Evidence map›Paper›PMID 35123536›Full record

ArticleDiagnostic pathology2022

LGR5 expression and clinicopathological features of the invasive front in the fat infiltration area of pancreatic cancer.

Masato Kamakura, Takeshi Uehara, Mai Iwaya, Shiho Asaka, Shota Kobayashi, Tomoyuki Nakajima, Yasuhiro Kinugawa, Tadanobu Nagaya, Takahiro Yoshizawa, Akira Shimizu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Diagnostic pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

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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

6 citing papers in PubMed, 7 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 1 country.

Masato KamakuraDepartment of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan.
Takeshi UeharaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan. tuehara@shinshu-u.ac.jp.
Mai IwayaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan.
Shiho AsakaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan.
Shota KobayashiDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan.
Tomoyuki NakajimaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan.
Yasuhiro KinugawaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan.
Tadanobu NagayaDepartment of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan.
Takahiro YoshizawaDepartment of Surgery, Shinshu University School of Medicine, Matsumoto, Japan.
Akira ShimizuDepartment of Surgery, Shinshu University School of Medicine, Matsumoto, Japan.
Hiroyoshi OtaDepartment of Laboratory Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, 390-8621, Matsumoto, Japan.
Takeji UmemuraDepartment of Gastroenterology, Shinshu University School of Medicine, Matsumoto, Japan.
Shinshu University · JP

Funding

Hokuto Foundation for Bioscience none
6 · The paper itself

Abstract

backgroundLeucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5) is a strong cancer stem cell marker in colorectal cancer; however, there are many unclear aspects of LGR5 expression in pancreatic cancer. It has been reported that the interaction between tumor cells and stroma at the fat infiltration site has a significant effect on pancreatic cancer prognosis. Therefore, we report a clinicopathological study of LGR5 expression at the fat invasion front in pancreatic cancer.

methodsLGR5 expression was analyzed in 40 pancreatic ductal adenocarcinoma cases with RNAscope, which is a newly developed high-sensitivity in situ hybridization method. Epithelial-mesenchymal transition (EMT) was analyzed by the expression of E-cadherin and vimentin via immunohistochemistry.

resultsLGR5-positive dots were identified in all cases, especially with glandular formation. In the fat invasion front, a high histological grade showed significantly reduced LGR5 expression compared with a low histological grade (p=0.0126). LGR5 expression was significantly higher in the non-EMT phenotype group than in EMT phenotype group (p=0.0003). Additionally, LGR5 expression was significantly lower in cases with high vascular invasion than in those with low vascular invasion (p=0.0244).

conclusionsThese findings suggest that decreased LGR5 expression in the fat invasion front is associated with more aggressive biological behavior in pancreatic ductal adenocarcinoma, with higher tumor grade, EMT phenotype, and higher vascular invasion.

Indexed as

AdenocarcinomaCarcinoma, Pancreatic DuctalPancreatic NeoplasmsBiomarkers, TumorEpithelial-Mesenchymal TransitionHumansNeoplastic Stem CellsPrognosisReceptors, G-Protein-CoupledBiomarkers, TumorLGR5 protein, humanReceptors, G-Protein-Coupledcancer stem cellFat invasionLeucine-rich repeat-containing G-protein-coupled receptor 5 (LGR5)Pancreatic ductal adenocarcinomaRNA in situ hybridization

Identifiers

PMID35123536
PMCPMC8818226
OpenAlexW4210576216

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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.