Evidence map›Paper›PMID 33178497›Full record

ArticleOncoimmunology2020

IAP inhibitor, Embelin increases VCAM-1 levels on the endothelium, producing lymphocytic infiltration and antitumor immunity.

Kosei Nakajima, Yoshinori Ino, Rie Yamazaki-Itoh, Chie Naito, Mari Shimasaki, Mami Takahashi, Minoru Esaki, Satoshi Nara, Yoji Kishi, Kazuaki Shimada and 1 more

Open access · goldAbstract read
In one paragraph

Article in Oncoimmunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 25% 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

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

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
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  7. Review
  8. 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

11 authors at 2 institutions in 3 countries.

Kosei NakajimaDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Yoshinori InoDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Rie Yamazaki-ItohDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Chie NaitoDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Mari ShimasakiDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Mami TakahashiCentral Animal Division, National Cancer Center Research Institute, Tokyo, Japan.
Minoru EsakiHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Satoshi NaraHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Yoji KishiHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Kazuaki ShimadaHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.
Nobuyoshi HiraokaDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.ORCID 0000-0003-4215-4385
National Cancer Research Institute · GBNational Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is an increasing unmet need for successful immunotherapeutic interventions. Lymphocyte extravasation via tumor tissue endothelial cells (TECs) is required for lymphocyte infiltration into tumor sites. This study aimed to investigate the clinical significance of dysfunctional TECs in pancreatic ductal adenocarcinoma (PDAC) and identify chemical compounds that boost tumor-infiltrating lymphocyte (TIL) numbers. We performed immunohistochemical detection and clinicopathological analysis of VCAM-1 on TECs, which is essential for lymphocyte trafficking. We characterized the gene expression profiles of TECs from fresh PDAC tissues. We isolated compounds that upregulated VCAM-1 and E-selectin expression in TECs and examined their biological activities. Compared to endothelial cells from chronic pancreatitis tissue, TECs showed significantly lower VCAM-1 and E-selectin expression and significant weaknesses in lymphocyte adhesion and transmigration, resulting in decreased T cell infiltration around vessels. Patients with a relatively high percentage of VCAM-1

Indexed as

Pancreatic NeoplasmsVascular Cell Adhesion Molecule-1BenzoquinonesEndothelial CellsEndotheliumHumansBenzoquinonesembelinVascular Cell Adhesion Molecule-1compound screeningimmunotherapylymphocyte infiltrationpancreas cancertumor endothelial cells

Identifiers

PMID33178497
PMCPMC7595596
OpenAlexW3094912610

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.