ArticleBreast cancer research and treatment1995
MCF-7 breast cancer cells overexpressing transfected c-erbB-2 have an in vitro growth advantage in estrogen-depleted conditions and reduced estrogen-dependence and tamoxifen-sensitivity in vivo.
Article in Breast cancer research and treatment, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 164 citations in OpenAlex.
- Review
- Review
- Fatty acid synthase regulates estrogen receptor-α signaling in breast cancer cells.Oncogenesis · 2017Article
- Oestrogen receptor negativity in breast cancer: a cause or consequence?Bioscience reports · 2016Review
- Prognostic Impact of HER2 and ER Status of Circulating Tumor Cells in Metastatic Breast Cancer Patients with a HER2-Negative Primary Tumor.Neoplasia (New York, N.Y.) · 2016Article
- Article
- Low Dose, Low Cost Estradiol Pellets Can Support MCF-7 Tumour Growth in Nude Mice without Bladder Symptoms.Journal of Cancer · 2015Article
- HER2 and uPAR cooperativity contribute to metastatic phenotype of HER2-positive breast cancer.Oncoscience · 2015Review
- Protein kinase D1 regulates ERα-positive breast cancer cell growth response to 17β-estradiol and contributes to poor prognosis in patients.Journal of cellular and molecular medicine · 2014Article
- ERBB2 overexpression suppresses stress-induced autophagy and renders ERBB2-induced mammary tumorigenesis independent of monoallelic Becn1 loss.Autophagy · 2014Article
- Modeling the estrogen receptor to growth factor receptor signaling switch in human breast cancer cells.FEBS letters · 2013Article
- The development, application and limitations of breast cancer cell lines to study tamoxifen and aromatase inhibitor resistance.The Journal of steroid biochemistry and molecular biology · 2012Review
- Clinical utility of the combination of lapatinib and letrozole in the management of hormone receptor-positive and HER2-positive advanced breast cancer.Breast cancer (Dove Medical Press) · 2011Review
- Adaptive changes result in activation of alternate signaling pathways and acquisition of resistance to aromatase inhibitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2011Article
- Dynamic modelling of oestrogen signalling and cell fate in breast cancer cells.Nature reviews. Cancer · 2011Review
- Article
- Status of HER-2/neu receptors and Ki-67 in breast cancer of Indian women.International journal of applied & basic medical research · 2011Article
- Somatic expression of PyMT or activated ErbB2 induces estrogen-independent mammary tumorigenesis.Neoplasia (New York, N.Y.) · 2010Article
- Epigenetic Reactivation of Estrogen Receptor: Promising Tools for Restoring Response to Endocrine Therapy.Molecular and cellular pharmacology · 2010Article
- Loss of HER2 amplification following trastuzumab-based neoadjuvant systemic therapy and survival outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2009Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
A c-erbB-2 expression vector was transfected into the estrogen receptor positive (ER+) MCF-7 human breast cancer cell line to determine if overexpression of this transmembrane tyrosine kinase could increase the malignant phenotype of this cell line. Loss of transfected c-erbB-2 expression was observed when cells were carried in medium containing estrogen. Homogeneous populations stably overexpressing levels of the 185 kDa c-erbB-2 observed in the SKBR-3 a breast cancer cell line which overexpresses c-erbB-2 as a result of gene amplification could be obtained by continually maintaining the transfected cell lines in estrogen-free conditions. Levels of constitutively activated c-erbB-2 varied among clonal isolates. Whereas some overexpressing lines did acquire the ability to form transient tumor nodules in ovariectomized nude mice without estrogen supplementation, as well as in mice that received the antiestrogen tamoxifen, one cell line that exhibited the highest levels of constitutively activated c-erbB-2 was able to form static tumors of a larger size under both conditions. This same cell line formed progressively growing tumors in estrogen-supplemented mice that were much larger than observed in mice injected with control cell lines, and also showed reduced sensitivity to antiestrogens in vitro, but it continued to have a low metastatic phenotype. These results suggest that signal transduction mediated by the c-erbB-2 tyrosine kinase can partially overcome the estrogen dependence of ER+breast cancer cells for growth and that c-erbB-2 overexpression confers a selective advantage to such cells in the absence of estrogen.
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Registered trials
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