Evidence map›Paper›PMID 25634113›Full record

ArticleOncology reports2015

AURKA upregulation plays a role in fibroblast-reduced gefitinib sensitivity in the NSCLC cell line HCC827.

Jia Chen, Huiqi Lu, Wang Zhou, Huabin Yin, Lishuang Zhu, Chang Liu, Pengfei Zhang, Huimin Hu, Yili Yang, Huanxing Han

Open access · bronzeAbstract read
In one paragraph

Article in Oncology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Antiproliferative Activity of a New Quinazolin-4(3Pharmaceuticals (Basel, Switzerland) · 2022
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. The role of Aurora-A in human cancers and future therapeutics.American journal of cancer research · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Design, synthesis and biological activity of NJournal of enzyme inhibition and medicinal chemistry · 2018
    Article
  16. 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

10 authors at 2 institutions in 2 countries.

Jia ChenTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Huiqi LuTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Wang ZhouDepartment of Bone Tumor Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, P.R. China.
Huabin YinDepartment of Bone Tumor Surgery, Changzheng Hospital, Second Military Medical University, Shanghai, P.R. China.
Lishuang ZhuTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Chang LiuTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Pengfei ZhangTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Huimin HuTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Yili YangCancer and Developmental Biology Laboratory, National Cancer Institute, Frederick, MD, USA.
Huanxing HanTranslational Medicine Center, Changzheng Hospital, Affiliated to The Second Military Medical University, Shanghai, P.R. China.
Second Military Medical University · CNNational Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs) have been used to treat non-small cell lung carcinoma (NSCLC) patients that have EGFR-activating mutations. EGFR-TKI monotherapy in most NSCLC patients with EGFR mutations who initially respond to EGFR-TKIs results in the development of acquired resistance. We investigated the role of fibroblasts in stromal cell-mediated resistance to gefitinib-induced apoptosis in EGFR-mutant NSCLC cells. While gefitinib induced apoptosis in EGFR-mutant NSCLC cells, apoptosis induction was diminished under stromal co-culture conditions. Protection appeared to be mediated in part by Aurora-A kinase (AURKA) upregulation. The protective effect of stromal cells was significantly reduced by pre-exposure to AURKA-shRNA. We suggest that combinations of AURKA antagonists and EGFR inhibitors may be effective in clinical trials targeting mutant EGFR NSCLCs.

Indexed as

Antineoplastic AgentsAurora Kinase ACarcinoma, Non-Small-Cell LungCell Line, TumorCoculture TechniquesDrug Resistance, NeoplasmEnzyme InductionErbB ReceptorsFibroblastsGefitinibGene Expression Regulation, NeoplasticGene Regulatory NetworksGenes, erbB-1HumansLung NeoplasmsNeoplasm ProteinsAntineoplastic AgentsAURKA protein, humanAurora Kinase AEGFR protein, humanErbB ReceptorsGefitinibMDM2 protein, humanNeoplasm ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins c-mdm2QuinazolinesRecombinant Fusion ProteinsRNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID25634113
PMCPMC4440218
OpenAlexW1979800807

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.