Evidence map›Paper›PMID 40285889›Full record

ArticleCancer immunology, immunotherapy : CII2025

Blockade of TIGAR prevents CD8

Jialin Cui, Wenjie Liu, Shiyang Zhong, Yiran Fang, Pei Xu, Cheng Xu, Rong Wang, Xingfei Hu, Wanting Zhou, Kening Li and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2025. 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

13 authors.

Jialin Cui *Department of Rehabilitation Medicine, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Wenjie Liu *Department of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Shiyang Zhong *Department of Bioinformatics, Nanjing Medical University, Nanjing, China.
Yiran FangDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Pei XuDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Cheng XuDepartment of Pathology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Rong WangDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Xingfei HuDepartment of Bioinformatics, Nanjing Medical University, Nanjing, China.
Wanting ZhouDepartment of Bioinformatics, Nanjing Medical University, Nanjing, China.
Kening LiDepartment of Bioinformatics, Nanjing Medical University, Nanjing, China.
Ming HongDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Sixuan QianDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China. qiansx@medmail.com.cn.ORCID http://orcid.org/0000-0003-1049-4238
Qian SunDepartment of Hematology, The First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China. kssq001@163.com.ORCID http://orcid.org/0000-0002-0297-5376

Funding

Jiangsu Province Hospital (the First Affiliated Hospital with Nanjing Medical University) Clinical Capacity Enhancement Project JSPH-MC-2023-11Medical Innovation Team CXZX202222National Natural Science Foundation of China 82170153Young Scholars Fostering Fund of the First Affiliated Hospital of Nanjing Medical University PY2023025
6 · The paper itself

Abstract

Acute myeloid leukemia (AML) cells and activated T cells rely on aerobic glycolysis for energy metabolism. The TP53-induced glycolysis and apoptosis regulator (TIGAR) inhibits glycolysis and protects AML cells from apoptosis. Preliminary studies suggest that combining TIGAR inhibition with the glycolysis inhibitor 2-deoxy-D-glucose (2-DG) may offer a therapeutic strategy for AML. However, it remains unclear whether silencing TIGAR can enhance T cell function and thereby improve AML prognosis. This study aims to investigate whether TIGAR silencing in host can eliminate AML cells and rejuvenate dysfunctional T cells with mouse models. TIGAR knockout mice on the C57BL/6J background were generated and AML mouse models were established through intravenous injection of C1498 cells. We found that TIGAR depletion enhanced CD8

Indexed as

CD8-Positive T-LymphocytesLeukemia, Myeloid, AcutePhosphoric Monoester HydrolasesAnimalsApoptosisApoptosis Regulatory ProteinsCell Line, TumorDisease Models, AnimalHumansMiceMice, Inbred C57BLMice, KnockoutApoptosis Regulatory ProteinsPhosphoric Monoester HydrolasesTIGAR protein, mouseAcute myeloid leukemiaKnockout miceSingle-cell RNA sequencingT-lymphocytesTP53-induced glycolysis and apoptosis regulator

Identifiers

PMID40285889
PMCPMC12033161

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.