Evidence map›Paper›PMID 26544866›Full record

ArticlePloS one2015

Up-Regulation of S100A11 in Lung Adenocarcinoma - Its Potential Relationship with Cancer Progression.

Tetsukan Woo, Koji Okudela, Hideaki Mitsui, Michihiko Tajiri, Yasushi Rino, Kenichi Ohashi, Munetaka Masuda

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  4. Review
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  7. Review
  8. Review
  9. The Calcium Binding Protein S100A11 and Its Roles in Diseases.Frontiers in cell and developmental biology · 2021
    Review
  10. Article
  11. Article
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  19. Active Secretion of Dimerized S100A11 Induced by the Peroxisome in Mesothelioma Cells.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2016
    Article
  20. 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

7 authors at 3 institutions in 1 country.

Tetsukan WooDepartment of Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Koji OkudelaDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Hideaki MitsuiDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Michihiko TajiriDepartment of Thoracic Surgery, Kanagawa Cardiovascular and Respiratory Center, Yokohama, Kanagawa, Japan.
Yasushi RinoDepartment of Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Kenichi OhashiDepartment of Pathology, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Munetaka MasudaDepartment of Surgery, Yokohama City University Graduate School of Medicine, Yokohama, Kanagawa, Japan.
Yokohama City University · JPKanagawa Cardiovascular and Respiratory Center · JPSaiseikai Yokohama Eastern Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that patients with lung adenocarcinomas with KRAS gene mutations and strong proliferating activity had poorer outcomes, even in the early stage of the disease. The aim of the present study was to elucidate the potential molecular basis of these highly malignant lung tumors by focusing on S100 proteins (S100A2, S100A7, and S100A11), which are downstream targets of oncogenic KRAS and promoters of tumor progression. The immunohistochemical expression of S100 proteins was examined in 179 primary lung adenocarcinomas, and the potential relationships between their levels and clinicopathologic factors were analyzed. Among the three subtypes, S100A11 levels were significantly higher in adenocarcinomas with KRAS mutations and strong proliferating activity. They were also higher in adenocarcinomas with poorly differentiated tumors. Furthermore, higher levels of S100A11 were associated with shorter disease-free survival. These results suggest that the up-regulation of S100A11 plays a role in tumor progression, particularly in KRAS-mutated lung adenocarcinomas.

Indexed as

AdenocarcinomaAdenocarcinoma of LungAgedCell DifferentiationCell ProliferationDisease-Free SurvivalDisease ProgressionFemaleHumansImmunohistochemistryKaplan-Meier EstimateLung NeoplasmsMaleMiddle AgedMutationProto-Oncogene Proteins p21(ras)KRAS protein, humanProto-Oncogene Proteins p21(ras)S100A11 protein, humanS100 Proteins

Identifiers

PMID26544866
PMCPMC4636248
OpenAlexW2224365682

What OpenQuestion holds

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LicenceCC BY
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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.