Evidence map›Paper›PMID 37872214›Full record

ArticleOncogene2023

Low doses of IFN-γ maintain self-renewal of leukemia stem cells in acute myeloid leukemia.

Xiaoling Xie, Wuju Zhang, Xuan Zhou, Binyan Xu, Hao Wang, Yingqi Qiu, Yuxing Hu, Bin Guo, Zhixin Ye, Le Hu and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.5field-weighted citation impact, top 7% of its field
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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Blockade of TIGAR prevents CD8Cancer immunology, immunotherapy : CII · 2025
    Article
  9. Review
  10. 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

13 authors at 2 institutions in 1 country.

Xiaoling Xie *Department of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China. xxl413@smu.edu.cn.ORCID 0000-0003-1970-4537
Wuju Zhang *Central Laboratory, The Fifth Affiliated Hospital, Southern Medical University, 510910, Guangzhou, China.
Xuan ZhouDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Binyan XuDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Hao WangDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Yingqi QiuDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Yuxing HuDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China.
Bin GuoGuangdong Provincial Key Laboratory of Bone and Joint Degenerative Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Zhixin YeGuangdong Provincial Key Laboratory of Bone and Joint Degenerative Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Le HuGuangdong Provincial Key Laboratory of Bone and Joint Degenerative Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China.
Honghao ZhangDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China.ORCID 0000-0003-1572-0425
Yuhua LiDepartment of Hematology, Zhujiang Hospital, Southern Medical University, 510280, Guangzhou, China. liyuhua1974@outlook.com.ORCID 0000-0002-0982-6680
Xiaochun BaiGuangdong Provincial Key Laboratory of Bone and Joint Degenerative Diseases, Department of Cell Biology, School of Basic Medical Sciences, Southern Medical University, 510515, Guangzhou, China. baixc15@smu.edu.cn.ORCID 0000-0001-9631-4781
Zhujiang Hospital · CNSouthern Medical University · CN

Funding

China Postdoctoral Science Foundation 2022M720060National Natural Science Foundation of China (National Science Foundation of China) 81991510National Natural Science Foundation of China (National Science Foundation of China) 81991511National Natural Science Foundation of China (National Science Foundation of China) 82100155
6 · The paper itself

Abstract

Conventional therapies for acute myeloid leukemia (AML) often fail to eliminate the disease-initiating leukemia stem cell (LSC) population, leading to disease relapse. Interferon-γ (IFN-γ) is a known inflammatory cytokine that promotes antitumor responses. Here, we found that low serum IFN-γ levels correlated with a higher percentage of LSCs and greater relapse incidence in AML patients. Furthermore, IFNGR1 was overexpressed in relapsed patients with AML and associated with a poor prognosis. We showed that high doses (5-10 μg/day) of IFN-γ exerted an anti-AML effect, while low doses (0.01-0.05 μg/day) of IFN-γ accelerated AML development and supported LSC self-renewal in patient-derived AML-LSCs and in an LSC-enriched MLL-AF9-driven mouse model. Importantly, targeting the IFN-γ receptor IFNGR1 by using lentiviral shRNAs or neutralizing antibodies induced AML differentiation and delayed leukemogenesis in vitro and in mice. Overall, we uncovered essential roles for IFN-γ and IFNGR1 in AML stemness and showed that targeting IFNGR1 is a strategy to decrease stemness and increase differentiation in relapsed AML patients.

Indexed as

Interferon-gammaLeukemia, Myeloid, AcuteAnimalsCarcinogenesisHumansMiceNeoplastic Stem CellsRecurrenceInterferon-gamma

Identifiers

PMID37872214
OpenAlexW4387879699

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.