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The PD model variables included tumor drug concentration for 50% inhibition of pEGFR (IC 50), the zero-order rate constant for the formation of pEGFR ( K in), the rate constant from the drug target compartment (pEGFR) to the response compartment (pERK; K tr), and a first-order rate constant for degradation and dephosphorylation of pERK ( K out).

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There were no detectable levels of phosphorylated EGFR in mouse lung tumors examined, which is the primary postulated target of these EGFR inhibitors ().

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Health-related quality of life in non-small-cell lung cancer: methodologic issues in randomized controlled trials.

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While specific requirements and approaches may vary somewhat from one country to another, or even between different accrediting organizations within one country (eg, Joint Commission versus CAP in the United States), the fundamental principles are conserved and retained; tests must be properly validated, undergo regular quality control and instrument maintenance, with monitoring of the laboratory environment and reagent integrity, be performed by competent personnel following clear and informative standard operating procedures, with participation in external proficiency testing procedures and subject to regular inspections by accrediting agencies.

If specimens are insufficient for molecular testing, patients may need to undergo another invasive diagnostic procedure before they can be treated.

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The mRNA levels of RAF1, ERK, MAPK14 and the EGFR increased in a dose-dependent manner after treatment with gemcitabine or doxorubicin.

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Correlation between EGFR gene mutation, cytologic tumor markers, 18F-FDG uptake in non-small cell lung cancer.

Similar to what we have observed in COS-7 cells, all EGFR variants, including the EGFRvIII mutant, are more sensitive to gefitinib than wild-type EGFR in H1299 cells.

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While there were no statistically significant differences between the groups for either parameter, further investigations into the most appropriate dose for gefitinib to treat patients with advanced GI tumors are warranted.

However, in this group of patients, it is also possible that the association of response with skin rash is a reflection of the fact that patients who responded or who had SD were likely to have been taking the drug long enough to develop the side effect, whereas the nonresponders tended to stop taking gefitinib early.

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They were required to have failed prior chemotherapy, and had no other treatment options available.

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However, most patients' tumors eventually become resistant to these drugs.

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

FOXA1 and FOXA2 also recruit HDACs via Groucho-related protein (GRG3) to suppress gene expression.

Patients who develop onset of new eye symptoms such as pain should be medically evaluated and managed appropriately, including IRESSA therapy interruption and removal of an aberrant eyelash if present.

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If used, such an approach should still meet the above TAT recommendations and should not be undertaken if the KRAS testing will exhaust the sample and thereby preclude EGFR and ALK testing.

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In our patient, we were concerned about the possibility of drug-induced liver injury recurring while on gefitinib.

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Radioactivity was well distributed into the tissues of the mouse and the profile of distribution was similar to that observed previously in the rat ().

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PREGNANCY and BREAST-FEEDING: Imatinib may cause harm to the fetus.

In the Elderly Lung Cancer Vinorelbine Italian Study, 154 patients who were older than 70 years were randomly assigned to vinorelbine or supportive care.

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This increase coincides with the widespread introduction of EGFR TKIs into the clinic; gefitinib was FDA approved for use in NSCLC in May 2003, and erlotinib was FDA approved in November 2004 (B).

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The medicine is processed with the use of gefitinib and basically belongs to a class of anti-cancer medications known as epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors.

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As a molecular test of the requirement for FGFR1 in gefitinib-resistant HCC4006 cells, both control and gefitinib-resistant HCC4006 cells were transiently transfected with an FGFR1-targeting small interfering RNA (siRNA) or a non-silencing control siRNA.

Already, new treatments targeting genetic alterations in other, less common driver oncogenes are being evaluated in lung cancer, and testing for these may be addressed in future versions of these guidelines.

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Gefitinib combined survival analysis of the mutation positives from the prospective phase II trials (I-CAMP).

As a result, EGFR mutations analysis has become a routine molecular test in many Chinese hospitals, and direct sequencing is the most frequently used method because it is readily available and relatively inexpensive to use as compared with assays of real-time PCR such as TaqMan probes, Amplification Refractory Mutation System (ARMS) and High Resolution Melting (HRM).

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The expression of Csf2rb1 was increased in control tumor compared with control normal and reversed by the treatment to normal level.

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The rapid pace of preclinical work in the field of EGFR mutations and mechanisms of resistance to gefitinib and erlotinib continues to shed light on potential clinical approaches for this NSCLC subtype.

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Gefitinib was well tolerated and yielded symptomatic improvement in one-third of patients.

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Other potential drug-sensitive mutations occur at much lower frequency: G719X (3%), L861X (2%), and exon 19 insertions (1%).

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With the increased understanding of molecular abnormalities in lung cancer, research efforts have focused heavily on identifying molecular targets and using this knowledge to develop molecular-targeted therapies.

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Effect of the tyrosine kinase inhibitor STI571 in a patient with a metastatic gastrointestinal stromal tumor".

In addition, several RTKs are known to play important roles in tumorigenesis, and have become effective therapeutic targets.

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However, the simulations conducted by varying the brain tumor partition coefficient ( R bt) reflect the spatial variations in the tumor accumulation of gefitinib, either within or between tumors as observed in patients (, ), which are often attributed to breakdown of the BBB.

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In the former trial (V-15-32), gefitinib did not reach non-inferiority in comparison with docetaxel ().

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However, the clinical relevance of detecting an activating EGFR mutation in NSCLC as assessed by DNA gene sequencing cannot be understated given the exquisite sensitivity that EGFR-mutated NSCLCs show to the 'reversible' EGFR-TK inhibitors (-TKIs) gefitinib or erlotinib (to which we will also refer to as 'first-generation' EGFR-TKIs) (), which allows patients to experience a particularly extended survival in the presence of EGFR-TKI treatment, thus in contrast with the historical data reported for NSCLCs when considered as a single disease entity ().

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This medicine work by blocking the epidermal growth factor receptor tyrosine kinase, thus, any cancer cell that expresses this protein in large amounts could be affected by the drug.

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IRESSA treatment should be interrupted or discontinued if the patient develops severe bullous, blistering or exfoliating conditions.

Based on the findings in this study and the increased efficacy of combined EGFR and FGFR inhibitors on specific NSCLC cell lines (Supplementary Figure S8), if supported by future demonstration of increased FGF2 and FGFR1 in lung tumor biopsies following progression on EGFR inhibitors, we suggest that treatment with combinations of EGFR and FGFR inhibitors may be superior to sequential treatment with an FGFR inhibitor.

Pharmacokinetic (PK) factors such as drug absorption, distribution, metabolism and elimination (ADME) limit the amount of a systemically administered drug that reaches the tumour.

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High-resolution genomic profiling of childhood ALL reveals novel recurrent genetic lesions affecting pathways involved in lymphocyte differentiation and cell cycle progression.

Gefitinib (Iressa, AstraZeneca Pharmaceuticals, Macclesfield, United Kingdom) is an orally active, selective EGFR tyrosine kinase inhibitor that blocks the signal transduction pathways involved in the proliferation and survival of cancer cells and other host-dependent processes promoting cancer growth.

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