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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Tumor resensitization to erlotinib following brief substitution of cetuximab.

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.[1]

References

  1. Tumor resensitization to erlotinib following brief substitution of cetuximab. Epstein, R.J., Leung, T.W. Cancer Chemother. Pharmacol. (2008) [Pubmed]
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