Evidence map›Paper›PMID 27821106›Full record

ArticleBMC cancer2016

Aberrant activation of Notch signaling in extrahepatic cholangiocarcinoma: clinicopathological features and therapeutic potential for cancer stem cell-like properties.

Shuichi Aoki, Masamichi Mizuma, Yayoi Takahashi, Yoichi Haji, Ryo Okada, Tomoya Abe, Hideaki Karasawa, Keiichi Tamai, Takaho Okada, Takanori Morikawa and 6 more

Abstract read
In one paragraph

Article in BMC cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

  1. Article
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  11. Review
  12. Review
  13. Notch Signaling Pathway in Pancreatobiliary Tumors.Medicina (Kaunas, Lithuania) · 2021
    Article
  14. Notch signalling pathway in development of cholangiocarcinoma.World journal of gastrointestinal oncology · 2020
    Review
  15. Cholangiocarcinoma 2020: the next horizon in mechanisms and management.Nature reviews. Gastroenterology & hepatology · 2020
    Review
  16. A Novel Flow Cytometric Assay to Identify Inhibitors of RBPJ-DNA Interactions.SLAS discovery : advancing life sciences R & D · 2020
    Article
  17. Article
  18. Article
  19. Article
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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

16 authors.

Shuichi AokiDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Masamichi MizumaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan. masamichi@surg1.med.tohoku.ac.jp.
Yayoi TakahashiDepartment of Pathology, Tohoku University Hospital, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Yoichi HajiDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Ryo OkadaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Tomoya AbeDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Hideaki KarasawaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Keiichi TamaiDivision of Cancer Stem Cell, Miyagi Cancer Center Research Institute, 47-1 Nodayama, Medeshimashiote aza, Natori, 981-1293, Japan.
Takaho OkadaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Takanori MorikawaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Hiroki HayashiDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Kei NakagawaDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Fuyuhiko MotoiDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Takeshi NaitohDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Yu KatayoseDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.
Michiaki UnnoDepartment of Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai, 980-8574, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLittle is known about the roles of Notch signaling in cholangiocarcinoma (CC). The expression of hairy and enhancer of split 1 (Hes-1) has not been investigated yet in resected specimens of CC. Notch signaling has been reported to be related to cancer stem cell (CSC) like properties in some malignancies. Our aim is to investigate the participation of Notch signaling in resected specimens of extrahepatic CC (EHCC) and to evaluate the efficacy of CC cells with CSC-like properties by Notch signaling blockade.

methodsFirst, the expression of Notch1, 2, 3, 4 and Hes-1 was examined by immunohistochemistry in 132 resected EHCC specimens. The clinicopathological characteristics in the expression of Notch receptors and Hes-1 were investigated. Second, GSI IX, which is a γ-secretase-inhibitor, was used for Notch signaling blockade in the following experiment. Alterations of the subpopulation of CD24

resultsNotch1, 2, 3, 4 and Hes-1 in the resected EHCC specimens were expressed in 50.0, 56.1, 42.4, 6.1, and 81.8 % of the total cohort, respectively. Notch1 and 3 expressions were associated with poorer histological differentiation (P = 0.008 and 0.053). The patients with the expression of at least any one of Notch1-3 receptors, who were in 80.3 % of the total, exhibited poorer survival (P = 0.050). Similarly, the expression of Hes-1 tended to show poor survival (P = 0.093). In all of the examined CC cell lines, GSI IX treatment significantly diminished the subpopulation of CD24

conclusionAberrant Notch signaling is involved with EHCC. Inhibition of Notch signaling is a novel therapeutic strategy for targeting cells with CSC-like properties.

Indexed as

Signal TransductionAdolescentAdultAgedAged, 80 and overAnimalsBile Duct NeoplasmsBiomarkersCell Line, TumorCell ProliferationCholangiocarcinomaDisease Models, AnimalFemaleGene ExpressionHeterograftsHumansBiomarkersHES1 protein, humanReceptors, NotchTranscription Factor HES-1Cancer stem cellCholangiocarcinomaHes-1Notch signaling

Identifiers

PMID27821106
PMCPMC5100105

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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.