Evidence map›Paper›PMID 30349952›Full record

ArticleVirchows Archiv : an international journal of pathology2019

EVI1 expression is associated with aggressive behavior in intrahepatic cholangiocarcinoma.

Mariko Tanaka, Junji Shibahara, Shumpei Ishikawa, Tetsuo Ushiku, Teppei Morikawa, Aya Shinozaki-Ushiku, Akimasa Hayashi, Kento Misumi, Atsushi Tanaka, Hiroto Katoh and 7 more

Abstract read
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In one paragraph

Article in Virchows Archiv : an international journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 27% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
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  4. Review
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  11. International journal of molecular sciences · 2022
    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

17 authors at 4 institutions in 1 country.

Mariko TanakaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Junji ShibaharaDepartment of Pathology, Kyorin University Hospital, Tokyo, Japan.
Shumpei IshikawaDepartment of Genomic Pathology, Medical Research Institute Tokyo Medical and Dental University, Tokyo, Japan.
Tetsuo UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Teppei MorikawaPathology Division, NTT Medical Center Tokyo, Tokyo, Japan.
Aya Shinozaki-UshikuDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Akimasa HayashiDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Kento MisumiDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Atsushi TanakaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Hiroto KatohDepartment of Genomic Pathology, Medical Research Institute Tokyo Medical and Dental University, Tokyo, Japan.
Kei SakumaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Takashi KokudoDepartment of Surgery, Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshinori InagakiDepartment of Surgery, Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Junichi AritaDepartment of Surgery, Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Yoshihiro SakamotoDepartment of Surgery, Kyorin University Hospital, Tokyo, Japan.
Kiyoshi HasegawaDepartment of Surgery, Hepato-Biliary-Pancreatic Surgery, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masashi FukayamaDepartment of Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan. mfukayama-tky@umin.org.
The University of Tokyo · JPKyorin University Hospital · JPTokyo Medical and Dental University · JPNTT Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ecotropic virus integration site 1 protein homolog (EVI1), a well-known oncogenic transcriptional factor of hematopoietic cells, contributes to pancreatic cancer oncogenicity through increased expression of KRAS. Because EVI1 was upregulated in cholangiocarcinoma by referring The Cancer Genome Atlas, we investigated the importance of EVI1 in intrahepatic cholangiocarcinoma (ICC) which has been regarded as a heterogeneous group of cancers. Immunohistochemical analysis results demonstrated that EVI1 was overexpressed in about half of ICC (53/101, 52.5%). Moreover, all intraductal papillary neoplasms of the bile duct cases expressed EVI1 regardless of histological grading and subtypes such as gastric, intestinal, pancreatobiliary, or oncocytic (20/20, 100%). EVI1-positive ICC showed higher frequencies of aggressive pathological indicators such as periductal infiltrative growth (p = 0.022), hilar invasion (p = 0.041), advanced UICC stage (p = 0.026), major vascular invasion (p = 0.026), and perineural invasion (p = 0.007) than EVI1-negative ICC. Patients with EVI1-positive ICC showed worse overall survival and recurrence-free survival in all resected cases and in curative resected cases. Recently, we proposed type 1/2 (large/small duct types) classification of ICC based on mucin productivity and immunophenotypes (S100P, N-cadherin, and NCAM). Type 1 predominantly consisted of EVI1-positive ICC (33/42 cases, 79%), and the frequency was significantly higher than type 2 (18/55 cases, 32.7%) (p < 0.0001). EVI1-positive ICC was likely to express stomach-specific claudin CLDN18 (correlation coefficient r = 0.55373) and mucin MUC5AC (r = 0.42718). EVI1-positive ICC is an aggressive ICC showing both large-duct and/or gastric phenotypes. Consequently, a transcriptional factor EVI1 is associated with aggressive behavior in ICC and can be a therapeutic target molecule, while EVI1 might be a key molecule for the development of intraductal papillary neoplasms of the bile duct.

Indexed as

AgedBile Duct NeoplasmsBiomarkers, TumorCholangiocarcinomaDisease ProgressionFemaleHepatectomyHumansImmunohistochemistryMaleMDS1 and EVI1 Complex Locus ProteinMiddle AgedProgression-Free SurvivalTime FactorsTreatment OutcomeBiomarkers, TumorMDS1 and EVI1 Complex Locus ProteinMECOM protein, humanEVI1Gastric phenotypeIntrahepatic cholangiocarcinomaType 1Type 2

Identifiers

PMID30349952
OpenAlexW2896442954

What OpenQuestion holds

Textmetadata
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.