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Serious adverse reactions were reported in 29% of patients treated with afatinib.
CYP2D6 could play a more prominent role in overall gefitinib clearance in the presence of continued CYP3A4 inhibition.
Interestingly, overexpression of wild-type FOXM1 or constitutively active FOXM1 did not efficiently overcome the antiproliferative effect of gefitinib, indicating that gefitinib may either have other cell cycle regulators as targets or also regulate FOXM1 activity through other post-transcriptional mechanisms.
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Engelman JA, Jänne PA, Mermel C, Pearlberg J, Mukohara T, Fleet C, Cichowski K, Johnson BE, Cantley LC: ErbB-3 mediates phosphoinositide 3-kinase activity in gefitinib-sensitive non-small cell lung cancer cell lines.
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MTE schedule was also effective in reducing proliferation of H292 and HCC827 cells, whereas an antagonistic effect was observed in the resistant cells, H460 and H1975.
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An Autopsy Case of Two Distinct, Acquired Drug Resistance Mechanisms in Epidermal Growth Factor Receptor-mutant Lung Adenocarcinoma: Small Cell Carcinoma Transformation and Epidermal Growth Factor Receptor T790M Mutation.
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Clinicians and patients were not masked to treatment allocation; independent review of tumour response was done in a blinded manner.
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The observation that certain subgroups of patients, particularly female patients, those who have never smoked, those who have adenocarcinoma histology, and those who are of Asian descent, have a higher response rate and clinical benefit with gefitinib and erlotinib therapy prompted research to elucidate the molecular mechanism responsible for this increased response.
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Seven (15 %) of these had also received further palliative systemic therapy (including platins, 5-fluorouracil, taxanes and triapine (a novel ribonucleotide reductase inhibitor)) prior to commencing gefitinib.
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Our work also underscores the need to consider incorporating repeated biopsies into clinical studies of novel targeted therapies, such as those involving mutant tyrosine kinases.
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Alternative explanations are the possibility that gefitinib acts as a cytostatic agent and, therefore, may potentially reduce the effect of chemotherapy when the drugs are given concomitantly.
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If these genes are damaged, out-of-control growth may result in cancer.
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Although both drugs also phosphorylated eIF2α in PC-9 cells, which are human lung cancer cell line and are extremely sensitive to EGFR inhibitors, the protective effect of TUDCA was not found in this cell line ( and Figs), suggesting that TUDCA treatment would not disturb the anti-cancer efficacy of EGFR inhibitors in non-small cell lung cancer patients.
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