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Gefitinib and G protein-coupled receptor (GPCR) interactions were assessed by β-arrestin recruitment, luciferase and radioligand competition assays.

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We imported the statistical results of our data set into the program and used GenMAPP to illustrate pathways containing differentially expressed genes ().

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They have also been associated with a poorer prognosis as well as resistance to chemotherapy and EGFR TKIs (-).

Role of hMLH1 promoter hypermethylation in drug resistance to 5-fluorouracil in colorectal cancer cell lines.

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We evaluated the efficacy and safety of a combination regimen of gefitinib and pemetrexed as first-line chemotherapy in EGFR-mutated NSCLC patients.

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Radiation therapy injures or destroys cells in the area being treated (the "target tissue") by damaging their genetic material, making it impossible for these cells to continue to grow and divide.

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The treatment of cancer has undergone evolutionary changes as understanding of the underlying biological processes has increased.

Electrocardiography, echocardiography, and hemodynamic analyses showed that affected mice developed aortic stenosis and regurgitation.

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Commonly employed strategies aimed at overcoming EGFR-tyrosine kinase inhibitor resistance are to: 1) irreversibly inhibit EGFR tyrosine kinase by covalent cross-linking of receptors 2) broaden the receptor tyrosine kinase targets of the drug using multi-kinase inhibitors 3) target downstream PI3K or STAT5 pathways 4) target a combination of pathways or 5) target mutant EGFR for degradation.

We found that ARMS could improve the mutation detection rate and the mutation positive patients responded well with TKIs therapy, but the correlation between mutation negative patients and TKIs therapy was still unsatisfactory.

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The PMDA package insert for gefitinib states that it is indicated for patients with EGFR activating mutation positive non-small cell lung cancer (NSCLC), and that EGFR mutation testing should be performed prior to beginning gefitinib treatment.

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A549 tumor xenografts in mouse is also markedly inhibited by gefitinib (, ), Calu-6 tumor xenografts are quite resistant to gefitinib treatment.

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Oncologists chose outcomes such as survival time, time to disease progression and tumour response as providing objective data.

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Therefore, PTEN expression in a cutaneous biopsy could be a marker for tumor response to gefitinib, although the relationship between PTEN expression in cutaneous cells and tumor response requires further investigation.

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Proteomics analyses across species can help reveal biologically conserved pathways and protein interactions.

However, because T790M is often not present in every tumor cell, conventional Sanger sequencing, even with microdissection, is considered insufficient for this testing.

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The break-apart FISH assay is generally more expensive than some other assays, and so its primary role in the detection of ALK rearrangement will need to be carefully evaluated for both performance and cost-effectiveness against other techniques that are currently being introduced.

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Despite considerable controversy (see ), it has become an acceptable treatment paradigm and both drugs are approved for maintenance therapy of advanced NSCLC patients in Europe and the USA.

Radiotherapy alone versus combined chemotherapy and radiotherapy in nonresectable non-small-cell lung cancer: first analysis of a randomized trial in 353 patients.

To validate these findings, we performed these experiments on another lung cancer cell line CL1-0 using transiently transfection methods.

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When competitive drugs came on the market, they were sold at a higher price to reflect the smaller population, and Novartis raised the price of Gleevec to match them.

This allows activation of the downstream effectors of EGFR even in the presence of an EGFR inhibitor.

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The level of EGFR expression and the extent of EGFR phosphorylation were compared between the vehicle control and low-dose gefitinib groups.

Briefly, over a period of 12 months, human CALU-3 lung adenocarcinoma cells were continuously exposed to increasing concentrations of gefitinib.

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Theme: Oncology - Molecular mechanisms determining the efficacy of EGF receptor-specific tyrosine kinase inhibitors help to identify biomarker candidates.

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The difference in the rates of objective response between gefitinib-treated patients with an EGFR mutation and those without an EGFR mutation (71.

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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.

Three research groups have presented studies showing a positive relationship between the presence of activating mutations in the EGFR TK domain and a clinical response to gefitinib.

HER2 inhibitor highly effective in preclinical lung cancer models.

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Long-term follow-up of children with chronic myeloid leukemia after hematopoietic stem cell transplantation and tyrosine kinase inhibitor therapy.

Dibutyryl-cAMP or PD98059 suppressed gefitinib-induced AML cell cytostasis and differentiation.

Another cause of resistance can be inactivating mutations of the tumour suppressor, which allow increased activation of independent of stimulation by EGFR.

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