ReviewCell death discovery2024
Crosstalk between autophagy and metabolism: implications for cell survival in acute myeloid leukemia.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 13 citations in OpenAlex.
- The Inv(16) Oncogene CBFB::MYH11 is Required for the Survival of Leukemia Cells in the Blood and Spleen, but not the Bone Marrow.Oncogene · 2026Article
- Inhibition of NHE1 Overcomes Temozolomide-Resistance in Glioblastoma via ROS-AKT/ERK Axis-Mediated Autophagy Suppression.Journal of biochemical and molecular toxicology · 2026Article
- AcTor, a novel mTOR stimulator, potentiates ixazomib for the treatment of acute myeloid leukemia.Molecular cancer · 2026Article
- AcTor, a novel mTOR stimulator, potentiates ixazomib for the treatment of acute myeloid leukemia.Research square · 2026Article
- Targeting LAPTM5 enhances AML sensitivity to cytarabine through autophagy inhibition.Cell death & disease · 2026Article
- Investigating autophagy and miRNAs as therapeutic targets in leukemia.Discover oncology · 2026Review
- Solubility based mechanistic profiling of combinatorial drug therapy.Nature communications · 2026Article
- Autophagy and Lipid Metabolism as a Therapeutic Target for Overcoming Drug Resistance in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2026Review
- LC3 gene expression as a marker of autophagy in acute myeloid and lymphoblastic leukemia: a systematic review.Discover oncology · 2026Review
- Glycolysis and glycolytic enzymes in acute myeloid leukemia: Warburg and beyond.Frontiers in pharmacology · 2026Review
- Metabolic reprogramming in tumor-associated cells of hematologic malignancies: mechanisms, crosstalk networks, and therapeutic implications in the tumor microenvironment.Frontiers in immunology · 2026Review
- Unraveling autophagy-metabolism crosstalk in cancer: Molecular insights and therapeutic strategies.Theranostics · 2026Review
- Discovery of Golgi membrane-associated degradation (GOMED) pathway: a focus on 15 years of ultrastructural analyses.Microscopy (Oxford, England) · 2025Review
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- Lysosome targeted therapies in hematological malignancies.Frontiers in oncology · 2025Review
- Dissecting L-glutamine metabolism in acute myeloid leukemia: single-cell insights and therapeutic implications.Journal of translational medicine · 2024Article
- Spatial metabolomics highlights metabolic reprogramming in acute myeloid leukemia mice through creatine pathway.Acta pharmaceutica Sinica. B · 2024Article
- Prediction of acute myeloid leukemia prognosis based on autophagy features and characterization of its immune microenvironment.Frontiers in immunology · 2024Article
- Cancer statistics, 2025.CA: a cancer journal for cliniciansArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML), a prevalent form of leukemia in adults, is often characterized by low response rates to chemotherapy, high recurrence rates, and unfavorable prognosis. A critical barrier in managing refractory or recurrent AML is the resistance to chemotherapy. Increasing evidence indicates that tumor cell metabolism plays a crucial role in AML progression, survival, metastasis, and treatment resistance. Autophagy, an essential regulator of cellular energy metabolism, is increasingly recognized for its role in the metabolic reprogramming of AML. Autophagy sustains leukemia cells during chemotherapy by not only providing energy but also facilitating rapid proliferation through the supply of essential components such as amino acids and nucleotides. Conversely, the metabolic state of AML cells can influence the activity of autophagy. Their mutual coordination helps maintain intrinsic cellular homeostasis, which is a significant contributor to chemotherapy resistance in leukemia cells. This review explores the recent advancements in understanding the interaction between autophagy and metabolism in AML cells, emphasizing their roles in cell survival and drug resistance. A comprehensive understanding of the interplay between autophagy and leukemia cell metabolism can shed light on leukemia cell survival strategies, particularly under adverse conditions such as chemotherapy. This insight may also pave the way for innovative targeted treatment strategies.
Identifiers
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.