Erlotinib: as maintenance monotherapy in non-small-cell lung cancer
VJ Muir, S Dhillon - BioDrugs, 2011 - Springer
VJ Muir, S Dhillon
BioDrugs, 2011•SpringerErlotinib is a low molecular weight, orally active, epidermal growth factor receptor (EGFR)
tyrosine kinase inhibitor. Inhibition of EGFR tyrosine kinase results in the disruption of
processes involved in cancer growth and development, including cell migration,
proliferation, angiogenesis, and apoptosis. In the well designed, phase III SATURN study,
oral erlotinib 150mg/day as maintenance treatment prolonged progression-free survival
(PFS) in patients with non-small-cell lung cancer (NSCLC) who had not progressed after …
tyrosine kinase inhibitor. Inhibition of EGFR tyrosine kinase results in the disruption of
processes involved in cancer growth and development, including cell migration,
proliferation, angiogenesis, and apoptosis. In the well designed, phase III SATURN study,
oral erlotinib 150mg/day as maintenance treatment prolonged progression-free survival
(PFS) in patients with non-small-cell lung cancer (NSCLC) who had not progressed after …
Abstract
Erlotinib is a low molecular weight, orally active, epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor. Inhibition of EGFR tyrosine kinase results in the disruption of processes involved in cancer growth and development, including cell migration, proliferation, angiogenesis, and apoptosis.
In the well designed, phase III SATURN study, oral erlotinib 150mg/day as maintenance treatment prolonged progression-free survival (PFS) in patients with non-small-cell lung cancer (NSCLC) who had not progressed after four cycles of first-line platinum doublet chemotherapy. PFS was significantly longer with erlotinib than with placebo in patients who were analyzable for PFS and in the subgroup of these patients with EGFR immunohistochemistry-positive tumors (co-primary endpoints).
The improvement in PFS was independent of several baseline and clinical characteristics, including histology, smoking status, and EGFR mutation status, although a greater treatment benefit was observed in patients with tumors bearing EGFR-activating mutations than in those with wild-type EGFR tumors.
Overall survival in the SATURN study was significantly longer with erlotinib than with placebo in the intent-to-treat population, in patients with EGFR immunohistochemistry-positive tumors, and in patients with wild-type EGFR tumors. Median overall survival had not yet been reached in patients with tumors bearing EGFR-activating mutations.
Oral erlotinib as maintenance therapy was generally well tolerated in patients with NSCLC in the SATURN study and had a tolerability profile generally similar to that observed in a trial of erlotinib monotherapy as second-line treatment in patients with NSCLC.
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