Literature DB >> 15355892

HER-2 amplification, HER-1 expression, and tamoxifen response in estrogen receptor-positive metastatic breast cancer: a southwest oncology group study.

Grazia Arpino1, Stephanie J Green, D Craig Allred, Dannika Lew, Silvana Martino, C Kent Osborne, Richard M Elledge.   

Abstract

PURPOSE: Preclinical data indicate that expression of the ErbB family of receptors, such as HER-2 and HER-1 (EGFR) may be involved in endocrine resistance. Evidence of resistance from clinical studies has been inconsistent. The present study examined whether HER-2 gene amplification or HER-1 expression predicted response to tamoxifen. PATIENTS AND METHODS: Three hundred and forty nine patients had estrogen receptor (ER)-positive breast cancer and received daily tamoxifen as initial therapy for advanced disease. HER-2 gene amplification, detected by fluorescence in situ hybridization, and HER-1 expression, evaluated by immunohistochemistry, was determined on 136 and 204 patients, respectively.
RESULTS: HER-2 amplification was correlated with lower ER (P = 0.02), HER-1 positivity (P = 0.004), and HER-2 protein overexpression (P < 0.00001). The response rate was 56% for HER-2 non-amplified versus 47% for HER-2 amplified tumors (P = 0.38), and 58% for HER-1-negative versus 36% for HER-1-positive (P = 0.05). Time to treatment failure (TTF) was 7 months for non-amplified HER-2 tumors and 5 months (P = 0.007) for amplified HER-2 tumors, and there was a trend toward a better overall survival (OS) in patients with non-amplified HER-2 tumors (median 31 versus 25 months, respectively, P = 0.07). For positive versus negative HER-1 tumors, TTF was 4 versus 8 months (P = 0.08) and median survival was 24 versus 31 months (P = 0.41). Combining HER-1 expression and HER-2 gene status, patients with both negative HER-1 expression and non-amplified HER-2 had longer TTF (P = 0.001) and OS (P = 0.03) than if either were positive. In multivariate analysis, HER-2 was not an independent factor for TTF and OS, although HER-1 was significant for TTF only (P </= 0.001).
CONCLUSION: Patients with HER-2 amplification and HER-1 expression had lower ER levels and were modestly less responsive to tamoxifen, suggesting that molecular events in addition to those involving the ErbB receptors are important in determining the endocrine-resistant phenotype.

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Year:  2004        PMID: 15355892     DOI: 10.1158/1078-0432.CCR-04-0110

Source DB:  PubMed          Journal:  Clin Cancer Res        ISSN: 1078-0432            Impact factor:   12.531


  83 in total

1.  Hyperactivation of phosphatidylinositol-3 kinase promotes escape from hormone dependence in estrogen receptor-positive human breast cancer.

Authors:  Todd W Miller; Bryan T Hennessy; Ana M González-Angulo; Emily M Fox; Gordon B Mills; Heidi Chen; Catherine Higham; Carlos García-Echeverría; Yu Shyr; Carlos L Arteaga
Journal:  J Clin Invest       Date:  2010-06-07       Impact factor: 14.808

2.  The tumor microenvironment modulates tamoxifen resistance in breast cancer: a role for soluble stromal factors and fibronectin through β1 integrin.

Authors:  Osvaldo Pontiggia; Rocio Sampayo; Diego Raffo; Andrea Motter; Ren Xu; Mina J Bissell; Elisa Bal de Kier Joffé; Marina Simian
Journal:  Breast Cancer Res Treat       Date:  2011-09-21       Impact factor: 4.872

Review 3.  Minireview: Inflammation: an instigator of more aggressive estrogen receptor (ER) positive breast cancers.

Authors:  Sarah C Baumgarten; Jonna Frasor
Journal:  Mol Endocrinol       Date:  2012-02-02

4.  Amplification of thymidylate synthetase in metastatic colorectal cancer patients pretreated with 5-fluorouracil-based chemotherapy.

Authors:  Roshawn G Watson; Filipe Muhale; Leigh B Thorne; Jinsheng Yu; Bert H O'Neil; Janelle M Hoskins; Michael O Meyers; Allison M Deal; Joseph G Ibrahim; Michael L Hudson; Christine M Walko; Howard L McLeod; James T Auman
Journal:  Eur J Cancer       Date:  2010-08-18       Impact factor: 9.162

Review 5.  Overcoming endocrine resistance in metastatic breast cancer: Current evidence and future directions.

Authors:  Andrea Milani; Elena Geuna; Gloria Mittica; Giorgio Valabrega
Journal:  World J Clin Oncol       Date:  2014-12-10

Review 6.  Pathways to tamoxifen resistance.

Authors:  Rebecca B Riggins; Randy S Schrecengost; Michael S Guerrero; Amy H Bouton
Journal:  Cancer Lett       Date:  2007-05-01       Impact factor: 8.679

7.  Leptin increases HER2 protein levels through a STAT3-mediated up-regulation of Hsp90 in breast cancer cells.

Authors:  Cinzia Giordano; Donatella Vizza; Salvatore Panza; Ines Barone; Daniela Bonofiglio; Marilena Lanzino; Diego Sisci; Francesca De Amicis; Suzanne A W Fuqua; Stefania Catalano; Sebastiano Andò
Journal:  Mol Oncol       Date:  2012-11-23       Impact factor: 6.603

8.  Estrogen receptor-α36 is involved in development of acquired tamoxifen resistance via regulating the growth status switch in breast cancer cells.

Authors:  Guangliang Li; Jing Zhang; Ketao Jin; Kuifeng He; Yi Zheng; Xin Xu; Haohao Wang; Haiyong Wang; Zhongqi Li; Xiongfei Yu; Xiaodong Teng; Jiang Cao; Lisong Teng
Journal:  Mol Oncol       Date:  2013-02-26       Impact factor: 6.603

9.  Epidermal growth factor receptor expression in breast cancer association with biologic phenotype and clinical outcomes.

Authors:  Mothaffar F Rimawi; Priya B Shetty; Heidi L Weiss; Rachel Schiff; C Kent Osborne; Gary C Chamness; Richard M Elledge
Journal:  Cancer       Date:  2010-03-01       Impact factor: 6.860

10.  Overcoming Tamoxifen Resistance of Human Breast Cancer by Targeted Gene Silencing Using Multifunctional pRNA Nanoparticles.

Authors:  Yijuan Zhang; Marissa Leonard; Yi Shu; Yongguang Yang; Dan Shu; Peixuan Guo; Xiaoting Zhang
Journal:  ACS Nano       Date:  2016-12-16       Impact factor: 15.881

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