Send to

Choose Destination
See comment in PubMed Commons below
Crit Rev Oncol Hematol. 2008 Nov;68(2):93-106. doi: 10.1016/j.critrevonc.2008.07.006. Epub 2008 Aug 3.

The biological properties of cetuximab.

Author information

Medical Oncology, Campus Bio-Medico University, Via Alvaro del Portillo 200, Rome, Italy.


Cetuximab is a recombinant chimeric human murine immunoglobulin G1 antibody that binds to the extra-cellular domain of epidermal growth factor receptor with a higher affinity than either endogenous ligand. This binding inhibits receptor phosphorylation and activation and it leads to receptor internalization and degradation. Several studies have shown that cetuximab is able to inhibit growth of epidermal growth factor receptor (EGFR)-expressing tumour cells in vitro. Moreover, treatment with cetuximab results in a marked inhibition of tumour growth in nude mice bearing xenografts of human cancer cell lines. These results are linked to cetuximab biological effects as inhibition of cell cycle, tumour progression, neo-angiogenesis, invasion and metastatization, as well as increase and activation of pro-apoptotic molecules. Additionally, cetuximab potentiates, in combination, the effects of chemotherapy and radiation therapy in eradicating well-established tumours in nude mice and it may even reverse the resistance to some cytotoxic agents in these xenografts. Moreover, numerous clinical trials demonstrated cetuximab efficacy in different tumour types. It has been approved by Food and Drugs Administration in the treatment of metastatic colorectal cancer as single agent or in combination with chemotherapy, in locally and regionally advanced head and neck squamous cell carcinoma in combination with radiation, and as monotherapy for recurrent and metastatic head and neck squamous cell carcinoma after failing platinum-based chemotherapy. This paper will overview all the experimental and pre-clinical data on the biological properties of cetuximab.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center