Gee, J.M. and Howell, A. and Gullick, W.J. and Benz, C.C. and Sutherland, R.L. and Santen, R.J. and Martin, L.A. and Ciardiello, F. and Miller, W.R. and Dowsett, M. and Barrett-Lee, P. and Robertson, J.F. and Johnston, S.R. and Jones, H.E. and Wakeling, A.E. and Duncan, R. and Nicholson, R.I. (2005) Consensus statement. Workshop on therapeutic resistance in breast cancer: impact of growth factor signalling pathways and implications for future treatment. Endocrine-Related Cancer, 12 (Suppl 1). S1-7. ISSN 1351-0088 .
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Anti-hormones (notably tamoxifen), chemotherapy and modern radiotherapeutic approaches are invaluable in the management of breast cancer, and collectively have contributed substantially to the improved survival in this disease. Moreover, there is promise that these successes will continue with the emergence of other endocrine agents (for example, aromatase inhibitors and pure anti-oestrogens). However, de novo and acquired resistance comprises a significant problem with all treatment approaches examined to date. This Workshop aimed to evaluate the contribution made by growth factor signalling pathways in the various resistant states, primarily focusing on resistance to anti-hormonal strategies and spanning experimental models and, where possible, clinical breast cancer data. The successes and limitations of therapeutic targeting of these pathways with various signal transduction inhibitors (STIs) were evaluated in model systems and from emerging clinical trials (including epidermal growth factor receptor inhibitors such as gefitinib). It was concluded that growth factor signalling is an important contributor in the development of endocrine resistance in breast cancer and that use of STIs provides a promising therapeutic strategy for this disease. However, the cancer cell is clearly able to harness alternative growth factor signalling pathways for growth and cell survival in the presence of STI monotherapy and, as a consequence, the efficacy of STIs is likely to be limited by the acquisition of resistance. A number of strategies were proposed from studies in model systems that appeared to enhance anti-tumour actions of existing STI monotherapy, notably including combination therapies targeting multiple pathways. With the increased availability of diverse STIs and improved drug delivery, there is much hope that the more complex therapeutic strategies proposed may ultimately be achievable in clinical practice.
|Additional information:||Research Support, Non-U.S. Gov't Review|
|Uncontrolled keywords:||Breast Neoplasms/*drug therapy Drug Resistance, Neoplasm Drug Therapy, Combination Female Growth Inhibitors/*therapeutic use Hormone Antagonists/*therapeutic use Humans *Signal Transduction/drug effects|
R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
|Divisions:||Faculties > Science Technology and Medical Studies > School of Biosciences > Biomedical Research Group|
|Depositing User:||Bill Gullick|
|Date Deposited:||01 Sep 2008 20:22|
|Last Modified:||05 Sep 2011 23:34|
|Resource URI:||http://kar.kent.ac.uk/id/eprint/3974 (The current URI for this page, for reference purposes)|
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