ReviewBlood2023
Metabolism in stem cell-driven leukemia: parallels between hematopoiesis and immunity.
Review in Blood, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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.
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.
Who cites it
18 citing papers in PubMed, 12 citations in OpenAlex.
- Exploiting Metabolic Vulnerabilities in Acute Myeloid Leukemia: Rationale and Evidence for Combining Metabolic Modulators with Conventional Chemotherapy.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Protein phosphatase 2A orchestrates hematopoietic fate determination via modulation of lactate metabolism.Haematologica · 2026Article
- The distinct roles of ROS in tumor immunity: from mechanisms to immunotherapeutic applications.Journal of hematology & oncology · 2026Review
- Decoding Leukemic Stem Cells in AML: From Identification to Targeted Eradication.Diseases (Basel, Switzerland) · 2026Review
- Leukemia stem cells in acute myeloid leukemia: biology, therapeutic resistance, and barriers to durable remission.Journal of biomed research · 2026Article
- Regulating Ferroptosis in Leukemic Stem Cells: From Stemness Preservation to Targeted Differentiation Strategies.Stem cell reviews and reports · 2026Review
- Hepatic Metabolic Dysregulation as a Potential Amplifier of Leukemogenesis Following mRNA Vaccination: A Novel Mechanistic Hypothesis.Medicina (Kaunas, Lithuania) · 2025Article
- Metabolic Signature ofJournal of personalized medicine · 2025Review
- Haematopoietic ageing in health and lifespan.Nature cell biology · 2025Review
- Glycolysis Induces Abnormal Transcription Through Histone Lactylation in T-cell Acute Lymphoblastic Leukemia.Genomics, proteomics & bioinformatics · 2025Article
- Epigenetic modifications in hematopoietic ecosystem: a key tuner from homeostasis to acute myeloid leukemia.Blood science (Baltimore, Md.) · 2024Review
- A metabolic atlas of blood cells in young and aged mice identifies uridine as a metabolite to rejuvenate aged hematopoietic stem cells.Nature aging · 2024Article
- Condensate-Promoting ENL Mutation Drives Tumorigenesis In Vivo Through Dynamic Regulation of Histone Modifications and Gene Expression.Cancer discovery · 2024Article
- Prognostic implications of metabolism-related genes in acute myeloid leukemia.Frontiers in genetics · 2024Article
- Zebrafish drug screening identifies Erlotinib as an inhibitor of Wnt/β-catenin signaling and self-renewal in T-cell acute lymphoblastic leukemia.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Article
- DNMT3A mutation promotes leukemia development through NAM-NAD metabolic reprogramming.Journal of translational medicine · 2023Article
- Therapeutic targeting of leukemia stem cells in acute myeloid leukemia.Frontiers in oncology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Our understanding of cancer metabolism spans from its role in cellular energetics and supplying the building blocks necessary for proliferation, to maintaining cellular redox and regulating the cellular epigenome and transcriptome. Cancer metabolism, once thought to be solely driven by upregulated glycolysis, is now known to comprise multiple pathways with great plasticity in response to extrinsic challenges. Furthermore, cancer cells can modify their surrounding niche during disease initiation, maintenance, and metastasis, thereby contributing to therapy resistance. Leukemia is a paradigm model of stem cell-driven cancer. In this study, we review how leukemia remodels the niche and rewires its metabolism, with particular attention paid to therapy-resistant stem cells. Specifically, we aim to give a global, nonexhaustive overview of key metabolic pathways. By contrasting the metabolic rewiring required by myeloid-leukemic stem cells with that required for hematopoiesis and immune cell function, we highlight the metabolic features they share. This is a critical consideration when contemplating anticancer metabolic inhibitor options, especially in the context of anticancer immune therapies. Finally, we examine pathways that have not been studied in leukemia but are critical in solid cancers in the context of metastasis and interaction with new niches. These studies also offer detailed mechanisms that are yet to be investigated in leukemia. Given that cancer (and normal) cells can meet their energy requirements by not only upregulating metabolic pathways but also utilizing systemically available substrates, we aim to inform how interlinked these metabolic pathways are, both within leukemic cells and between cancer cells and their niche.
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What OpenQuestion holds
Registered trials
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.