Evidence map›Paper›PMID 27590506›Full record

ArticleOncotarget2016

A novel application of E1A in combination therapy with EGFR-TKI treatment in breast cancer.

Chih-Ming Su, Ting-Yu Chang, Hui-Ping Hsu, Hui-Huang Lai, Jie-Ning Li, Yu-Jhen Lyu, Kuang-Tai Kuo, Ming-Te Huang, Jen-Liang Su, Pai-Sheng Chen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. 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 5 institutions in 1 country.

Chih-Ming SuDivision of General Surgery, Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei City, Taiwan, ROC.
Ting-Yu ChangNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan, ROC.
Hui-Ping HsuDepartment of Surgery, National Cheng Kung University Hospital, Tainan, Taiwan, ROC.
Hui-Huang LaiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Jie-Ning LiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Yu-Jhen LyuDepartment of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
Kuang-Tai KuoDivision of Thoracic Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan, ROC.
Ming-Te HuangDivision of General Surgery, Department of Surgery, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan, ROC.
Jen-Liang SuNational Institute of Cancer Research, National Health Research Institutes, Zhunan, Miaoli Country, Taiwan, ROC.
Pai-Sheng ChenInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan, ROC.
National Cheng Kung University · TWNational Health Research Institutes · TWTaipei Medical University-Shuang Ho Hospital · TWNational Cheng Kung University Hospital · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epidermal growth factor receptor (EGFR) is commonly overexpressed in breast cancer and is associated with poor clinical outcomes; however, an increasing number of patients have shown a poor effective response to EGFR tyrosine kinase inhibitors (EGFR-TKI). Here, we found that AXL expression was positively correlated with poor progression in breast cancer patients. Suppression of AXL by an anti-tumor protein, E1A, enhanced EGFR-TKI (gefitinib, erlotinib and lapatinib) sensitization, resulting in significant inhibition of tumor growth in breast cancer cells. Additionally, AXL overexpression dramatically impaired E1A-mediated EGFR-TKI sensitization. These findings show that downregulation of AXL expression by E1A contributes to sensitization to EGFR-TKI in breast cancer, suggesting that combinatorial therapy of AXL inhibitors or E1A gene therapy with EGFR-TKI may be a potential therapeutic strategy for treatment of breast cancer patients.

Indexed as

Adenovirus E1A ProteinsAnimalsApoptosisAxl Receptor Tyrosine KinaseBreast NeoplasmsCell Line, TumorCell SurvivalDisease ProgressionDown-RegulationDrug Resistance, NeoplasmErbB ReceptorsErlotinib HydrochlorideFemaleGefitinibGenetic TherapyHumansAdenovirus E1A ProteinsAxl Receptor Tyrosine KinaseEGFR protein, humanErbB ReceptorsErlotinib HydrochlorideGefitinibLapatinibProtein Kinase InhibitorsProto-Oncogene ProteinsQuinazolinesReceptor Protein-Tyrosine Kinasescombination therapyE1A

Identifiers

PMID27590506
PMCPMC5325414
OpenAlexW2509553765

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.