ReviewOncogene2001
Pathways of retinoic acid- or arsenic trioxide-induced PML/RARalpha catabolism, role of oncogene degradation in disease remission.
Review in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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
57 citing papers in PubMed, 151 citations in OpenAlex.
- All-trans retinoic acid/As2O3 combination yields a high quality remission and survival in newly diagnosed acute promyelocytic leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2004Trial
- Fusion Genes in Myeloid Malignancies.Cancers · 2024Review
- Design and Synthesis of Thiourea-Conjugating Organic Arsenic D-Glucose with Anticancer Activities.Molecules (Basel, Switzerland) · 2024Article
- A machine learning model identifies M3-like subtype in AML based on PML/RARα targets.iScience · 2024Article
- Understanding a high-risk acute myeloid leukemia by analyzing the interactome of its major driver mutation.PLoS genetics · 2022Article
- Article
- Excellent Early Outcomes of Combined Chemotherapy With Arsenic Trioxide for Stage 4/M Neuroblastoma in Children: A Multicenter Nonrandomized Controlled Trial.Oncology research · 2021Article
- Emerging role of tumor cell plasticity in modifying therapeutic response.Signal transduction and targeted therapy · 2020Review
- Targeting positive feedback between BASP1 and EGFR as a therapeutic strategy for lung cancer progression.Theranostics · 2020Article
- Acute Promyelocytic Leukemia: Update on the Mechanisms of Leukemogenesis, Resistance and on Innovative Treatment Strategies.Cancers · 2019Review
- Acute Promyelocytic Leukemia: A History over 60 Years-From the Most Malignant to the most Curable Form of Acute Leukemia.Oncology and therapy · 2019Review
- Article
- RNF8 is responsible for ATRA resistance in variant acute promyelocytic leukemia with GTF2I/RARA fusion, and inhibition of the ubiquitin-proteasome pathway contributes to the reversion of ATRA resistance.Cancer cell international · 2019Article
- Carbohydrate-conjugated 4-(1,3,2-dithiarsolan-2-yl)aniline as a cytotoxic agent against colorectal cancer.RSC advances · 2018Article
- Arsenic trioxide: insights into its evolution to an anticancer agent.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2018Review
- Differentiation therapy revisited.Nature reviews. Cancer · 2018Review
- PML: Regulation and multifaceted function beyond tumor suppression.Cell & bioscience · 2018Review
- Establishment and characterization of arsenic trioxide resistant KB/ATO cells.Acta pharmaceutica Sinica. B · 2017Article
- Selenite promotes all-trans retinoic acid-induced maturation of acute promyelocytic leukemia cells.Oncotarget · 2016Article
- p53 as an Effector or Inhibitor of Therapy Response.Cold Spring Harbor perspectives in medicine · 2015Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although there is evidence to suggest that PML/RARalpha expression is not the sole genetic event required for the development of acute promyelocytic leukemia (APL), there is little doubt that the fusion protein plays a central role in the initiation of leukemogenesis. The two therapeutic agents, retinoic acid and arsenic, that induce clinical remissions in APL, both target the oncogenic fusion protein, representing the first example of oncogene-directed cancer therapy. This review focuses on the molecular mechanisms accounting for PML/RARalpha degradation. Each drug targets a specific moiety of the fusion protein (RARalpha for retinoic acid, PML for arsenic) to the proteasome. Moreover, both activate a common caspase-dependent cleavage in the PML part of the fusion protein. Specific molecular determinants (the AF2 transactivator domain of RARalpha for retinoic acid and the K160 SUMO-binding site in PML for arsenic) are respectively implicated in RA- or arsenic-triggered catabolism. The respective roles of PML/RARalpha activation versus its catabolism are discussed with respect to differentiation or apoptosis induction in the context of single or dual therapies.
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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.