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Absence of epidermal growth factor receptor gene mutations in patients with hormone refractory prostate cancer not responding to gefitinib
Author(s) -
Curigliano Giuseppe,
Pelosi Giuseppe,
De Pas Tommaso,
Renne Giuseppe,
De Cobelli Ottavio,
Manzotti Michela,
Spitaleri Gianluca,
de Braud Filippo
Publication year - 2007
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/pros.20530
Subject(s) - gefitinib , prostate cancer , epidermal growth factor receptor , cancer research , medicine , exon , cancer , prostate , oncology , endocrinology , biology , gene , genetics
BACKGROUND Mutations in the tyrosine kinase (TK) domain of the epidermal growth factor receptor (EGFR) gene in human cancers are associated with increased sensitivity to anilinoquinazoline EGFR inhibitors. To our knowledge no data have been reported on EGFR gene mutations in hormone refractory prostate cancer (HRPC). METHODS Between March 2003 and December 2004, 23 patients with HRPC received 250 mg oral gefitinib daily in addition to antiandrogen plus luteinizing hormone‐releasing hormone (LH‐RH) analog for at least 2 months or until disease progression. Patients with unresected prostate cancer prospectively underwent trans‐rectal biopsy of primary tumor (before starting gefitinib treatment). RESULTS None of the patients demonstrated PSA or objective response to gefitinib. We sequenced exons 18–21 of the EGFR TK domain from genomic DNA isolated from 8 HRPC patients. No patient showed EGFR TK domain mutations. CONCLUSIONS Our results show EGFR mutations did not occur in these patients suggesting that gefitinib is unlikely to be effective in patients with tumors not harboring specific EGFR TK domain. Prostate 67: 603–604, 2007. © 2007 Wiley‐Liss, Inc.