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Growth factor signalling and response to endocrine therapy: the Royal Marsden Experience.

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Date
2005-07
ICR Author
Smith, Ian
Johnston, Stephen
Martin, Lesley-Ann
Dowsett, Mitch
Author
Dowsett, M
Johnston, S
Martin, L-A
Salter, J
Hills, M
Detre, S
Gutierrez, MC
Mohsin, SK
Shou, J
Allred, DC
Schiff, R
Osborne, CK
Smith, I
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Type
Journal Article
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Abstract
De novo resistance to endocrine therapy is a near-universal feature of oestrogen receptor (ER)- negative breast cancer. Although many ER-positive breast cancers also show no response to tamoxifen or aromatase inhibitors on objective clinical grounds the large majority show reduced proliferation indicating that some oestrogen dependence is present in almost all ER-positive breast cancer. In neoadjuvant studies HER2 positivity is associated with poor response rates to tamoxifen but not aromatase inhibitors, consistent with preclinical models. Acquired resistance to tamoxifen is associated with decreases in ER positivity but most recurrent lesions remain ER-positive. A small proportion of these show increased HER2 expression and in these patients increased phospho-p38 may contribute to the tamoxifen-resistant phenotype. There is an unfortunate paucity of clinical and biological data on acquired resistance to aromatase inhibitors.
URI
https://repository.icr.ac.uk/handle/internal/2043
DOI
https://doi.org/10.1677/erc.1.01044
Collections
  • Breast Cancer Research
  • Clinical Studies
  • Molecular Pathology
Subject
Humans
Breast Neoplasms
Neoplasms, Hormone-Dependent
Tamoxifen
Receptor, erbB-2
Receptors, Estrogen
Antineoplastic Agents, Hormonal
Aromatase Inhibitors
Estrogens
Signal Transduction
Drug Resistance, Neoplasm
Female
Research team
Endocrine Therapy Resistance
Medicine (RMH Smith Cunningham)
Endocrinology
Language
eng
License start date
2005-07
Citation
Endocrine-related cancer, 2005, 12 Suppl 1 pp. S113 - S117

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