Evidence map›Paper›PMID 27100677›Full record

ArticlePloS one2016

Clinical, Pathological, and Molecular Features of Lung Adenocarcinomas with AXL Expression.

Katsuaki Sato, Kenichi Suda, Shigeki Shimizu, Kazuko Sakai, Hiroshi Mizuuchi, Kenji Tomizawa, Toshiki Takemoto, Kazuto Nishio, Tetsuya Mitsudomi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Katsuaki SatoDivision of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.ORCID 0000-0003-4045-7796
Kenichi SudaDivision of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Shigeki ShimizuDepartment of Pathology, Hyogo College of Medicine, Hyogo, Japan.
Kazuko SakaiDepartment of Genome Biology, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Hiroshi MizuuchiDivision of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Kenji TomizawaDivision of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Toshiki TakemotoDivision of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Kazuto NishioDepartment of Genome Biology, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Tetsuya MitsudomiDivision of Thoracic Surgery, Department of Surgery, Kinki University Faculty of Medicine, Osaka-Sayama, Japan.
Kindai University · JPHyogo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The receptor tyrosine kinase AXL is a member of the Tyro3-Axl-Mer receptor tyrosine kinase subfamily. AXL affects several cellular functions, including growth and migration. AXL aberration is reportedly a marker for poor prognosis and treatment resistance in various cancers. In this study, we analyzed clinical, pathological, and molecular features of AXL expression in lung adenocarcinomas (LADs). We examined 161 LAD specimens from patients who underwent pulmonary resections. When AXL protein expression was quantified (0, 1+, 2+, 3+) according to immunohistochemical staining intensity, results were 0: 35%; 1+: 20%; 2+: 37%; and 3+: 7% for the 161 samples. AXL expression status did not correlate with clinical features, including smoking status and pathological stage. However, patients whose specimens showed strong AXL expression (3+) had markedly poorer prognoses than other groups (P = 0.0033). Strong AXL expression was also significantly associated with downregulation of E-cadherin (P = 0.025) and CD44 (P = 0.0010). In addition, 9 of 12 specimens with strong AXL expression had driver gene mutations (6 with EGFR, 2 with KRAS, 1 with ALK). In conclusion, we found that strong AXL expression in surgically resected LADs was a predictor of poor prognosis. LADs with strong AXL expression were characterized by mesenchymal status, higher expression of stem-cell-like markers, and frequent driver gene mutations.

Indexed as

AdenocarcinomaAgedAnaplastic Lymphoma KinaseAntineoplastic AgentsAxl Receptor Tyrosine KinaseCadherinsDown-RegulationErbB ReceptorsFemaleGefitinibHumansHyaluronan ReceptorsImmunohistochemistryKaplan-Meier EstimateLungLung NeoplasmsALK protein, humanAnaplastic Lymphoma KinaseAntineoplastic AgentsAXL protein, humanAxl Receptor Tyrosine KinaseCadherinsErbB ReceptorsGefitinibHyaluronan ReceptorsKRAS protein, humanProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)QuinazolinesReceptor Protein-Tyrosine Kinases

Identifiers

PMID27100677
PMCPMC4839706
OpenAlexW2342308623

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.