Evidence map›Paper›PMID 28596680›Full record

ArticleWorld journal of gastroenterology2017

Role of AXL in invasion and drug resistance of colon and breast cancer cells and its association with p53 alterations.

Wael M Abdel-Rahman, Noura A Al-Khayyal, Vidhya A Nair, S R Aravind, Maha Saber-Ayad

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastroenterology, 2017. 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
1.3field-weighted citation impact, top 21% 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, 29 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Receptor tyrosine kinase inhibitors in cancer.Cellular and molecular life sciences : CMLS · 2023
    Review
  7. Article
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  14. Calponin 3 promotes invasion and drug resistance of colon cancer cells.World journal of gastrointestinal oncology · 2019
    Article
  15. Review
  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

5 authors at 1 institution in 1 country.

Wael M Abdel-RahmanWael M Abdel-Rahman, Department of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, United Arab Emirates.
Noura A Al-KhayyalWael M Abdel-Rahman, Department of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, United Arab Emirates.
Vidhya A NairWael M Abdel-Rahman, Department of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, United Arab Emirates.
S R AravindWael M Abdel-Rahman, Department of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, United Arab Emirates.
Maha Saber-AyadWael M Abdel-Rahman, Department of Medical Laboratory Sciences, College of Health Sciences and Sharjah Institute for Medical Research, University of Sharjah, Sharjah 27272, United Arab Emirates.
University of Sharjah · AE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo characterize AXL receptor tyrosine kinase (AXL) expression in relationship to tumor protein P53 (

methodsWe used 14 cell lines, including 3 isogenic pairs carrying mutant/knockout p53, to gain insight into the relationship between AXL and

resultsWe showed that the introduction of p53 mutations or knockout increased expression levels of AXL in isogenic cells compared to the matching p53 wild-type parental cells. Overall, we found a trend for correlation between the potential EMT candidate AXL, p53 alterations, and EMT markers in colorectal and breast cancers. The expression of AXL in RKO cells, a rare colon cancer cell line with inactive Wnt signaling, suggests that the AXL oncogene might provide an alternative genetic pathway for colorectal carcinogenesis in the absence of Wnt signaling activation and

conclusionAXL is influenced by p53 status and could cause the emergence of aggressive clones after exposure to chemotherapy. These findings could have applications in cancer management.

Indexed as

AnimalsAxl Receptor Tyrosine KinaseBreast NeoplasmsCamptothecinCell Line, TumorCell SurvivalColonic NeoplasmsDoxorubicinFluorouracilGene Expression Regulation, NeoplasticGene SilencingHCT116 CellsHeLa CellsHumansIrinotecanMCF-7 CellsAxl Receptor Tyrosine KinaseCamptothecinDoxorubicinFluorouracilIrinotecanProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRNA, Small InterferingTP53 protein, humanTumor Suppressor Protein p53AXLBreast cancerChemotherapyColon cancerInvasion

Identifiers

PMID28596680
PMCPMC5442080
OpenAlexW2615678201

What OpenQuestion holds

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LicenceCC BY-NC
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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.