Evidence map›Paper›PMID 25091415›Full record

ArticleScientific reports2014

Structural signature of the G719S-T790M double mutation in the EGFR kinase domain and its response to inhibitors.

George Priya C Doss, B Rajith, Chiranjib Chakraborty, N NagaSundaram, Shabana Kouser Ali, Hailong Zhu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Mutant-Selective Binding ofInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Article
  10. E2Computers in biology and medicine · 2022
    Article
  11. Article
  12. Article
  13. Observational
  14. Strategies to overcome acquired resistance to EGFR TKI in the treatment of non-small cell lung cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

George Priya C DossMedical Biotechnology Division, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu, India.
B RajithMedical Biotechnology Division, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu, India.
Chiranjib ChakrabortyDepartment of Bio-informatics, School of Computer and Information Sciences, Galgotias University, India.
N NagaSundaramMedical Biotechnology Division, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu, India.
Shabana Kouser AliMedical Biotechnology Division, School of Biosciences and Technology, VIT University, Vellore, Tamil Nadu, India.
Hailong ZhuDepartment of Computer Science, Hong Kong Baptist University, Kowloon Tong, Hong Kong.
Vellore Institute of Technology University · INGalgotias University · INHong Kong Baptist University · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Some individuals with non-small-cell lung cancer (NSCLC) benefit from therapies targeting epidermal growth factor receptor (EGFR), and the characterization of a new mechanism of resistance to the EGFR-specific antibody gefitinib will provide valuable insight into how therapeutic strategies might be designed to overcome this particular resistance mechanism. The G719S and T790M mutations and their combination were involved in causing different conformational redistribution of EGFR. In the present computational study, we analyzed the impact and structural influence of G719S/T790M double mutation (DM) in EGFR with ligand (gefitinib) through molecular dynamic simulation (50 ns) and docking analysis. We observed the escalation in distance between the functional loop and activation loop with respect to T790M mutation compared to the G719S mutation. Furthermore, we confirmed that the G719S mutation causes the ligand to move closer to the hinge region, whereas T790M makes the ligand escape from the binding pocket. Obtained results provide with an explanation for the resistance induced by T790M and a vital clue for the design of drugs to combat gefitinib resistance.

Indexed as

Antineoplastic AgentsCarcinoma, Non-Small-Cell LungDrug Resistance, NeoplasmErbB ReceptorsGefitinibGene ExpressionHumansLigandsLung NeoplasmsMolecular Docking SimulationMolecular Dynamics SimulationMutationNeoplasm ProteinsPrincipal Component AnalysisProtein Kinase InhibitorsProtein Structure, SecondaryAntineoplastic AgentsEGFR protein, humanErbB ReceptorsGefitinibLigandsNeoplasm ProteinsProtein Kinase InhibitorsQuinazolines

Identifiers

PMID25091415
PMCPMC4121614
OpenAlexW2004226562

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.