Evidence map›Paper›PMID 41763448›Full record

ReviewCancer letters2026

PPARδ: An underappreciated tumor accelerator in pancreatic ductal adenocarcinoma.

Danping Niu, Daoyan Wei, Yi Liu, James C Yao, Imad Shureiqi, Xiangsheng Zuo

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cancer letters, 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

6 authors.

Danping NiuDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Daoyan WeiDepartment of Gastroenterology and Hepatology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Yi LiuDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
James C YaoDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.
Imad ShureiqiDivision of Hematology and Oncology, Department of Internal Medicine, University of Michigan, USA; Rogel Cancer Center, University of Michigan, USA. Electronic address: ishureiq@med.umich.edu.
Xiangsheng ZuoDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. Electronic address: xzuo@mdanderson.org.

Funding

ALOX15 regulation of colon cancer invasiveness via PI3P-linoleic acid metabolismR01CA266223 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Imad Shureiqi · 2022 to 2026
$3.2M
PPARD hyperactivation promotes pancreatic intraepithelial neoplasia progression into pancreatic ductal adenocarcinomaR01CA273732 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Imad Shureiqi · 2024 to 2026
$1.9M
Molecular Understanding and Targeting of Determinant Factors in Gastric TumorigenesisR01CA236905 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI ZUO, XIANGSHENG · 2021 to 2025
$1.8M
NCI NIH HHS R01 CA236905NCI NIH HHS R01 CA266223NCI NIH HHS R01 CA273732
6 · The paper itself

Abstract

Pancreatic cancer, primarily pancreatic ductal adenocarcinoma (PDAC), is one of the leading causes of cancer-related death, largely due to its late diagnosis and highly aggressive nature. Although precursors such as pancreatic intraepithelial neoplasia (PanIN), often harboring KRAS mutations, are commonly detected in adults; PanIN rarely progresses to invasive PDAC. The molecular mechanisms that govern this PanIN-to-PDAC transition remain poorly understood. Peroxisome proliferator-activated receptor delta (PPARδ), a ligand-activated nuclear transcription factor, plays critical roles in lipid metabolism, inflammation and tumorigenesis across multiple cancer types. In this brief review, we summarize recent advances and emerging evidence implicating PPARδ activation in oncogenic KRAS-initiated pancreatic tumorigenesis and progression, with emphasis on mechanisms such as metabolic reprogramming and immune suppression. These integrated insights underscore PPARδ as a potential therapeutic target in this lethal malignancy.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsPPAR deltaAnimalsDisease ProgressionHumansMetabolic ReprogrammingProto-Oncogene Proteins p21(ras)Signal TransductionKRAS protein, humanPPAR deltaProto-Oncogene Proteins p21(ras)iTMEMetabolic remodelingOncogenic KRASPanIN to PDAC progressionPPARδTargeted anti-cancer therapy

Identifiers

PMID41763448
PMCPMC13054940

What Socratic holds

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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 Socratic graph.