Title |
Integrin-mediated resistance to epidermal growth factor receptor-targeted therapy: an inflammatory situation
|
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Published in |
Breast Cancer Research, September 2014
|
DOI | 10.1186/s13058-014-0448-0 |
Pubmed ID | |
Authors |
Wells S Brown, Michael K Wendt |
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. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 19 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Master | 6 | 32% |
Student > Bachelor | 3 | 16% |
Student > Ph. D. Student | 3 | 16% |
Professor | 2 | 11% |
Student > Doctoral Student | 1 | 5% |
Other | 1 | 5% |
Unknown | 3 | 16% |
Readers by discipline | Count | As % |
---|---|---|
Biochemistry, Genetics and Molecular Biology | 6 | 32% |
Agricultural and Biological Sciences | 5 | 26% |
Medicine and Dentistry | 2 | 11% |
Pharmacology, Toxicology and Pharmaceutical Science | 1 | 5% |
Psychology | 1 | 5% |
Other | 1 | 5% |
Unknown | 3 | 16% |