Evidence map›Paper›PMID 42728345›Full record

ArticleOncogene2026

Propionyl-CoA catabolism is a metabolic gatekeeper for fatty acid oxidation in pancreatic cancer.

Weidong Yu, Bo Wang, Fanhao Meng, Xiaojun Ren, Danyi Zhou, Huanxin Wei, Zhengquan Yang, Hongwei Sun, Minghua Jiang, Tao Xia and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Weidong Yu *Department of Clinical Laboratory, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Bo Wang *School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.
Fanhao Meng *School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.
Xiaojun RenLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, China.
Danyi ZhouSchool of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.
Huanxin WeiSchool of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, China.
Zhengquan YangLaboratory Medicine Center, Department of Clinical Laboratory, Zhejiang Provincial People's Hospital, Affiliated People's Hospital, Hangzhou Medical College, Hangzhou, China.
Hongwei SunDepartment of Hepatobiliary and Pancreatic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Minghua JiangDepartment of Clinical Laboratory, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.
Tao XiaDepartment of Hepatobiliary and Pancreatic Surgery, The Affiliated Lihuili Hospital of Ningbo University, Ningbo, China. taoxia@zju.edu.cn.ORCID http://orcid.org/0009-0005-3825-3235
Wei CuiDepartment of Clinical Laboratory, State Key Laboratory of Molecular Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, 100000, China. cui123@cicams.ac.cn.
Hezhi FangDepartment of Clinical Laboratory, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China. fangh@cicams.ac.cn.ORCID http://orcid.org/0000-0003-0956-3160

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82272435National Natural Science Foundation of China (National Science Foundation of China) 82472332Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LQ24H200004Natural Science Foundation of Zhejiang Province (Zhejiang Provincial Natural Science Foundation) LRG25H200001
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) cells rely on fatty acid oxidation (FAO) for proliferation; however, the regulatory mechanisms governing this dependency and their clinical implications remain unclear. Here, we report that PDAC patients exhibit decreased plasma levels of propionyl-CoA intermediates, alongside accelerated propionyl-CoA catabolic activity within both human PDAC tumors and Pdx1-Cre/Kras

Identifiers

PMID42728345

What OpenQuestion holds

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Registered trials

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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.