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Activation of downstream epidermal growth factor receptor (EGFR) signaling provides gefitinib-resistance in cells carrying EGFR mutation.

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Management: If such combinations cannot be avoided, the ceritinib dose should be reduced by approximately one-third (to the nearest 150 mg).

Vaidya was supported by the National Institutes of Diabetes and Digestive and Kidney Disease of the National Institutes of Health under award R01 DK107407, by the National Heart, Lung, and Blood Institute under award K23 HL111771, and by grant 2015085 from the Doris Duke Charitable Foundation.

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T790, located in the ATP binding pocket, is named “the gatekeeper residue” as it determines the affinity of ATP-competitive EGFR-TK inhibitors to EGFR-TK.

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The performance of the FISH assay has been rigorously evaluated and shown to be effective in analyzing FFPE NSCLC specimens.

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In these populations, such treatment is associated with favorable rates of objective responses, progression-free survival, and overall survival.

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This work was supported by grants from National Health Research Institutes (MG-093-PP-08 and MG-093-PP-07 to SF Huang and Y-R Chen, respectively), Department of Health (DOH94-TD-G-111-016 to Y-R Chen), and National Science Council, Taiwan (NHRI92A1-NSCCA16-5 to S-F Tsai).

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The exponential functions for K out in each tumor group were quite similar (see ), and thus, whatever the underlying mechanism, it is not unique to a particular tumor type.

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Gefitinib was purchased from Tocris Bioscience (Bristol, UK).

To identify specific genes or pathways that may directly or indirectly contribute to the protective effect of gefitinib on tumorigenesis, three to four independent tumors and normal tissues from gefitinib treatment and control groups were used for this analysis.

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The mRNA expression levels of MDR proteins were not significantly altered by gefitinib (5 μM) in Bxpc-3 cells.

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EGFR mutation status was available for 21 of these patients, with 5 testing positive, but all were in the chemotherapy arm.

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NSCLC reported that EGFR activating mutations were the most important independent predictors for time to treatment failure compared with other mutations, among which exon 19 deletion and L858R mutations were the best predictors for longer time to treatment failure in a multivariate analysis ().

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Because gefitinib targets FOXM1 through FOXO3a in breast cancer, it is therefore possible to increase the efficacy of gefitinib or treat gefitinib-resistant diseases through targeting FOXM1.

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In this study, the gene expression of MDR proteins (MRP1, MRP2, and MRP3) was induced by conventional chemotherapeutic agents in pancreatic carcinoma cell line, especially by gemcitabine in a dose-dependent manner.

Take L858R as example, which is a frequent EGFR mutation in NSCLC where leucine (L) is substituted by arginine (R) at the locus.

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The epidermal growth factor receptor (EGFR or ErbB1) was one of the first growth factor receptors to be characterized and is the founding member of a family of receptor tyrosine kinases, which also include HER-2 (ErbB2, neu), HER-3 (ErbB3), and HER-4 (ErbB4; refs.

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To establish evidence-based recommendations for the molecular analysis of lung cancers that are that are required to guide EGFR- and ALK-directed therapies, addressing which patients and samples should be tested, and when and how testing should be performed.

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Tumor samples from patients who consented to have biomarkers assessed were analyzed at two central laboratories to determine biomarker status, with EGFR mutation status the first priority.

Jeremy Geffen, MD, FACP, who is described as a board certified medical oncologist and leading expert in integrative medicine and oncology and is the author of the book The Journey Through Cancer: Healing and Transforming the Whole Person.

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Patients must be prepared to have treatment on and off for the rest of their lives to control the disease.

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MHO administered the chemotherapy and the patient was taken to the emergency room and hospitalized.

H1299 cells were selected as permanently transfected cells for wild-type and mutated EGFRs because they express wild-type EGFR and respond well to EGF treatment.

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Comparison of Gefitinib Versus VMP in the Combination with Radiotherapy for Multiple Brain Metastases from Non-small Cell Lung Cancer.

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If a person's tumor is negative for the most common KRAS mutation, tests for other less common mutations not detected by the current test may be used to help predict therapeutic responses.

OBJECTIVES: Epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) is a specific lung cancer subtype characterized by sensitivity to treatment with EGFR tyrosine kinase inhibitors (TKIs).

Radiation myelopathy: estimates of risk in 1048 patients in three randomized trials of palliative radiotherapy for non-small cell lung cancer: the Medical Research Council Lung Cancer Working Party.

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Although gefitinib shows pronounced penetration into tumor tissue in mouse, rat, and human, this distribution profile seems compound specific and differs markedly from that of its metabolite, M523595, and the structurally related compound, erlotinib.

CA125 is a tumor marker frequently elevated in ovarian cancer and useful for following response to therapy.

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Figure 2 Mutations in the EGFR Gene in Gefitinib-Responsive Tumors.

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In those patients who experience disease progression only in the brain but not in the rest of the body, brain metastasis treatment should be administered, but erlotinib at standard daily doses can be resumed after completion of the radiation course.

Multiple genetic mutations are apparent, including both overexpression of the receptor as well as rearrangements that result in truncated isoforms.

Concomitant administration of itraconazole (200 mg QD for 12 days), an inhibitor of CYP3A4, with gefitinib (250 mg single dose) to healthy male volunteers, increased mean gefitinib AUC by 88% (see section).

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