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The updates reflect the most current clinical practices and safety and efficacy data after more than 15 years of use.

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The study compared, prospectively or retrospectively, the sensitivity, specificity, negative predictive value, or positive predictive value of EGFR or ALK tests for detection of an EGFR mutation, ALK rearrangement, or response to a targeted EGFR or ALK TKI; the study described technical comparisons across various assay platforms; the study examined potential testing algorithms for NSCLC molecular testing; or the study examined the correlation of EGFR or ALK status in primary versus metastatic tumors from the same patients.

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The study population characteristics were: median age 65 years, age 75 years or older (25%), age less than 65 years (49%), white (100%), female (71%), never smokers (64%), WHO PS 0 (45%), WHO PS 1 (48%), WHO PS 2 (7%), and adenocarcinoma histology (97%).

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NCI-H1975 cells were treated with gefitinib (3 µM) or V1801 (3 µM) for indicated time points, lysed, and Western blot analysis was performed.

The inhibition of EGFR phosphorylation and of downstream signaling by adding gefitinib to metformin treatment abrogated this phenomenon and induced a strong apoptotic effect in vitro and in vivo.

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Recent, large, randomized phase III trials have demonstrated that platinum-based chemotherapy combinations yield a median survival time of 8-11 months, a 1-year survival rate of 30-45% and a 2-year survival rate of 10-20% ().

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Gefitinib Treatment for Pulmonary Sarcomatoid Carcinoma Driven by an EGFR Mutation: Two Cases.

Two Steps Forward in the Treatment of Colorectal Cancer".

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New insights into the pathobiology and treatment of chronic myelogenous leukemia.

Ku GY, Chopra A, Lopes Gde L: Successful treatment of two lung cancer patients with erlotinib following gefitinib-induced hepatotoxicity.

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Pharmacogenomic biomarkers for personalized cancer treatment.

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Four patients achieved partial remission, 11 stable disease and 10 progressive disease.

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Conclusion Gefitinib showed no added benefit in survival, TTP, or RR compared with standard chemotherapy alone.

Total RNA was extracted from paraffin-embedded tumor samples with the use of an RNA isolation kit (Optimum FFPE, Ambion Diagnostics).

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Oncogene addiction as a foundational rationale for targeted anti-cancer therapy: promises and perils.

EGFR-mutated patients treated with a reversible EGFR-TKI might have led to miscalculation of the optimal sample size required to detect a statistically significant difference in survival ().

Fatal adverse drug reactions of anticancer drugs detected by all-case post-marketing surveillance in Japan.

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Obstacles to precision oncology: confronting current factors affecting the successful introduction of biomarkers to the clinic.

Small-Cell Lung Cancer Patients with Brain Metastases or Leptomeningeal Disease.

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EGFR mutation respond to gefitinib.

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Experience has shown, however, that imatinib is much less effective in patients with this mutation, and patients with the mutation comprise nearly 90% of cases of mastocytosis.

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Another interesting finding in this study is the acquired resistance of HER2-overexpressing gastric cancer cell lines to gefitinib.

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Iran also approved its own version of the monoclonal antibody in January 2016, and announced its readiness to export the drug to other countries in the Middle-East and Central Asia when were lifted.

He completed his residency in internal medicine at The University of Texas Health Science Center in Houston and his fellowship training in medical oncology at The University of Texas MD Anderson Cancer Center.

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Only four (9 %) patients received gefitinib as first-line therapy, the majority (35, 74 %) receiving it as second- or third-line therapy, with eight (17 %) receiving it as their fourth to seventh line of treatment.

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Treatment with low-dose gefitinib also caused earlier emergence of acquired resistance in a transgenic mouse model.

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Using the gefitinib-sensitive breast carcinoma cell lines BT474 and SKBR3 as well as the resistant lines MCF-7, MDA-MB-231, and MDA-MB-453, we showed that gefitinib represses the expression of the transcription factor FOXM1 in sensitive, but not resistant, cells.

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