D EGF-R regarding the processes causing cetuximab resistance in tumour cells [27].Goerner et al. Head Neck Oncology 2010, 2:8 http://www.headandneckoncology.org/content/2/1/Page 4 ofDual targeted treatment approaches directed at both EGF-R and Src might, therefore, be a feasible strategy for overcoming or preventing acquired resistance to cetuximab. Dasatinib is a potent inhibitor of multiple oncogenic kinases including Src, cKIT, BCR-ABL, PDGFR, and ephrin A. Because of its ability to inhibit BCR-ABL, it was approved for treatment of chronic myeloid leukemia in 2006. Currently dasatinib is being evaluated in phase I clinical trials for solid tumours either alone or in combination with cetuximab [28]. Proteasomes are proteinases, which play a critical role in degradation of the proteins responsible for the control of cell growth. Inhibitors of proteasomes have demonstrated antitumour effects associated with the induction of apoptosis and sensitization of malignant cells to conventional cytotoxic drugs. Bortezomib, a small molecule inhibitor of proteasomes, has shown efficacy against myeloma and lymphomas, and was recently tested in phase II trials in HNSCC in combination with docetaxel or irinotecan, respectively[29]. Preliminary results have shown 50 disease control rates in recurrent or metastasizing HNSCC patients with the use of low-dose bortezomib[30]. Phase III trials with optimized dosing schedules are needed to confirm these promising new treatment options, which were usually associated with acceptable toxicity.Chicago, IL, USA. 3Community Hospital Bielefeld, Department of Otolaryngology, Teutoburger Str. 60, 33604 Bielefeld, Germany. Authors’ contributions MG and HS performed the literature research and composed the manuscript. TS critically revised the manuscript. All authors approved the final version of the manuscript. Competing interests The authors declare that they have no competing interests. Received: 12 March 2010 Accepted: 14 April 2010 Published: 14 April 2010 References 1. Bozec A, Gros F-X, Penault-Llorca F, Patricia AUY922 site Formento, Anne Cayre, Cl ia Dental, Marie-Christine Etienne-Grimaldi, Jean-Louis Fischel, G ard Milano: Vertical VEGF targeting: A combination of ligand blockade with receptor tyrosine kinase inhibition. Eur J Cancer 2008, 13:1922-1930. 2. Goon PK, Stanley MA, Ebmeyer J, Lars Steinstr ser, Tahwinder Upile, Waseem Jerjes, Manuel Bernal-Sprekelsen, Martin G ner, Holger H Sudhoff: HPV head and neck cancer: a descriptive update. Head Neck Oncol 2009, 1:36. 3. Segal NH, Saltz LB: Evolving treatment of advanced PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27385778 colon cancer. Annu Rev Med 2009, 207-219. 4. Iwase M, Takaoka S, Uchida M, Sayaka Yoshiba, Gen Kondo, Hitoshi Watanabe, Masaru Ohashi, Masao Nagumo: Epidermal growth factor receptor inhibitors enhance susceptibility to Fas-mediated apoptosis in oral squamous cell carcinoma cells. Oral Oncol 2008, 4:361-368. 5. Kalyankrishna S, Grandis JR: Epidermal growth factor receptor biology in head and neck cancer. J Clin Oncol 2006, 17:2666-2672. 6. Grandis JR, Tweardy DJ: Elevated levels of transforming growth factor alpha and epidermal growth factor receptor messenger RNA are early markers of carcinogenesis in head and neck cancer. Cancer Res 1993, 15:3579-3584. 7. Hoang T, Huang S, Armstrong E, Jens C Eickhoff, Paul M Harari: Augmentation of radiation response with the vascular targeting agent ZD6126. Int J Radiat Oncol Biol Phys 2006, 5:1458-1465. 8. Huang SM, Bock JM, Harari PM: Epidermal growth factor.