101. Change in expression of epidermal growth factor receptor and c-erb-B2 during the development of tamoxifen resistance in human breast cancer

Newby, Jacqueline C.; Johnston, Stephen; Smith, Ian; Dowsett, Mitch

doi:10.1016/0960-9776(95)90193-0

Cited by 73 publications

(82 citation statements)

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“…It has been demonstrated that patients who had either EGF receptorpositive and/or c-erbB2-positive disease had a significantly lower response rate to endocrine therapy than those who were negative for both (Newby et al, 1997). The overexpression of c-erbB2 may result in some oestrogenic growth factor pathways becoming independent of the ER, and explain our observations of relative resistance to endocrine therapy in such cases.…”

Section: Discussionsupporting

confidence: 46%

Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

et al. 1999

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The present study investigated the interaction between c-erbB2 overexpression and the response to first-line endocrine therapy in patients with advanced breast cancer. The primary tumours of 241 patients who were treated at first relapse with endocrine therapy were assessed for overexpression of c-erbB2 by immunohistochemistry. c-erbB2 was overexpressed in 76 (32%) of primary breast cancers and did not correlate with any other prognostic factor. The overall response to treatment and time to progression were significantly lower in patients with c-erbB2-positive tumours compared to those that were c-erbB2-negative (38% vs 56%, P = 0.02; and 4.1 months vs 8.7 months, P < 0.001, respectively). In multivariate analysis, c-erbB2 status was the most significant predictive factor for a short time to progression ( P = 0.0009). In patients with ER-positive primary tumours treated at relapse with tamoxifen ( n = 170), overexpression of c-erbB2 was associated with a significantly shorter time to progression (5.5 months vs 11.2 months, P < 0.001). In conclusion, overexpression of c-erbB2 in the primary tumour is an independent marker of relative resistance to first-line endocrine therapy in patients with advanced breast cancer. In patients with ER-positive primary tumours, the overexpression of c-erbB2 defines a subgroup less likely to respond to endocrine therapy. © 1999 Cancer Research Campaign

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Section: Discussionsupporting

confidence: 46%

Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

et al. 1999

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“…It is therefore a possibility that HER2 may contribute to acquired resistance by becoming overexpressed during the period of endocrine treatment, and thereby providing an alternative pathway for autonomous tumor growth. At our institution HER2 status was assessed in 155 patients who were progressing on tamoxifen treatment (Newby et al 1997). Marginally higher levels of HER2 positivity were present in samples taken from patients who were progressing on tamoxifen compared with untreated tumors.…”

Section: Peptide Growth Factor Signalling Pathwaymentioning

confidence: 99%

Mechanisms of tamoxifen resistance

Ring

Dowsett²

2004

Endocr Relat Cancer

552

472

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The anti-oestrogen tamoxifen is the most commonly used treatment for patients with oestrogenreceptor (ER)-positive breast cancer. Although many patients benefit from tamoxifen in the adjuvant and metastatic settings, resistance is an important clinical problem. The target of tamoxifen in vivo is the ER. Over the last decade many advances have been made in our understanding of the biology of the ER which may help to explain how resistance to tamoxifen develops. Such mechanisms may include changes in the expression of ERa or ERb, alterations in co-regulatory proteins, and the influences of cellular kinase signal transduction pathways. The experimental and clinical evidence supporting these mechanisms of tamoxifen resistance are discussed in this review.

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“…Preclinical studies have demonstrated that EGFR-TKI therapy reduces proliferation and increases apoptosis in the epithelium, and, either alone or combined with antiestrogen therapy, EGFR-TKI may represent a novel form of chemoprevention. Clinical trials should investigate evidence that breast cancers that have become tamoxifen-resistant use the EGFR signalling pathway which would suggest that the combination of tamoxifen and Iressa would be potent at chemopreventing cancer [111].…”

Section: New Agents and New Strategies For Medical Treatment?mentioning

confidence: 99%

The management of ductal intraepithelial neoplasia (DIN): open controversies and guidelines of the Istituto Europeo di Oncologia (IEO), Milan, Italy

Farante

Zurrida

Galimberti

et al. 2010

Breast Cancer Res Treat

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101. Change in expression of epidermal growth factor receptor and c-erb-B2 during the development of tamoxifen resistance in human breast cancer

Cited by 73 publications

References 0 publications

Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

Overexpression of c-erbB2 is an independent marker of resistance to endocrine therapy in advanced breast cancer

Mechanisms of tamoxifen resistance

The management of ductal intraepithelial neoplasia (DIN): open controversies and guidelines of the Istituto Europeo di Oncologia (IEO), Milan, Italy

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