Anthony J Maxwell1, Karen Clements2, Bridget Hilton3, David J Dodwell4, Andrew Evans5, Olive Kearins6, Sarah E Pinder7, Jeremy Thomas8, Matthew G Wallis9, Alastair M Thompson10. 1. Nightingale Centre, Wythenshawe Hospital, Manchester, M23 9LT, UK; Division of Informatics, Imaging & Data Sciences, School of Health Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester, M13 9PT, UK. Electronic address: anthony.maxwell@manchester.ac.uk. 2. Screening Quality Assurance Service (Midlands and East), Public Health England, 1st Floor, 5 St Philip's Place, Birmingham, B3 2PW, UK. Electronic address: karen.clements@phe.gov.uk. 3. Screening Quality Assurance Service (Midlands and East), Public Health England, 1st Floor, 5 St Philip's Place, Birmingham, B3 2PW, UK. Electronic address: bridget.hilton@phe.gov.uk. 4. Nuffield Department of Population Health, University of Oxford, Richard Doll Building, Old Road Campus, Oxford, OX3 7LF, UK. Electronic address: david.dodwell@nhs.net. 5. Ninewells Hospital and Medical School, Mailbox 4, Level 6, Dundee, DD1 9SY, UK. Electronic address: a.z.evans@dundee.ac.uk. 6. Screening Quality Assurance Service (Midlands and East), Public Health England, 1st Floor, 5 St Philip's Place, Birmingham, B3 2PW, UK. Electronic address: olive.kearins@phe.gov.uk. 7. Cancer Studies, King's College London, 9th Floor, Innovation Hub, Comprehensive Cancer Centre, Guy's Hospital, Great Maze Pond, London, SE1 9RT, UK. Electronic address: sarah.pinder@kcl.ac.uk. 8. Department of Pathology, Western General Hospital, Edinburgh, EH4 2XU, UK. Electronic address: jeremy.thomas@luht.scot.nhs.uk. 9. Cambridge Breast Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge & NIHR Cambridge Biomedical Research Centre, Cambridge, CB2 0QQ, UK. Electronic address: matthew.wallis@addenbrookes.nhs.uk. 10. Department of Breast Surgical Oncology, University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA. Electronic address: AThompson1@mdanderson.org.
Abstract
BACKGROUND: The natural history of ductal carcinoma in situ (DCIS) remains uncertain. The risk factors for the development of invasive cancer in unresected DCIS are unclear. METHODS: Women diagnosed with DCIS on needle biopsy after 1997 who did not undergo surgical resection for ≥1 year after diagnosis were identified by breast centres and the cancer registry and outcomes were reviewed. RESULTS: Eighty-nine women with DCIS diagnosed 1998-2010 were identified. The median age at diagnosis was 75 (range 44-94) years with median follow-up (diagnosis to death, invasive disease or last review) of 59 (12-180) months. Twenty-nine women (33%) developed invasive breast cancer after a median interval of 45 (12-144) months. 14/29 (48%) with high grade, 10/31 (32%) with intermediate grade and 3/17 (18%) with low grade DCIS developed invasive cancer after median intervals of 38, 60 and 51 months. The cumulative incidence of invasion was significantly higher in high grade DCIS than other grades (p = .0016, log-rank test). Invasion was more frequent in lesions with calcification as the predominant feature (23/50 v. 5/25; p = .042) and in younger women (p = .0002). Endocrine therapy was associated with a lower rate of invasive breast cancer (p = .048). CONCLUSIONS: High cytonuclear grade, mammographic microcalcification, young age and lack of endocrine therapy were risk factors for DCIS progression to invasive cancer. Surgical excision of high grade DCIS remains the treatment of choice. Given the uncertain long-term natural history of non-high grade DCIS, the option of active surveillance of women with this condition should be offered within a clinical trial. Crown
BACKGROUND: The natural history of ductal carcinoma in situ (DCIS) remains uncertain. The risk factors for the development of invasive cancer in unresected DCIS are unclear. METHODS:Women diagnosed with DCIS on needle biopsy after 1997 who did not undergo surgical resection for ≥1 year after diagnosis were identified by breast centres and the cancer registry and outcomes were reviewed. RESULTS: Eighty-nine women with DCIS diagnosed 1998-2010 were identified. The median age at diagnosis was 75 (range 44-94) years with median follow-up (diagnosis to death, invasive disease or last review) of 59 (12-180) months. Twenty-nine women (33%) developed invasive breast cancer after a median interval of 45 (12-144) months. 14/29 (48%) with high grade, 10/31 (32%) with intermediate grade and 3/17 (18%) with low grade DCIS developed invasive cancer after median intervals of 38, 60 and 51 months. The cumulative incidence of invasion was significantly higher in high grade DCIS than other grades (p = .0016, log-rank test). Invasion was more frequent in lesions with calcification as the predominant feature (23/50 v. 5/25; p = .042) and in younger women (p = .0002). Endocrine therapy was associated with a lower rate of invasive breast cancer (p = .048). CONCLUSIONS: High cytonuclear grade, mammographic microcalcification, young age and lack of endocrine therapy were risk factors for DCIS progression to invasive cancer. Surgical excision of high grade DCIS remains the treatment of choice. Given the uncertain long-term natural history of non-high grade DCIS, the option of active surveillance of women with this condition should be offered within a clinical trial. Crown
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