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Previous Volume 354:525-526 February 2, 2006 Number 5 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: Mellinghoff et al. (Nov. 10 issue)¹ identified coexpression of epidermal growth factor receptor (EGFR) deletion mutant variant III (EGFRvIII) and the tumor-suppressor protein PTEN as a molecular signature in pretreatment glioblastoma tissue that predicts sensitivity to EGFR inhibitors. However, several tumors that were responsive to erlotinib in the validation data set exhibited PTEN loss, and one of these did not express EGFRvIII, suggesting that alternative mechanisms of action exist. Although the effects of EGFR inhibitors on EGFR activity and signaling were analyzed in vitro, ideally tissue from patients in the training and validation sets would also be . . . [Full Text of this Article]

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