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Breast Cancer Res. 2014 Sep 23;16(5):448. doi: 10.1186/s13058-014-0448-0.

Integrin-mediated resistance to epidermal growth factor receptor-targeted therapy: an inflammatory situation.

Abstract

Targeting the function of epidermal growth factor receptor (EGFR) has failed as an effective clinical option for breast cancer. Understanding the drivers of inherent resistance has been a challenge. One possible mechanism is the acquisition of stem-like properties through the process of epithelial-mesenchymal transition. A recent study by Seguin and colleagues adds to our understanding of this process by demonstrating a functional role for unligated αvβ3 integrin in mediating a stem-like phenotype and facilitating resistance to EGFR-targeted therapy via enhanced downstream coupling to a KRAS:RalB:NF-κB pathway. Importantly, the identified mechanism may reveal a possible strategy for sensitizing breast cancer cells to EGFR-targeted therapies.

PMID:
25255930
PMCID:
PMC4728772
DOI:
10.1186/s13058-014-0448-0
[Indexed for MEDLINE]
Free PMC Article

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