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. 2016 Sep 12;3(6):e1232186.
doi: 10.1080/23723556.2016.1232186. eCollection 2016.

A phenotypic and mechanistic perspective on heterogeneity of HER2-positive breast cancers

Affiliations

A phenotypic and mechanistic perspective on heterogeneity of HER2-positive breast cancers

Anthony Ferrari et al. Mol Cell Oncol. .

Abstract

Analysis of gene expression and whole-genome features of 64 human epidermal growth factor 2 (HER2)-positive breast tumors supports the idea that their intrinsic heterogeneity actually reflects their cell of origin, suggesting that HER2 amplification is an embedded event in the natural history of these tumors. Possible mechanisms for this event involve breakage-fusion-bridge and chromothripsis.

Keywords: Breakage-Fusion-Bridge; Breast cancer; ERBB2 amplification; cancer genomics; mammary epithelial hierarchy.

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Figures

Figure 1.
Figure 1.
Mammary epithelial hierarchy and genomic features of epidermal growth factor 2-positive breast cancer. From left to right: developmental stage of normal epithelial mammary cells; amplification events: erb-b2 receptor tyrosine kinase 2 (ERBB2), cyclin D1 (CCND1), and zinc finger protein 703 (ZNF703); RNA expression groups (A, B, C, and D); PAM50 intrinsic subtypes (luminal A, luminal B, HER2-enriched, and basal); genomic features: fraction of genome altered (FGA); mutations in tumor protein p53 (TP53) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit α (PIK3CA).

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