Epidermal growth factor receptor expression in breast cancer: Association with response to endocrine therapy

Nicholson, Robert Ian; McClelland, Richard Andrew; Gee, Julia Margaret Wendy; Manning, David L.; Cannon, P.; Robertson, J. F. R.; Ellis, Ian O.; Blamey, R.W.

doi:10.1007/bf00666187

Cited by 179 publications

(107 citation statements)

References 14 publications

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“…This probably reflects the inverse relationship between EGFR and ERα expression that has been demonstrated in several studies on both cell lines and clinical material (Sainsbury et al 1985, Davidson et al 1987, Klijn et al 1994, Larsen et al 1999) and found to be associated with progression towards estrogen-independence and lack of response to endocrine therapy (Harris et al 1989, Nicholson et al 1994). In the estrogen-independent LCC cell system, however, the basal expression level of EGFR in MCF-7/LCC1 is dramatically increased compared with MCF-7 (DCS) but without a concomitant decrease in ERα mRNA level.…”

Section: Discussionmentioning

confidence: 79%

Validation of real-time RT-PCR for analysis of human breast cancer cell lines resistant or sensitive to treatment with antiestrogens.

Crémoux

Tran-Perennou²,

Brockdorff³

et al. 2003

Endocrine-Related Cancer

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Using a quantitative real-time RT-PCR technique we have compared the expression of a number of genes in two different human breast cancer model systems for development of acquired resistance to antiestrogens. The model system developed at the Danish Cancer Society comprises the cell lines MCF-7, MCF-7/TAM R -1, MCF-7/182 R -6 and MCF-7/182 R -7, and the model system developed at the Lombardi Cancer Research Center consists of the cell lines MCF-7/LCC1, MCF-7/LCC2 and MCF-7/ LCC9. The findings on the well-known parameters estrogen receptor (ER)α, progesterone receptor (PR) and epidermal growth factor receptor (EGFR) are in good agreement with previous reports, thus documenting the usefulness of the real-time RT-PCR technique for multiparametric RNA analysis. The gene expression levels in the two model systems were found to be quite similar in relation to ERα, AIB1 (amplified in breast cancer-1), breast cancer antiestrogen resistance gene 1 (BCAR1) and ErbB-2 mRNA expression, whereas significant differences were observed on the expression of ERβ, multidrug resistance gene 1 (MDR1), PR and EGFR. Furthermore, the presented data suggest that ERβ, AIB1, BCAR1, CYP19 and MDR1 are unlikely to be causally involved in development of antiestrogen resistance in these breast cancer cell lines.

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Section: Discussionmentioning

confidence: 79%

Validation of real-time RT-PCR for analysis of human breast cancer cell lines resistant or sensitive to treatment with antiestrogens.

Crémoux

Tran-Perennou²,

Brockdorff³

et al. 2003

Endocrine-Related Cancer

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show abstract

“…Furthermore, Watanabe and co-workers described a correlation between HER2 overexpression and the absence of estrogen receptors in breast carcinomas which is consistent with the non-responsiveness of HER2-positive tumours to endocrine therapy (Watanabe et al 1993, Nicholson et al 1994, Wright et al 1989.…”

Section: Egfr and Her2 Gene Aberrations In Human Cancersmentioning

confidence: 72%

The epidermal growth factor receptor family as a central element for cellular signal transduction and diversification.

Prenzel¹,

Fischer²,

Streit³

et al. 2001

Endocrine-Related Cancer

594

471

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Homeostasis of multicellular organisms is critically dependent on the correct interpretation of the plethora of signals which cells are exposed to during their lifespan. Various soluble factors regulate the activation state of cellular receptors which are coupled to a complex signal transduction network that ultimately generates signals defining the required biological response. The epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases represents both key regulators of normal cellular development as well as critical players in a variety of pathophysiological phenomena. The aim of this review is to give a broad overview of signal transduction networks that are controlled by the EGFR superfamily of receptors in health and disease and its application for target-selective therapeutic intervention. Since the EGFR and HER2 were recently identified as critical players in the transduction of signals by a variety of cell surface receptors, such as G-protein-coupled receptors and integrins, our special focus is the mechanisms and significance of the interconnectivity between heterologous signalling systems.

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“…The epidermal growth factor receptor (EGFR) 2 is considered a major oncogenic factor, and its presence in tumors is indicative of poor prognosis (1,2). EGFRs not only modulate growth properties of transformed cells but are causally involved in survival signaling, cell migration, angiogenesis, and metastasis (3)(4)(5).…”

mentioning

confidence: 99%

ADP-ribosylation Factor 1 Controls the Activation of the Phosphatidylinositol 3-Kinase Pathway to Regulate Epidermal Growth Factor-dependent Growth and Migration of Breast Cancer Cells

Boulay

Cotton

Melançon

et al. 2008

Journal of Biological Chemistry

110

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Activation of intracellular signaling pathways by growth factors is one of the major causes of cancer development and progression. Recent studies have demonstrated that monomeric G proteins of the Ras family are key regulators of cell proliferation, migration, and invasion. Using an invasive breast cancer cell lines, we demonstrate that the ADP-ribosylation factor 1 (ARF1), a small GTPase classically associated with the Golgi, is an important regulator of the biological effects induced by epidermal growth factor. Here, we show that this ARF isoform is activated following epidermal growth factor stimulation and that, in MDA-MB-231 cells, ARF1 is found in dynamic plasma membrane ruffles. Inhibition of endogenous ARF1 expression results in the inhibition of breast cancer cell migration and proliferation. The underlying mechanism involves the activation of the phosphatidylinositol 3-kinase pathway. Our data demonstrate that depletion of ARF1 markedly impairs the recruitment of the phosphatidylinositol 3-kinase catalytic subunit (p110␣) to the plasma membrane, and the association of the regulatory subunit (p85␣) to the activated receptor. These results uncover a novel molecular mechanism by which ARF1 regulates breast cancer cell growth and invasion during cancer progression.

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Epidermal growth factor receptor expression in breast cancer: Association with response to endocrine therapy

Cited by 179 publications

References 14 publications

Validation of real-time RT-PCR for analysis of human breast cancer cell lines resistant or sensitive to treatment with antiestrogens.

Validation of real-time RT-PCR for analysis of human breast cancer cell lines resistant or sensitive to treatment with antiestrogens.

The epidermal growth factor receptor family as a central element for cellular signal transduction and diversification.

ADP-ribosylation Factor 1 Controls the Activation of the Phosphatidylinositol 3-Kinase Pathway to Regulate Epidermal Growth Factor-dependent Growth and Migration of Breast Cancer Cells

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