Evidence map›Paper›PMID 20934974›Full record

ArticleThe American journal of pathology2010

Co-activation of epidermal growth factor receptor and c-MET defines a distinct subset of lung adenocarcinomas.

Daisuke Matsubara, Shumpei Ishikawa, Oguni Sachiko, Hiroyuki Aburatani, Masashi Fukayama, Toshiro Niki

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. 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
3.1field-weighted citation impact, top 8% 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, 49 citations in OpenAlex.

  1. Randomized phase II trial of Onartuzumab in combination with erlotinib in patients with advanced non-small-cell lung cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2013
    Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Phase Ib Study of Telisotuzumab Vedotin in Combination With Erlotinib in Patients With c-Met Protein-Expressing Non-Small-Cell Lung Cancer.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023
    Article
  9. Article
  10. Article
  11. Understanding the Mechanisms of Resistance inInternational journal of molecular sciences · 2019
    Review
  12. Article
  13. BeyondAnnals of translational medicine · 2018
    Review
  14. Review
  15. Article
  16. Targeting MET in Lung Cancer: Will Expectations Finally Be MET?Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2017
    Review
  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 2 institutions in 1 country.

Daisuke MatsubaraDepartment of Integrative Pathology, Jichi Medical University, 3311-1 Yakushiji, Shimotsuke-shi, Tochigi, 329-0498, Japan.
Shumpei Ishikawa
Oguni Sachiko
Hiroyuki Aburatani
Masashi Fukayama
Toshiro Niki
Jichi Medical University · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) and MET are molecular targets for lung cancer treatment. The relationships between expression, activation, and gene abnormalities of these two targets are currently unclear. Here, we demonstrate that a panel of 40 lung cancer cell lines could be classified into two groups. Group I was characterized by (1) high phosphorylations of MET and EGFR, (2) frequent mutation or amplification of EGFR, MET, and human epidermal growth factor receptor-2 (HER2), (3) high expressions of bronchial epithelial markers (thyroid transcription factor-1 (TTF-1), MUC1, and Cytokeratin 7 (CK7)); and (4) high expressions of MET, human epidermal growth factor receptor-3, E-cadherin, cyclooxygenase-2, and laminin gamma2. In contrast, Group II exhibited little or no phosphorylation of MET and EGFR; no mutation or amplification of EGFR, MET, and HER2; were triple-negative for TTF-1, MUC1, and CK7; and showed high expressions of vimentin, fibroblast growth factor receptor-1, and transcription factor 8. Importantly, Group I was more sensitive to gefitinib and more resistant to cisplatin and paclitaxel than Group II. The clinical relevance was confirmed in publicly available data on 442 primary lung adenocarcinoma patients; survival benefits by postoperative chemotherapy were seen in only patients with tumors corresponding to Group II. Overall, co-activation of EGFR and MET defines a distinct subgroup of lung carcinoma with characteristic genetic abnormalities, gene expression pattern, and response to chemotherapeutic reagents.

Indexed as

AdenocarcinomaAnimalsAntineoplastic AgentsBiomarkers, TumorCell Line, TumorCell ProliferationCisplatinCluster AnalysisEnzyme ActivationErb-b2 Receptor Tyrosine KinasesErbB ReceptorsGefitinibGene Expression ProfilingHumansLung NeoplasmsOligonucleotide Array Sequence AnalysisAntineoplastic AgentsBiomarkers, TumorCisplatinErb-b2 Receptor Tyrosine KinasesErbB ReceptorsGefitinibKRAS protein, humanPaclitaxelProto-Oncogene ProteinsProto-Oncogene Proteins c-metProto-Oncogene Proteins p21(ras)Quinazolinesras Proteins

Identifiers

PMID20934974
PMCPMC2966779
OpenAlexW2124717208

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.