Evidence map›Paper›PMID 38843841›Full record

ArticleCell reports. Medicine2024

A CD36-dependent non-canonical lipid metabolism program promotes immune escape and resistance to hypomethylating agent therapy in AML.

He-Zhou Guo, Rui-Xue Feng, Yan-Jie Zhang, Ye-Hua Yu, Wei Lu, Jia-Jia Liu, Shao-Xin Yang, Chong Zhao, Zhao-Li Zhang, Shan-He Yu and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Coixenolide Enhances Antitumor Immunity of Cytotoxic CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  6. CD36: bridging metabolism, inflammation, and reproduction.npj metabolic health and disease · 2026
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Senescent fibroblasts drive CD8Journal of translational medicine · 2026
    Article
  13. Article
  14. Dual relevance ofFrontiers in oncology · 2026
    Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

15 authors.

He-Zhou GuoDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China; Shanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital, Shanghai Jiao-Tong University School of Medicine and School of Life Sciences and Biotechnology, Shanghai Jiao-Tong University, Shanghai, China.
Rui-Xue FengShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital, Shanghai Jiao-Tong University School of Medicine and School of Life Sciences and Biotechnology, Shanghai Jiao-Tong University, Shanghai, China.
Yan-Jie ZhangDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Ye-Hua YuDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Wei LuDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Jia-Jia LiuDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Shao-Xin YangDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Chong ZhaoDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Zhao-Li ZhangDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China.
Shan-He YuShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital, Shanghai Jiao-Tong University School of Medicine and School of Life Sciences and Biotechnology, Shanghai Jiao-Tong University, Shanghai, China.
Hui JinDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Si-Xuan QianDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Jian-Yong LiDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China. Electronic address: lijianyonglm@126.com.
Jiang ZhuShanghai Institute of Hematology, State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine at Shanghai, Collaborative Innovation Center of Hematology, Ruijin Hospital, Shanghai Jiao-Tong University School of Medicine and School of Life Sciences and Biotechnology, Shanghai Jiao-Tong University, Shanghai, China. Electronic address: zhujiang@shsmu.edu.cn.
Jun ShiDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. Electronic address: junshi@sjtu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Environmental lipids are essential for fueling tumor energetics, but whether these exogenous lipids transported into cancer cells facilitate immune escape remains unclear. Here, we find that CD36, a transporter for exogenous lipids, promotes acute myeloid leukemia (AML) immune evasion. We show that, separately from its established role in lipid oxidation, CD36 on AML cells senses oxidized low-density lipoprotein (OxLDL) to prime the TLR4-LYN-MYD88-nuclear factor κB (NF-κB) pathway, and exogenous palmitate transfer via CD36 further potentiates this innate immune pathway by supporting ZDHHC6-mediated MYD88 palmitoylation. Subsequently, NF-κB drives the expression of immunosuppressive genes that inhibit anti-tumor T cell responses. Notably, high-fat-diet or hypomethylating agent decitabine treatment boosts the immunosuppressive potential of AML cells by hijacking CD36-dependent innate immune signaling, leading to a dampened therapeutic effect. This work is of translational interest because lipid restriction by US Food and Drug Administration (FDA)-approved lipid-lowering statin drugs improves the efficacy of decitabine therapy by weakening leukemic CD36-mediated immunosuppression.

Indexed as

CD36 AntigensDecitabineLeukemia, Myeloid, AcuteLipid MetabolismLipoproteins, LDLAcyltransferasesAnimalsCell Line, TumorDrug Resistance, NeoplasmHumansImmunity, InnateMiceMice, Inbred C57BLMyeloid Differentiation Factor 88NF-kappa BSignal TransductionAcyltransferasesCD36 AntigensCD36 protein, humanDecitabineLipoproteins, LDLMyeloid Differentiation Factor 88NF-kappa Boxidized low density lipoproteinToll-Like Receptor 4

Identifiers

PMID38843841
PMCPMC11228649

What OpenQuestion 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 OpenQuestion graph.