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Reports of success with these agents are mixed due to the lack of available data with consistent methodologies, trial populations, and optimal design.

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Our study suggested that, as regards ORR or PFS, NSCLC non-smoker patients have better sensitivity to gefitinib than smoker patients.

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Acquired Resistance of Lung Adenocarcinomas to Gefitinib or Erlotinib Is Associated with a Second Mutation in the EGFR Kinase Domain.

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Phase II results for breast cancer that over-expresses the protein (Her2-positive breast cancer) were described as promising by the authors, with 19 of 41 patients achieving benefit from afatinib.

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In this study, the toxicity of palliative gefitinib was mild, although the folliculitis previously reported with gefitinib was more prevalent and florid than has been previously reported.

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Nine percent of sunitinib patients and 8% of placebo patients discontinued therapy due to an adverse event.

In animal reproductive studies, oral administration of gefitinib from organogenesis through weaning resulted in fetotoxicity and neonatal death at doses below the recommended human dose.

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Otro experto, el Dr. Bruce Rutkin, cardilogo del Hospital de la Universidad de North Shore en Manhasset, Nueva York, dijo que es bastante difcil sacar conclusiones definitivas a partir de un metaanlisis.

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The following adverse reactions have been reported with IRESSA across NSCLC trials (Study 2, Study 3 and Study 4) and are not listed elsewhere in Section 6: nausea (18%), asthenia (17%), pyrexia (9%), alopecia (4.

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Erlotinib versus standard chemotherapy as first-line treatment for European patients with advanced EGFR mutation-positive non-small-cell lung cancer (EURTAC): a multicentre, open-label, randomised phase 3 trial.

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Mir-660 is downregulated in lung cancer patients and its replacement inhibits lung tumorigenesis by targeting MDM2-p53 interaction.

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Tissue was not available from the other patients with a response to gefitinib, most commonly because diagnostic specimens were limited to needle aspirates.

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Two hundred and sixteen patients received IRESSA, 102 (47%) and 114 (53%) receiving 250 mg and 500 mg daily doses, respectively.

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In the present study, we show that another forkhead transcription factor FOXM1 is a downstream cellular target and a marker for gefitinib action and that gefitinib activates FOXO3a to repress FOXM1 expression in breast cancer cells.

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SOURCES: Canadian Medical Association Journal, news release, Jan. 10, 2011; Canadian Medical Association Journal, Jan.

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P753insS mutations were introduced into the full-length EGFR coding sequence with the use of site-directed mutagenesis and inserted into a cytomegalovirus promoter-driven expression construct (pUSE, Upstate).

No significant differences for refusal or dropout rates were detected between pharmacotherapy alone and combination treatments, or between psychotherapy alone and combination treatments.

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As a first-line therapy, gefitinib has been assessed in combination with two different chemotherapy regimens in two large randomized studies (INTACT 1 and INTACT 2).

Research, was funded by drug maker Wyeth BioPharma.

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However, many reports have demonstrated that patients who acquire resistance can re-respond to EGFR TKIs after a drug holiday.

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This finding suggested that the presence of EGFR mutations is the best criterion for selection of patients who benefit from gefitinib, an idea that is validated by the present study.

The preponderance of evidence indicates that postoperative cisplatin combination chemotherapy provides a significant survival advantage to patients with resected NSCLC with occult N2 disease discovered at surgery.

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In a subset analysis which included patients with EGFR-mutated disease (161 patients: 102 on erlotinib and 59 on placebo), DFS favored erlotinib in comparison with placebo.

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In addition, patients on afatinib had a significantly longer time on treatment, and risk of treatment failure was reduced by 27% versus gefitinib.

In patients without EGFR mutations for whom chemotherapy fails, erlotinib may be administered as a second-line agent.

Some of these biomarkers may be detectable 1 - 3 years before a clinical diagnosis of lung cancer.

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In a tumor with the 2240del18 mutation from a patient with nonsmall cell lung cancer who showed responsiveness to gefitinib with complete remission over a 2-year period, identified the development of a second mutation in EGFR, thr790 to met (T790M; ), responsible for secondary resistance to gefitinib.

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The alternate strategy of increasing the dose level in the wild-type EGFR group was ruled out as the doses of gefitinib would likely be toxic ().

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