Evidence map›Paper›PMID 36747147›Full record

ArticleBMC cancer2023

1,5-Anhydroglucitol promotes pre-B acute lymphocytic leukemia progression by driving glycolysis and reactive oxygen species formation.

Huasu Zhu, Huixian Ma, Na Dong, Min Wu, Dong Li, Linghong Liu, Qing Shi, Xiuli Ju

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. 1,5-Anhydroglucitol Aggravates Acute Liver Failure via the PPARα Signaling Pathway.Journal of clinical and translational hepatology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
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 at 1 institution in 1 country.

Huasu ZhuDepartment of Pediatrics, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Huixian MaLaboratory of Cryomedicine, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Na DongDepartment of Pediatrics, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Min WuDepartment of Pediatrics, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Dong LiLaboratory of Cryomedicine, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Linghong LiuLaboratory of Cryomedicine, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Qing ShiLaboratory of Cryomedicine, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China.
Xiuli JuDepartment of Pediatrics, Qilu Hospital of Shandong University, Jinan, 250012, Shandong Province, China. jxlqlyy@163.com.
Qilu Hospital of Shandong University · CN

Funding

Clinical Research Center of Shandong University No. 2020SDUCRCA010
6 · The paper itself

Abstract

backgroundPrecursor B-cell acute lymphoblastic leukemia (pre-B ALL) is the most common hematological malignancy in children. Cellular metabolic reorganization is closely related to the progression and treatment of leukemia. We found that the level of 1,5-anhydroglucitol (1,5-AG), which is structurally similar to glucose, was elevated in children with pre-B ALL. However, the effect of 1,5-AG on pre-B ALL was unclear. Here, we aimed to reveal the roles and mechanisms of 1,5-AG in pre-B ALL progression.

methodsThe peripheral blood plasma level of children with initial diagnosis of pre-B ALL and that of healthy children was measured using untargeted metabolomic analysis. Cell Counting Kit-8 assay, RNA sequencing, siRNA transfection, real-time quantitative PCR, and western blot were performed using pre-B ALL cell lines Reh and HAL-01. Cell cycle, cell apoptosis, ROS levels, and the positivity rate of CD19 were assessed using flow cytometry. Oxygen consumption rates and extracellular acidification rate were measured using XFe24 Extracellular Flux Analyzer. The lactate and nicotinamide adenine dinucleotide phosphate levels were measured using kits. The effect of 1,5-AG on pre-B ALL progression was verified using the In Vivo Imaging System in a xenotransplantation leukemia model.

resultsWe confirmed that 1,5-AG promoted the proliferation, viability, and intracellular glycolysis of pre-B ALL cells. Mechanistically, 1,5-AG promotes glycolysis while inhibiting mitochondrial respiration by upregulating pyruvate dehydrogenase kinase 4 (PDK4). Furthermore, high levels of intracellular glycolysis promote pre-B ALL progression by activating the reactive oxygen species (ROS)-dependent mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway. Conversely, N-acetylcysteine or vitamin C, an antioxidant, effectively inhibited 1,5-AG-mediated progression of leukemia cells.

conclusionsOur study reveals a previously undiscovered role of 1,5-AG in pre-B ALL, which contributes to an in-depth understanding of anaerobic glycolysis in the progression of pre-B ALL and provides new targets for the clinical treatment of pre-B ALL.

Indexed as

Precursor B-Cell Lymphoblastic Leukemia-LymphomaPrecursor Cell Lymphoblastic Leukemia-LymphomaApoptosisCell Line, TumorCell ProliferationChildDeoxyglucoseExtracellular Signal-Regulated MAP KinasesGlycolysisHumansReactive Oxygen Species1,5-anhydroglucitolDeoxyglucoseExtracellular Signal-Regulated MAP KinasesReactive Oxygen Species1,5-anhydroglucitolGlucose metabolismPre-B acute lymphoblastic leukemiaReactive oxygen speciesRedox homeostasis

Identifiers

PMID36747147
PMCPMC9903573
OpenAlexW4319302233

What OpenQuestion holds

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LicenceCC BY
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.