recurrence. We hypothesised that copy number aberrations could predict likelihood of recurrence. We analysed a cohort of pure DCIS cases treated only with wide local excision for genome-wide copy number and loss of heterozygosity using Affymetrix OncoScan MIP arrays. Cases included those without recurrence within 7 years (n = 25) and with recurrence between 1 and 5 years after diagnosis (n = 15). Pure DCIS were broadly similar in copy number changes compared with invasive breast cancer, with the consistent exception of a greater frequency of ERBB2 amplification in DCIS. There were no significant differences in age or ER status between the cases with a recurrence vs those without. Overall, the DCIS cases with recurrence had more copy number events than the DCIS without recurrence. The increased copy number appeared non-random with several genomic regions showing an increase in frequency in recurrent cases, including 20 q gain, ERBB2 amplification and 15q loss. Copy number changes may provide prognostic information for DCIS recurrence, but validation in additional cohorts is required.
DOI: 10.1038/modpathol.2015.75
ORCID: 0000-0003-3414-112X
PubMed URL: 26321097
Type: Journal Article
Appears in Collections:Journal articles

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