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We are analyzing https://link.springer.com/article/10.1007/s11684-016-0488-1.

Title:
Mechanisms of resistance to third-generation EGFR tyrosine kinase inhibitors | Frontiers of Medicine
Description:
The tyrosine kinase inhibitors (TKI) of the epidermal growth factor receptor (EGFR) are becoming the first line of therapy for advanced non-small cell lung cancer (NSCLC). Acquired mutations in EGFR account for one of the major mechanisms of resistance to the TKIs. Three generations of EGFR TKIs have been used in clinical applications. AZD9291 (osimertinib; Tagrisso) is the first and only FDA approved third-generation EGFR TKI for T790M-positive advanced NSCLC patients. However, resistance to AZD9291 arises after 9–13 months of therapy. The mechanisms of resistance to third-generation inhibitors reported to date include the EGFR C797S mutation, EGFR L718Q mutation, and amplifications of HER-2, MET, or ERBB2. To overcome the acquired resistance to AZD9291, EAI045 was discovered and recently reported to be an allosteric EGFR inhibitor that overcomes T790M- and C797S-mediated resistance. This review summarizes recent investigations on the mechanisms of resistance to the EGFR TKIs, as well as the latest development of EAI045 as a fourth-generation EGFR inhibitor.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {πŸ“š}

  • Science
  • Education
  • Health & Fitness

Content Management System {πŸ“}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {πŸ“ˆ}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
However, some sources were not loaded, we suggest to reload the page to get complete results.

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How Does Link.springer.com Make Money? {πŸ’Έ}

We see no obvious way the site makes money.

Not every website is profit-driven; some are created to spread information or serve as an online presence. Websites can be made for many reasons. This could be one of them. Link.springer.com might be plotting its profit, but the way they're doing it isn't detectable yet.

Keywords {πŸ”}

pubmed, article, google, scholar, cancer, egfr, cas, lung, central, oncol, resistance, inhibitors, cell, hematol, liu, mutation, wang, nonsmall, advanced, thirdgeneration, inhibitor, lee, kim, kinase, zhang, acquired, azd, phase, res, chen, nonsmallcell, med, mechanisms, tyrosine, patients, versus, treatment, song, receptor, nsclc, zhou, park, yang, access, privacy, cookies, content, epidermal, growth, factor,

Topics {βœ’οΈ}

month download article/chapter mirna-based therapeutic intervention nonsmall-cell lung cancer small-cell lung cancer structure-based design approach egfr-mutant lung cancer fourth-generation egfr inhibitor targeting drug resistance related subjects selumetinib-enhanced radioiodine uptake mutant-selective covalent inhibitor mutant-selective allosteric inhibitors xpo1/crm1-selective inhibitors overcomes t790m-mediated resistance tyrosine kinase inhibitors phase 3 trials phase iii study egfr mutation-positive advanced advanced egfr mutation-positive full article pdf monitor egfr-tki treatment phase iii affiliated cancer hospital allosteric egfr inhibitor randomised controlled trial privacy choices/manage cookies generation egfr inhibitors advanced squamous-cell egfr mutation-positive egfr-mutation- positive egfr mutation positive egfr mutation status selective bcl-2 inhibitor egfr c797s mutation afatinib versus erlotinib irreversible egfr tki c797s-mediated resistance generation alk inhibitors egfr-mutated nsclc article frontiers lung cancer patients tumor egfr status generation egfr tki egfr l718q mutation generation inhibitors reported erlotinib versus chemotherapy c797s mutation acquired acquired c797s mutation article wang advanced thyroid cancer

Questions {❓}

  • Can EGFR mutations in plasma or serum be predictive markers of non-small-cell lung cancer?
  • Nivolumab as first line monotherapy for advanced non-small cell lung cancer: could we replace first line chemotherapy with immunotherapy?

Schema {πŸ—ΊοΈ}

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         headline:Mechanisms of resistance to third-generation EGFR tyrosine kinase inhibitors
         description:The tyrosine kinase inhibitors (TKI) of the epidermal growth factor receptor (EGFR) are becoming the first line of therapy for advanced non-small cell lung cancer (NSCLC). Acquired mutations in EGFR account for one of the major mechanisms of resistance to the TKIs. Three generations of EGFR TKIs have been used in clinical applications. AZD9291 (osimertinib; Tagrisso) is the first and only FDA approved third-generation EGFR TKI for T790M-positive advanced NSCLC patients. However, resistance to AZD9291 arises after 9–13 months of therapy. The mechanisms of resistance to third-generation inhibitors reported to date include the EGFR C797S mutation, EGFR L718Q mutation, and amplifications of HER-2, MET, or ERBB2. To overcome the acquired resistance to AZD9291, EAI045 was discovered and recently reported to be an allosteric EGFR inhibitor that overcomes T790M- and C797S-mediated resistance. This review summarizes recent investigations on the mechanisms of resistance to the EGFR TKIs, as well as the latest development of EAI045 as a fourth-generation EGFR inhibitor.
         datePublished:2016-12-23T00:00:00Z
         dateModified:2016-12-23T00:00:00Z
         pageStart:383
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      headline:Mechanisms of resistance to third-generation EGFR tyrosine kinase inhibitors
      description:The tyrosine kinase inhibitors (TKI) of the epidermal growth factor receptor (EGFR) are becoming the first line of therapy for advanced non-small cell lung cancer (NSCLC). Acquired mutations in EGFR account for one of the major mechanisms of resistance to the TKIs. Three generations of EGFR TKIs have been used in clinical applications. AZD9291 (osimertinib; Tagrisso) is the first and only FDA approved third-generation EGFR TKI for T790M-positive advanced NSCLC patients. However, resistance to AZD9291 arises after 9–13 months of therapy. The mechanisms of resistance to third-generation inhibitors reported to date include the EGFR C797S mutation, EGFR L718Q mutation, and amplifications of HER-2, MET, or ERBB2. To overcome the acquired resistance to AZD9291, EAI045 was discovered and recently reported to be an allosteric EGFR inhibitor that overcomes T790M- and C797S-mediated resistance. This review summarizes recent investigations on the mechanisms of resistance to the EGFR TKIs, as well as the latest development of EAI045 as a fourth-generation EGFR inhibitor.
      datePublished:2016-12-23T00:00:00Z
      dateModified:2016-12-23T00:00:00Z
      pageStart:383
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External Links {πŸ”—}(218)

Analytics and Tracking {πŸ“Š}

  • Google Tag Manager

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