Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Cooke, T.
Right arrow Articles by Stanton, P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cooke, T.
Right arrow Articles by Stanton, P.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Annals of Oncology 12:S23-S28, 2001
© 2001 European Society for Medical Oncology


Symposium Article

HER2 as a prognostic and predictive marker for breast cancer

T. Cooke, J. Reeves, A. Lanigan and P. Stanton

University Department of Surgery, Royal Infirmary Glasgow, UK

Correspondence to: T. Cooke, MD University Department of Surgery Royal Infirmary Queen Elizabeth Building Alexandra Parade Glasgow G31 2ER UK E-mail: t.cooke{at}clinmed.gla.ac.uk

In recent years investigators have looked at the human epidermal growth factor receptor-2 (HER2), which is overexpressed in 20%–30% of breast cancer patients, with regard to its role as a prognostic and predictive factor. Although many studies have suggested that HER2 overexpression may be associated with a poor clinical outcome, other studies have not fully supported this observation. The inconsistencies between studies may be due in part to discrepancies between different HER2 testing methods. To overcome this problem, a radioimmuno-histochemical method was developed to quantitatively measure HER2 overexpression levels in breast tumor samples. The application of this method demonstrated that 85% of all breast tumor samples expressed HER2 at levels greater than normal. Of these, 23% expressed HER2 at levels between 45 and 480 times greater than normal, and this was associated with poor clinical outcome. The investigation of HER2 status as a predictor of response to therapy has also yielded many conflicting results. Overall, it appears that HER2 overexpression may correlate with resistance to hormonal therapy, sensitivity to anthracycline-based chemotherapy and resistance to CMF. With the development of targeted anti-HER2 therapies, assessment of HER2 status will be important in stratifying patients to the most appropriate treatment regimens.

breast cancer, HER2, prognostic factor, predictor


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Ann OncolHome page
J. F. R. Robertson, G. G. Steger, P. Neven, S. Barni, F. Gieseking, F. Nole, K. I. Pritchard, F. P. O'Malley, S. D. Simon, B. Kaufman, et al.
Activity of fulvestrant in HER2-overexpressing advanced breast cancer
Ann. Onc., October 29, 2009; (2009) mdp447v1.
[Abstract] [Full Text] [PDF]


Home page
J Hand Surg Eur VolHome page
O. A. ANAKWENZE, W. L. PARKER, L. E. WOLD, K. K AMRAMI, and P. C. AMADIO
Ewing's Sarcoma of the Hand
J Hand Surg Eur Vol., February 1, 2009; 34(1): 35 - 39.
[Abstract] [Full Text] [PDF]


Home page
Endocr Relat CancerHome page
P Kauraniemi and A Kallioniemi
Activation of multiple cancer-associated genes at the ERBB2 amplicon in breast cancer.
Endocr. Relat. Cancer, March 1, 2006; 13(1): 39 - 49.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.