Cetuximab and Other Anti–Epidermal Growth Factor Receptor Monoclonal Antibodies in the Treatment of Non-Small Cell Lung Cancer

Gridelli, Cesare; Maione, Paolo; Ferrara, Marianna; Rossi, Antonio

doi:10.1634/theoncologist.2008-0153

Cited by 33 publications

(20 citation statements)

References 63 publications

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“…In an unselected population, cetuximab treatment, as many other biological agents, only benefits a small percentage of NSCLC patients [28]. The body of knowledge that has paved the way for more targeted use of cetuximab has been recently reviewed [29].…”

Section: Resultsmentioning

confidence: 99%

Complement activation mediates cetuximab inhibition of non-small cell lung cancer tumor growth in vivo

Hsu¹,

Ajona²,

Corrales³

et al. 2010

Mol Cancer

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BackgroundCetuximab, an antibody targeting the epidermal growth factor receptor (EGFR), increases survival in patients with advanced EGFR-positive non-small cell lung cancer when administrated in combination with chemotherapy. In this study, we investigated the role of complement activation in the antitumor mechanism of this therapeutic drug.ResultsEGFR-expressing lung cancer cell lines were able to bind cetuximab and initiate complement activation by the classical pathway, irrespective of the mutational status of EGFR. This activation led to deposition of complement components and increase in complement-mediated cell death. The influence of complement activation on the activity of cetuximab in vivo was evaluated in xenografts of A549 lung cancer cells on nude mice. A549 cells express wild-type EGFR and have a KRAS mutation. Cetuximab activity against A549 xenografts was highly dependent on complement activation, since complement depletion completely abrogated the antitumor efficacy of cetuximab. Moreover, cetuximab activity was significantly higher on A549 cells in which a complement inhibitor, factor H, was genetically downregulated.ConclusionsWe demonstrate for the first time that the in vivo antitumor activity of cetuximab can be associated with a complement-mediated immune response. These results may have important implications for the development of new cetuximab-based therapeutic strategies and for the identification of markers that predict clinical response.

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Section: Resultsmentioning

confidence: 99%

Complement activation mediates cetuximab inhibition of non-small cell lung cancer tumor growth in vivo

Hsu¹,

Ajona²,

Corrales³

et al. 2010

Mol Cancer

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show abstract

“…Cetuximab was initially introduced as treatment for metastatic colorectal cancer and is now well established in all lines of treatment [10]. Among all anti-EGF-R monoclonal antibodies, cetuximab has been extensively studied in the treatment of NSCLC and has recently been reviewed [11]. Cetuximab has also demonstrated activity in the first-line setting for NSCLC treatment.…”

Section: Cetuximabmentioning

confidence: 99%

Targeted therapies for non-small cell lung cancer

2010

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“…28 It is supposed that the blockade of EGFR activation by tyrosine kinase inhibitors (TKIs), monoclonal antibodies, ligand-linked toxins and antisense approaches may ultimately lead to inhibition of cancer cell proliferation. 29 The incidence of EGFR mutation varies with ethnicity, with up to 50% of tumours being driven by activating EGFR mutations in Asian populations compared with 10% to 15% in Caucasians. 30,31 Detection of EGFR mutations has involved tissue biopsy but less invasive methods are becoming available, including the use of circulating tumour DNA.…”

Section: Targeting Molecular Drivers Of Carcinogenesismentioning

confidence: 99%

Advancing the Management of Non-small Cell Lung Cancer

Fakih¹

2017

European Oncology &Amp; Haematology

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A dvances in the development of targeted therapies and immunotherapy have transformed the management of non small-cell lung cancer (NSCLC). Targeting angiogenesis and molecular drivers of carcinogenesis has led to the approval of several new therapies. More recently, immunotherapeutic approaches have been investigated in the treatment setting of NSCLC. These include immune checkpoint inhibitors (e.g. anti-cytotoxic T-lymphocyte antigen-4 [CTLA-4], anti-programmed death-1 (PD-1) and anti-programmed deathligand 1 [PD-L1] agents). The emergence of so many therapeutic options offers the potential for personalised therapy. Molecular profiling can inform treatment decisions but there is a need for more data to determine the optimal sequencing and combination of targeted and immunotherapeutic agents.

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Cetuximab and Other Anti–Epidermal Growth Factor Receptor Monoclonal Antibodies in the Treatment of Non-Small Cell Lung Cancer

Abstract: This article is available for continuing medical education credit at CME.TheOncologist.com.

Cited by 33 publications

References 63 publications

Complement activation mediates cetuximab inhibition of non-small cell lung cancer tumor growth in vivo

Complement activation mediates cetuximab inhibition of non-small cell lung cancer tumor growth in vivo

Targeted therapies for non-small cell lung cancer

Advancing the Management of Non-small Cell Lung Cancer

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