Evidence map›Paper›PMID 41939310›Full record

ArticleACS omega2026

Tumor Lipidomic Changes after Treatment with Polymeric Hydroxychloroquine in a Syngeneic Murine Model of Pancreatic Cancer.

Sai Sundeep Kollala, Ling Ding, Sudipta Panja, Amar B Singh, David Oupicky, Daryl J Murry

Abstract read
In one paragraph

Article in ACS omega, 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.

Sai Sundeep KollalaDepartment of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska 68198-7400, United States.
Ling DingCenter for Drug Delivery and Nanomedicine, Department of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States.
Sudipta PanjaCenter for Drug Delivery and Nanomedicine, Department of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States.ORCID https://orcid.org/0000-0001-5692-450X
Amar B SinghDepartment of Medicine, The University of Kansas Medical Center, Kansas City, Kansas 66160, United States.
David OupickyCenter for Drug Delivery and Nanomedicine, Department of Pharmaceutical Sciences, College of Pharmacy, University of Nebraska Medical Center, Omaha, Nebraska 68198, United States.
Daryl J MurryDepartment of Pharmacy Practice and Science, University of Nebraska Medical Center, Omaha, Nebraska 68198-7400, United States.ORCID https://orcid.org/0000-0002-4169-5027

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most lethal malignancies, with limited treatment options. Altered lipid metabolism, including dysregulated eicosanoid pathways, plays a role in PDAC progression and therapy resistance. In this study, we investigated the impact of a treatment with polymeric hydroxychloroquine (PCQ), a novel macromolecular derivative of hydroxychloroquine (HCQ), on tumor lipid metabolism in a syngeneic mouse model of PDAC. Using a validated LC-MS/MS method, we quantified 72 eicosanoids in tumors to assess the metabolic changes induced by PCQ and HCQ treatment. Our findings revealed significant PCQ-mediated downregulation of multiple protumorigenic eicosanoids, including PGD2, PGJ2, LTE4, LTB4, and HETEs, and upregulation of antitumor resolvins. This was further confirmed by Partial Least Squares Discriminant Analysis (PLS-DA) and heatmap analysis. The parent compound HCQ showed minimal impact on eicosanoid concentrations in the tumors, with no significant alterations at 24-h and modulation of only six eicosanoids downregulated at 72-h post treatment. Overall, our data highlight a novel role of PCQ in modulating tumor lipid metabolism, suggesting a unique mechanism of action and its potential as an adjuvant agent in the therapy of PDAC.

Identifiers

PMID41939310
PMCPMC13044646

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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.