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Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

Cetuximab insufficiently inhibits glioma cell growth due to persistent EGFR downstream signaling

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  1. Biomarkers in Recurrent Grade III Glioma Patients Treated with Bevacizumab and Irinotecan

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Outcome of Bevacizumab Therapy in Patients with Recurrent Glioblastoma Treated with Angiotensin System Inhibitors

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. The effect of adenovirus-mediated gene expression of FHIT in small cell lung cancer cells

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Improved response by co-targeting EGFR/EGFRvIII and Src family kinases in human cancer cells

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  1. Phase 1 study of the immunotoxin LMB-100 in patients with mesothelioma and other solid tumors expressing mesothelin

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Larotrectinib versus Prior Therapies in Tropomyosin Receptor Kinase Fusion Cancer: An Intra-Patient Comparative Analysis

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Dabrafenib plus trametinib in patients with BRAFV600E-mutated biliary tract cancer - Authors' reply

    Publikation: Bidrag til tidsskriftKommentar/debatForskningpeer review

Vis graf over relationer
Overexpression and/or amplification of the epidermal growth factor receptor (EGFR) is present in 35-45% of primary glioblastoma multiforme tumors and has been correlated with a poor prognosis. In this study, we investigated the effect of cetuximab and intracellular signaling pathways downstream of EGFR, important for cell survival and proliferation. We show insufficient EGFR downregulation and competition with endogenous EGFR ligands upon cetuximab treatment. Dose-response experiments showed inhibition of EGFR phosphorylation without affecting two of the prominent downstream signaling pathways. Our results indicate that amplification and/or overexpression of EGFR is an unsatisfactory predictor for response to cetuximab.
OriginalsprogEngelsk
TidsskriftCancer Investigation
Vol/bind28
Udgave nummer8
Sider (fra-til)775-87
Antal sider13
ISSN0735-7907
DOI
StatusUdgivet - 1 okt. 2010

ID: 32224869