ArticleBlood2012
Autophagic degradation of the BCR-ABL oncoprotein and generation of antileukemic responses by arsenic trioxide.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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.
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
74 citing papers in PubMed, 129 citations in OpenAlex.
- Autophagy modulation in cancer.Nature reviews. Drug discovery · 2026Review
- The autophagy switch: A critical determinant of arsenic-induced carcinogenesis and cancer therapy.Toxicology reports · 2026Review
- Structure-Activity Relationship Studies Enable Optimization of a Small-Molecule Autophagy Activator and Evaluation of Effects on Cell Death Pathways.ACS pharmacology & translational science · 2026Article
- Independent PML::RARA-positive acute promyelocytic leukemia arising during BCR::ABL1-positive chronic myeloid leukemia.Journal of clinical and experimental hematopathology : JCEH · 2026Article
- Comprehensive pan-cancer analysis of p62 reveals its contribution to shaping tumor microenvironment and anti-tumor immunity.Discover oncology · 2025Article
- Deciphering the dual role of autophagy in gastric cancer and gastroesophageal junction cancer: from tumor suppression to cancer progression.Discover oncology · 2025Review
- SUMOylation facilitates the stability of BCR-ABL to promote chronic myeloid leukemia progression.Oncogene · 2025Article
- Folate-Appended Hydroxypropyl-β-Cyclodextrin Induces Autophagic Cell Death in Acute Myeloid Leukemia Cells.International journal of molecular sciences · 2023Article
- Histone lysine demethylase 3B regulates autophagy via transcriptional regulation ofInternational journal of oncology · 2023Article
- The new insights into autophagy in thyroid cancer progression.Journal of translational medicine · 2023Review
- Article
- The Question of Survival or Death: What Is the Role of Autophagy in Acute Myeloid Leukemia (AML)?International journal of hematology-oncology and stem cell research · 2022Review
- Endosomal LC3C-pathway selectively targets plasma membrane cargo for autophagic degradation.Nature communications · 2022Article
- The dual role of autophagy in acute myeloid leukemia.Journal of hematology & oncology · 2022Review
- Detoxified pneumolysin derivative ΔA146Ply inhibits autophagy and induces apoptosis in acute myeloid leukemia cells by activating mTOR signaling.Experimental & molecular medicine · 2022Article
- Review
- The Key Role of the WNT/β-Catenin Pathway in Metabolic Reprogramming in Cancers under Normoxic Conditions.Cancers · 2021Review
- Article
- Sequestosome 1/p62: A multitasker in the regulation of malignant tumor aggression (Review).International journal of oncology · 2021Review
- Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
We provide evidence that arsenic trioxide (As(2)O(3)) targets the BCR-ABL oncoprotein via a novel mechanism involving p62/SQSTM1-mediated localization of the oncoprotein to the autolysosomes and subsequent degradation mediated by the protease cathepsin B. Our studies demonstrate that inhibitors of autophagy or cathepsin B activity and/or molecular targeting of p62/SQSTM1, Atg7, or cathepsin B result in partial reversal of the suppressive effects of AS(2)O(3) on BCR-ABL expressing leukemic progenitors, including primitive leukemic precursors from chronic myelogenous leukemia (CML) patients. Altogether, these findings indicate that autophagic degradation of BCR-ABL is critical for the induction of the antileukemic effects of As(2)O(3) and raise the potential for future therapeutic approaches to target BCR-ABL expressing cells by modulating elements of the autophagic machinery to promote BCR-ABL degradation.
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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.