Molecular markers and therapeutic targets in ductal carcinoma in situ
Version of Record online: 19 SEP 2002
Copyright © 2002 Wiley-Liss, Inc.
Microscopy Research and Technique
Special Issue: Histology and Cell Biology of Breast Cancer—Part I
Volume 59, Issue 1, pages 3–11, 1 October 2002
How to Cite
Boland, G. P., Knox, W. F. and Bundred, N. J. (2002), Molecular markers and therapeutic targets in ductal carcinoma in situ. Microsc. Res. Tech., 59: 3–11. doi: 10.1002/jemt.10172
- Issue online: 19 SEP 2002
- Version of Record online: 19 SEP 2002
- Manuscript Accepted: 29 OCT 2001
- Manuscript Received: 16 AUG 2001
- Royal College of Surgeons of England
- breast cancer;
Ductal carcinoma in situ (DCIS) of the breast is a premalignant condition which accounts for approximately 20% of all new breast cancers and up to 40% of neoplastic lesions detected by mammographic screening. Since recurrence is common after DCIS treated with breast conservation surgery, there is a need to determine molecular factors that predict recurrence. In parallel with this and with the finding that oestrogen receptor (ER) positive breast cancer can be prevented with anti-oestrogens, there have been recent advances in the understanding of the molecular biology of DCIS. Receptor coexpression in DCIS has been determined largely by immunohistochemistry. Animal models have provided evidence for the signalling pathways involved in the regulation and dysregulation of proliferation and apoptosis in both normal breast and in situ cancer. ER-negative DCIS has been shown to be hormone-independent. Blockade of the pathways involved in cell proliferation in ER-negative DCIS is possible and will be necessary to prevent ER-negative breast cancers if the goal of breast cancer chemoprevention is to be realistically achieved. Microsc. Res. Tech. 59:3–11, 2002. © 2002 Wiley-Liss, Inc.