Inverse regulation of EGFR/HER1 and HER2-4 in normal and malignant human breast tissue

Cross-talk between the estrogen and the EGFR/HER signalling pathways has been suggested as a potential cause of resistance to endocrine therapy in breast cancer. Here, we determined HER1-4 receptor and neuregulin-1 (NRG1) ligand mRNA expression levels in breast cancers and corresponding normal breas...

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Veröffentlicht in:	PloS one 2013-08, Vol.8 (8), p.e74618-e74618
Hauptverfasser:	Flågeng, Marianne Hauglid, Knappskog, Stian, Haynes, Ben P, Lønning, Per Eystein, Mellgren, Gunnar
Format:	Artikel
Sprache:	eng
Schlagworte:	17β-Estradiol Adult Aged Aged, 80 and over Base Sequence Breast - metabolism Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Cancer therapies Cancer treatment Comparative analysis Correlation Deoxyribonucleic acid DNA DNA Primers Endocrine therapy Epidermal growth factor Epidermal growth factor receptors ErbB-2 protein Estradiol Estrogen receptors Estrogens Female Gene amplification Gene expression Gene Expression Regulation, Neoplastic Genes Genes, erbB-2 Health aspects Humans Kinases Laboratories Metastasis Middle Aged Neuregulin Neuregulin 1 Oncology Patients Post-menopause Postmenopausal women Protein expression Real-Time Polymerase Chain Reaction Receptor, Epidermal Growth Factor - genetics Receptor, ErbB-3 - genetics Receptor, ErbB-4 RNA Sex hormones Signal transduction Signaling Tumors Womens health
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Zusammenfassung:	Cross-talk between the estrogen and the EGFR/HER signalling pathways has been suggested as a potential cause of resistance to endocrine therapy in breast cancer. Here, we determined HER1-4 receptor and neuregulin-1 (NRG1) ligand mRNA expression levels in breast cancers and corresponding normal breast tissue from patients previously characterized for plasma and tissue estrogen levels. In tumours from postmenopausal women harbouring normal HER2 gene copy numbers, we found HER2 and HER4, but HER3 levels in particular, to be elevated (2.48, 1.30 and 22.27 -fold respectively; P
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0074618