Nuclear EGFR contributes to acquired resistance to cetuximab
- Author
- LI, C1 ; IIDA, M1 ; DUNN, E. F1 ; GHIA, A. J1 ; WHEELER, D. L1
[1] Department of Human Oncology, University of Wisconsin School of Medicine and Public Health, Madison, WI, United States - Source
Oncogene (Basingstoke). 2009, Vol 28, Num 43, pp 3801-3813, 13 p ; ref : 1 p
- ISSN
- 0950-9232
- Scientific domain
- Cell biology, histology; Medical oncology; Genetics
- Publisher
- Nature Publishing Group, Basingstoke
- Publication country
- United Kingdom
- Document type
- Article
- Language
- English
- Author keyword
- EGFR cetuximab dasatinib nuclear resistance src-family kinases
- Keyword (fr)
- Anticancéreux Carcinogenèse Cétuximab Dasatinib Immunomodulateur Kinase Protein-tyrosine kinase Résistance Enzyme Transferases
- Keyword (en)
- Antineoplastic agent Carcinogenesis Cetuximab Dasatinib Immunomodulator Kinase Protein-tyrosine kinase Resistance Enzyme Transferases
- Keyword (es)
- Anticanceroso Carcinogénesis Cetuximab Dasatinib Inmunomodulador Kinase Protein-tyrosine kinase Resistencia Enzima Transferases
- Classification
- Pascal
- 002 Biological and medical sciences / 002A Fundamental and applied biological sciences. Psychology / 002A04 Molecular and cellular biology / 002A04H Cell physiology / 002A04H04 Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
- Discipline
- Molecular and cell biology
- Origin
- Inist-CNRS
- Database
- PASCAL
- INIST identifier
- 22098935
Sauf mention contraire ci-dessus, le contenu de cette notice bibliographique peut être utilisé dans le cadre d’une licence CC BY 4.0 Inist-CNRS / Unless otherwise stated above, the content of this bibliographic record may be used under a CC BY 4.0 licence by Inist-CNRS / A menos que se haya señalado antes, el contenido de este registro bibliográfico puede ser utilizado al amparo de una licencia CC BY 4.0 Inist-CNRS
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DOI
10.1038/onc.2009.234 
https://dx.doi.org/10.1038/onc.2009.234
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