Evidence map›Paper›PMID 40349055›Full record

ArticleDiagnostic pathology2025

Long-chain fatty acyl CoA synthetase 4 expression in pancreatic cancer: a marker for malignant lesions and prognostic indicator for recurrence.

Daiki Uchihara, Shohei Shimajiri, Yoshikazu Harada, Keiichiro Kumamoto, Shinji Oe, Koichiro Miyagawa, Koichi Nakamura, Eisuke Katafuchi, Fariza Nuratdinova, Yuichi Honma and 3 more

Abstract read
In one paragraph

Article in Diagnostic pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

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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

4 citing papers in PubMed.

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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

13 authors.

Daiki UchiharaDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan. uchihara-daiki1127@med.uoeh-u.ac.jp.
Shohei ShimajiriDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Yoshikazu HaradaDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Keiichiro KumamotoDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Shinji OeThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Koichiro MiyagawaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Koichi NakamuraDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Eisuke KatafuchiDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Fariza NuratdinovaDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Yuichi HonmaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Michihiko ShibataThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Masaru HaradaThird Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Toshiyuki NakayamaDepartment of Pathology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLong-chain fatty acyl CoA synthetase 4 (ACSL4) is crucial for lipid metabolism, primarily catalyzing the formation of 12-20 carbon chain fatty acids. ACSL4 is upregulated in various cancers and linked to aggressive behavior and poor survival. A bioinformatics study showing ACSL4 upregulation in pancreatic cancer. However, utility for actual pathological diagnosis and clinical significance in pancreatic ductal adenocarcinoma (PDAC) and intraductal papillary mucinous neoplasm (IPMN) are unexplored. This study aimed to investigate ACSL4 expression in PDAC and IPMN, and evaluate its clinical implications.

methodsWe examined ACSL4 expression using immunohistochemistry in 165 patients with PDAC and IPMN. Differences in ACSL4 expression between malignant and benign lesions were evaluated using the Pearson χ2 test. The association between ACSL4 expression, pathological parameters, and survival was assessed through Kaplan-Meier and Cox regression analyses in 96 patients with invasive cancer.

resultsCompared to normal pancreatic ducts, low-grade pancreatic intraepithelial neoplasm, and intraductal papillary mucinous adenoma (IPMA) (3.3%, 3.4%, and 2.7%, respectively), ACSL4 expression was significantly higher in invasive PDAC, noninvasive intraductal papillary mucinous carcinoma (IPMC), and invasive IPMC (77%, 86.7%, and 93.9%, respectively). In invasive cancers, low ACSL4 expression was associated with a higher frequency of lymphovascular invasion and recurrence and shorter disease-free survival (P = 0.006). Additionally, low ACSL4 expression was an independent prognostic factor for shorter disease-free survival in multivariable Cox regression analysis (HR = 2.409, 95% CI: 1.121-5.180, P = 0.024).

conclusionACSL4 expression helps differentiate cancerous from precancerous lesions in pancreatic cancer, but low expression is linked to a higher frequency of lymphovascular invasion and shorter disease-free survival in invasive cases. Due to the limited sample size and broad confidence intervals, the findings of this study should be interpreted with caution and require validation in larger, independent cohorts.

Indexed as

Adenocarcinoma, MucinousBiomarkers, TumorCarcinoma, Pancreatic DuctalCoenzyme A LigasesNeoplasm Recurrence, LocalPancreatic Intraductal NeoplasmsPancreatic NeoplasmsAdultAgedAged, 80 and overFemaleHumansImmunohistochemistryKaplan-Meier EstimateLong-Chain-Fatty-Acid-CoA LigaseMaleBiomarkers, TumorCoenzyme A LigasesLong-Chain-Fatty-Acid-CoA LigaseACSL4DiagnosisIntraductal papillary mucinous neoplasmPancreatic ductal adenocarcinomaPrognosis

Identifiers

PMID40349055
PMCPMC12065365

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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.