Jump to main content
US EPA
United States Environmental Protection Agency
Search
Search
Main menu
Environmental Topics
Laws & Regulations
About EPA
Health & Environmental Research Online (HERO)
Contact Us
Print
Feedback
Export to File
Search:
This record has one attached file:
Add More Files
Attach File(s):
Display Name for File*:
Save
Citation
Tags
HERO ID
1338903
Reference Type
Journal Article
Title
Erlotinib has better efficacy than gefitinib in adenocarcinoma patients without EGFR-activating mutations, but similar efficacy in patients with EGFR-activating mutations
Author(s)
Wu, WS; Chen, YM; Tsai, CM; Shih, JF; Chiu, CH; Chou, KT; Lai, SL; Wu, CH; Luo, YH; Huang, CY; Lee, YC; Perng, RP; Whang-Peng, J
Year
2012
Is Peer Reviewed?
Yes
Journal
Experimental and Therapeutic Medicine
ISSN:
1792-0981
EISSN:
1792-1015
Volume
3
Issue
2
Page Numbers
207-213
Language
English
PMID
22969870
DOI
10.3892/etm.2011.383
Abstract
Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are an effective treatment for advanced non-small cell lung cancer. The objective of the present study was to compare the efficacy of gefitinib and erlotinib in patients with pulmonary adenocarcinoma, whose tumor EGFR mutation status was known. Pulmonary adenocarcinoma patients who began receiving gefitinib or erlotinib treatment from January 2005 to December 2010, and whose tumor EGFR mutation status had been determined, were included. Clinical data, type of treatment response and survival time data were collected. Of the 224 patients enrolled, 124 received gefitinib treatment and 100 received erlotinib treatment. Of these patients, 146 individuals had tumors with EGFR-activating mutations (exon 19 deletions and/point mutation of L858R in exon 21) and 78 did not. There was no difference in treatment response whether or not the patients had tumors with EGFR-activating mutations at the time they received gefitinib or erlotinib treatment. The median progression-free survival (PFS) of the gefitinib and erlotinib groups was 7.6 and 7.9 months, respectively (p=0.4731). PFS was significantly longer for patients without EGFR-activating mutations who received erlotinib treatment (n=48; median, 4.5 months) than for those who received gefitinib treatment (n=30; median, 2.3 months), with a hazard ratio of 0.58 (95% CI, 0.35-0.96; p=0.0339). Patients whose tumors had EGFR-activating mutations displayed no difference in PFS with either gefitinib (n=94; median, 10.5 months) or erlotinib treatment (n=52; median, 10.4 months). In conclusion, PFS showed no difference with either agent in patients whose tumors had EGFR-activating mutations, but was significantly longer in patients whose tumors did not have EGFR-activating mutations when receiving erlotinib treatment.
Tags
IRIS
•
Arsenic Hazard ID
1. Initial Lit Search
PubMed
4. Considered through Oct 2015
6. Cluster Filter through Oct 2015
•
Arsenic (Inorganic)
1. Literature
PubMed
4. Adverse Outcome Pathways/Networks Screening
Excluded/Not relevant
Electronic discard
•
Arsenic MOA
2. Electronic Discard
1. MOA Literature Screening
MOA Cluster
Home
Learn about HERO
Using HERO
Search HERO
Projects in HERO
Risk Assessment
Transparency & Integrity