Evidence map›Paper›PMID 34824448›Full record

ArticleBritish journal of cancer2022

Neoadjuvant therapy alters the collagen architecture of pancreatic cancer tissue via Ephrin-A5.

Kosei Nakajima, Yoshinori Ino, Chie Naito, Satoshi Nara, Mari Shimasaki, Utako Ishimoto, Toshimitsu Iwasaki, Noriteru Doi, Minoru Esaki, Yoji Kishi and 2 more

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 20 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

12 authors at 1 institution in 2 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.
Chie NaitoDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Satoshi NaraHepato-Biliary and Pancreatic Surgery Division, National Cancer Center Hospital, Tokyo, Japan.ORCID http://orcid.org/0000-0002-3516-8765
Mari ShimasakiDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Utako IshimotoDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Toshimitsu IwasakiDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Noriteru DoiDivision of Molecular Pathology, National Cancer Center Research Institute, Tokyo, Japan.
Minoru EsakiHepato-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. nhiraoka@ncc.go.jp.ORCID http://orcid.org/0000-0003-4215-4385
National Cancer Centre Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe treatment of pancreatic cancer (PDAC) remains clinically challenging, and neoadjuvant therapy (NAT) offers down staging and improved surgical resectability. Abundant fibrous stroma is involved in malignant characteristic of PDAC. We aimed to investigate tissue remodelling, particularly the alteration of the collagen architecture of the PDAC microenvironment by NAT.

methodsWe analysed the alteration of collagen and gene expression profiles in PDAC tissues after NAT. Additionally, we examined the biological role of Ephrin-A5 using primary cultured cancer-associated fibroblasts (CAFs).

resultsThe expression of type I, III, IV, and V collagen was reduced in PDAC tissues after effective NAT. The bioinformatics approach provided comprehensive insights into NAT-induced matrix remodelling, which showed Ephrin-A signalling as a likely pathway and Ephrin-A5 (encoded by EFNA5) as a crucial ligand. Effective NAT reduced the number of Ephrin-A5

conclusionThese results suggest that effective NAT changes the extracellular matrix with collagen profiles through CAFs and their Ephrin-A5 expression.

Indexed as

Antineoplastic AgentsCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalCell ProliferationCollagenEphrin-A5Gene Expression ProfilingGene Expression Regulation, NeoplasticHumansNeoadjuvant TherapyPancreatic NeoplasmsPrimary Cell CultureRetrospective StudiesSignal TransductionTumor Cells, CulturedTumor MicroenvironmentAntineoplastic AgentsCollagenEphrin-A5

Identifiers

PMID34824448
PMCPMC8854423
OpenAlexW3216877735

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.