Evidence map›Paper›PMID 41525037›Full record

ArticleClinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico2026

Single-cell and spatial transcriptomics reveal mTOR-driven cellular fate of spindle cells and immune evasion in classic Kaposi's sarcoma.

Ting Su, Yongkai Yu, Xuechen Cao, Yidan Wang, Zhonglan Su, Guoxin Song, Lu Sun, Yue Chen, Yan Lu

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Article in Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico, 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
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0citing papers in PubMed
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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

9 authors.

Ting Su *Department of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yongkai Yu *Department of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Xuechen CaoDepartment of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yidan WangDepartment of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Zhonglan SuDepartment of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Guoxin SongDepartment of Patology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Lu SunDepartment of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Yue ChenDepartment of Dermatology, The Friendship Hospital of Ili Kazakh Autonomous Prefecture, Ili & Jiangsu Joint Institute of Health, Ili, China. 809740563@qq.com.
Yan LuDepartment of Dermatology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China. luyan6289@163.com.ORCID http://orcid.org/0000-0001-8372-3324

Funding

Basic Research Program of Jiangsu Province SBK2022023090National Natural Science Foundation of China 82273549the Science Foundation Project of Ili & Jiangsu Joint Institute of Health yl2022zd01
6 · The paper itself

Abstract

backgroundClassic Kaposi's sarcoma (CKS) is an angiogenic tumor with no standardized treatment. Increased mTOR pathway activity in tumors fuels oncogenesis by stimulating anabolic metabolism, cell proliferation, and angiogenesis. This study aimed to assess the therapeutic potential of mTOR inhibitor metformin in CKS patients.

methodsTwo consecutive patients with biopsy-proven, CKS received metformin as monotherapy, and we further leverage single-cell RNA sequencing and spatial transcriptomics to uncover its underlying molecular mechanisms.

resultsRapid clinical response with no adverse effects was observed in 2 CKS patients. Further investigation identified characteristic spindle cells (SCs) exhibiting heightened activity in VEGF, mTOR, and hypoxia signaling pathways, suggestive of a terminal stromal differentiation state. Besides, the immune landscape was characterized by a high proportion of CD8+ Tex and NK cells displaying suppressed cytotoxicity and migration functions. Crucially, SCs were found to interact with immune cells predominantly via the CXCL9-CXCR3 signaling axis.

conclusionThis study reveals the mTOR-driven differentiation of SCs in KS pathogenesis aligning with rapid clinical improvement in CKS patients, which provides compelling evidence for metformin's therapeutic potential in CKS.

Indexed as

MetforminMTOR InhibitorsSarcoma, KaposiTOR Serine-Threonine KinasesTumor EscapeChemokine CXCL9FemaleHumansKiller Cells, NaturalMaleReceptors, CXCR3Signal TransductionSingle-Cell Gene Expression AnalysisSpatial TranscriptomicsVascular Endothelial Growth Factor AChemokine CXCL9CXCL9 protein, humanCXCR3 protein, humanMetforminMTOR InhibitorsMTOR protein, humanReceptors, CXCR3TOR Serine-Threonine KinasesVascular Endothelial Growth Factor AChromatin accessibilityKaposi’s sarcomaSingle-cell sequencingSpatial transcriptomeSpindle cell

Identifiers

PMID41525037

What Socratic 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 Socratic graph.