Evidence map›Paper›PMID 41973605›Full record

ArticleEuropean thyroid journal2026

Preliminary study on ketone body metabolism in anaplastic thyroid cancer.

Jiaqi Wang, Yuting Mao, Ziyang Xuan, Zhihao Li, Xi Tang, Ke Yang, Mingluan Xing, Xin Zhu

Abstract read
In one paragraph

Article in European thyroid journal, 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

8 authors.

Jiaqi WangDepartment of Pathology, Ningbo Clinical Pathology Diagnosis Center, Ningbo, Zhejiang, China.
Yuting MaoPostgraduate Training Base Alliance of Wenzhou Medical University (Zhejiang Cancer Hospital), Hangzhou, China.
Ziyang XuanPostgraduate Training Base Alliance of Wenzhou Medical University (Zhejiang Cancer Hospital), Hangzhou, China.
Zhihao LiPostgraduate Training Base Alliance of Wenzhou Medical University (Zhejiang Cancer Hospital), Hangzhou, China.
Xi TangZhejiang Cancer Institute, Zhejiang Cancer Hospital, Hangzhou, China.
Ke YangZhejiang Cancer Institute, Zhejiang Cancer Hospital, Hangzhou, China.
Mingluan XingDepartment of Environmental Health, Zhejiang Provincial Center for Disease Control and Prevention, Hangzhou, China.
Xin ZhuPostgraduate Training Base Alliance of Wenzhou Medical University (Zhejiang Cancer Hospital), Hangzhou, China.ORCID 0000-0001-5337-4661

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Anaplastic thyroid cancer (ATC) is characterized by high invasiveness and rapid progression and has a poor prognosis. The aim of this study was to investigate the role of ketone body metabolism in ATC and provide a novel approach for ATC treatment. Methods: Human ATC cell lines, including 8505C and CAL-62, were used as the research objects. Cell Counting Kit-8 and colony formation assays appraised cell proliferation. Flow cytometry was performed to evaluate the cell cycle and apoptosis. Wound healing and transwell assays verified the migration and invasion of cells. Furthermore, tumor xenograft models were established to investigate the therapeutic effect of ketogenic diet in vivo. Immunohistochemistry was used to quantify the expression level of Ki67, Bcl-2, and caspase-3 in tumor tissues. Importantly, autophagy analyses included fluorescence microscopy for the observation of monodansylcadaverine staining, western blotting, and tissue immunofluorescence to determine autophagic protein (LC3, Beclin1, and p62) expression. Results: Acetoacetate (AcAc) inhibited the proliferation, migration, and invasion of ATC cells (8505C and CAL-62) and induced cell cycle arrest. Ketogenic diet significantly inhibited tumor growth in vivo. AcAc markedly elevated the level of autophagy. Autophagy inhibitor weakened the extent to which AcAc hindered cell proliferation, migration, and invasion and blocked cell cycle. Conclusion: The study demonstrated that the ketone body metabolite AcAc inhibits the proliferation, migration, and invasion of ATC cells and induces cell cycle arrest by inducing autophagy. Ketogenic diet provides a new strategy for the treatment of ATC.

Indexed as

AcetoacetatesKetone BodiesThyroid Carcinoma, AnaplasticThyroid NeoplasmsAnimalsApoptosisAutophagyCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationDiet, KetogenicHumansMiceMice, NudeNeoplasm InvasivenessAcetoacetatesacetoacetic acidKetone Bodiesacetoacetateanaplastic thyroid cancerautophagyketogenic dietketone body metabolism

Identifiers

PMID41973605
PMCPMC13130877

What Socratic holds

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LicenceCC BY-NC-ND
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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.