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.

journal_name

Breast Cancer Res

authors

Brown WS,Wendt MK

doi

10.1186/s13058-014-0448-0

subject

Has Abstract

pub_date

2014-09-23 00:00:00

pages

448

issue

5

eissn

1465-5411

issn

1465-542X

pii

s13058-014-0448-0

journal_volume

16

pub_type

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