Abstract
Targeted inhibition of epidermal growth factor receptors (EGFR) is becoming a standard anticancer treatment in defined clinical scenarios. EGFR inhibition may be achieved either by small-molecule orally bioavailable tyrosine kinase inhibitors, such as gefitinib or erlotinib, or else by large-molecule receptor antibodies, such as cetuximab or panitumumab. Here, we describe a case of pancreatic cancer in which the small-molecule EGFR antagonist erlotinib was used before and after the EGFR antibody cetuximab, with unexpected potentiation of both toxic and therapeutic sequelae.
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Epstein, R.J., Leung, T.W. Tumor resensitization to erlotinib following brief substitution of cetuximab. Cancer Chemother Pharmacol 62, 1111–1112 (2008). https://doi.org/10.1007/s00280-008-0698-6
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DOI: https://doi.org/10.1007/s00280-008-0698-6