Evidence map›Paper›PMID 20156777›Full record

ReviewClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2010

Non-small-cell lung cancer harbouring mutations in the EGFR kinase domain.

Rafael Rosell, Teresa Morán, Enric Carcereny, Vanessa Quiroga, Miguel Angel Molina, Carlota Costa, Susana Benlloch, Miquel Tarón

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Hereditary lung cancer syndrome targets never smokers with germline EGFR gene T790M mutations.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2014
    Article
  17. Article
  18. Oncogenic driver mutations in lung cancer.Translational respiratory medicine · 2013
    Review
  19. Article
  20. Article
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

8 authors at 3 institutions in 1 country.

Rafael RosellCatalan Institute of Oncology, Hospital Germans Trias i Pujol, Badalona, Barcelona, Spain. rrosell@ico.scs.es
Teresa Morán
Enric Carcereny
Vanessa Quiroga
Miguel Angel Molina
Carlota Costa
Susana Benlloch
Miquel Tarón
Institut Català d'Oncologia · ESUSP Institut Universitari Dexeus · ESHospital Universitari Germans Trias i Pujol · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Key "driver" mutations have been discovered in specific subgroups of non-small-cell lung cancer (NSCLC) patients. Activating mutations in the form of deletions in exon 19 (del 19) or the missense mutation L858R in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) predict outcome to EGFR tyrosine kinase inhibitors (TKIs) such as gefitinib and erlotinib. Pooled data from several phase II studies show that gefitinib and erlotinib induce responses in over 70% of NSCLC patients harbouring EGFR mutations, with progression-free survival (PFS) ranging from 9 to 13 months and median survival of around 23 months. Two studies in Caucasian and Asian patients have confirmed that these subgroups of patients attain response rates of 70% with erlotinib and ge- fitinib, including complete responses, PFS up to 14 months and median survival up to 27 months. These landmark outcomes have been accompanied by new challenges: the additional role of chemotherapy and the management of tumours with the secondary T790M mutation that confers resistance to EGFR TKIs. Mechanisms of resistance to reversible EGFR TKIs should be further clarified and could be related to modifications in DNA repair. The presence of double mutations (T790M plus either L858R or del 19) at the time of diagnosis could be much more frequent than originally thought. The sensitivity to EGFR TKIs could be greatly influenced by the expression of genes involved in the repair of DNA double-strand breaks by homologous recombination and non-homologous end joining.

Indexed as

MutationAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorDatabases, GeneticDrug Resistance, NeoplasmErbB ReceptorsHumansLung NeoplasmsModels, BiologicalPhosphotransferasesProtein Structure, TertiarySpainAntineoplastic AgentsEGFR protein, humanErbB ReceptorsPhosphotransferases

Identifiers

PMID20156777
OpenAlexW1986348452

What OpenQuestion holds

Textmetadata
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.