ArticleLeukemia2013
Anti-leukemic mechanisms of pegylated arginase I in acute lymphoblastic T-cell leukemia.
Article in Leukemia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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.
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Who cites it
38 citing papers in PubMed, 48 citations in OpenAlex.
- The role of L-Arginine metabolism in the hallmarks of cancer as an emerging pathway to drug design.Frontiers in pharmacology · 2026Review
- Polyamines at the crossroad between cell metabolism and epigenetic regulation in acute leukemias.Cell death discovery · 2025Review
- Exploring Metabolic Approaches for Epithelial Ovarian Cancer Therapy.Journal of cellular physiology · 2025Review
- Multifaceted role of GCN2 in tumor adaptation and therapeutic targeting.Translational oncology · 2024Review
- Loss of Anti-Tumor Efficacy by Polyamine Blocking Therapy in GCN2 Null Mice.Biomedicines · 2023Article
- Amino acids in hematologic malignancies: Current status and future perspective.Frontiers in nutrition · 2023Review
- Preclinical investigation of Pegylated arginase 1 as a treatment for retina and brain injury.Experimental neurology · 2022Article
- Arginine-dependent immune responses.Cellular and molecular life sciences : CMLS · 2021Review
- The Importance of Cellular Metabolic Pathways in Pathogenesis and Selective Treatments of Hematological Malignancies.Frontiers in oncology · 2021Review
- Adaptive Mechanisms of Tumor Therapy Resistance Driven by Tumor Microenvironment.Frontiers in cell and developmental biology · 2021Review
- Inhibition of arginase modulates T-cell response in the tumor microenvironment of lung carcinoma.Oncoimmunology · 2021Article
- The Role of Amino Acids in the Crosstalk Between Mesenchymal Stromal Cells and Neoplastic Cells in the Hematopoietic Niche.Frontiers in cell and developmental biology · 2021Review
- Cancer Cell Metabolism Bolsters Immunotherapy Resistance by Promoting an Immunosuppressive Tumor Microenvironment.Frontiers in oncology · 2020Review
- Metabolic dependencies and vulnerabilities in leukemia.Genes & development · 2019Review
- Role of tumor and host autophagy in cancer metabolism.Genes & development · 2019Review
- ER stress-induced mediator C/EBP homologous protein thwarts effector T cell activity in tumors through T-bet repression.Nature communications · 2019Article
- Rewiring urea cycle metabolism in cancer to support anabolism.Nature reviews. Cancer · 2018Review
- Arginase 1 promotes retinal neurovascular protection from ischemia through suppression of macrophage inflammatory responses.Cell death & disease · 2018Article
- Sensitivity of Colorectal Cancer to Arginine Deprivation Therapy is Shaped by Differential Expression of Urea Cycle Enzymes.Scientific reports · 2018Article
- Time-resolved analysis of amino acid stress identifies eIF2 phosphorylation as necessary to inhibit mTORC1 activity in liver.The Journal of biological chemistry · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
New treatments for adults with acute lymphoblastic T-cell leukemia (T-ALL) are urgently needed, as the current rate of overall remission in these patients is only about 40 percent. We recently showed the potential therapeutic benefit of the pegylated-human-arginase I (peg-Arg I) in T-ALL. However, the mechanisms by which peg-Arg I induces an anti-T-ALL effect remained unknown. Our results show the induction of T-ALL cell apoptosis by peg-Arg I, which associated with a global arrest in protein synthesis and with the phosphorylation of the eukaryotic-translation-initiation factor 2 alpha (eIF2α). Inhibition of eIF2α phosphorylation in T-ALL cells prevented the apoptosis induced by peg-Arg I, whereas the expression of a phosphomimetic eIF2α form increased the sensibility of T-ALL cells to peg-Arg I. Phosphorylation of eIF2α by peg-Arg I was mediated through kinases PERK and GCN2 and down-regulation of phosphatase GADD34. GCN2 and decreased GADD34 promoted T-ALL cell apoptosis after treatment with peg-Arg I, whereas PERK had an unexpected anti-apoptotic role. Additional results showed that phospho-eIF2α signaling further increased the anti-leukemic effects induced by peg-Arg I in T-ALL-bearing mice. These results suggest the central role of phospho-eIF2α in the anti-T-ALL effects induced by peg-Arg I and support its study as a therapeutic target.
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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.