SynthesisOncogene2011
BCR-ABL-mediated upregulation of PRAME is responsible for knocking down TRAIL in CML patients.
Synthesis in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- DNA methylation screening identifies driver epigenetic events of cancer cell survival.Cancer cell · 2012Pooled it
- Emergence of the cancer antigen PRAME as key player in epigenetic dysregulation and renal tumorigenesis.Cell death and differentiation · 2026Article
- DNA methylation in primary myelofibrosis is partly associated with driver mutations and distinct from other myeloid malignancies.Clinical epigenetics · 2025Article
- Article
- Joint multi-omics discriminant analysis with consistent representation learning using PANDA.Research square · 2024Article
- TNFSF10, an autophagy related gene, was a prognostic and immune infiltration marker in skin cutaneous melanoma.Journal of Cancer · 2023Article
- Article
- PRAME protein expression in DICER1-related tumours.The journal of pathology. Clinical research · 2022Article
- BCR-ABL1 Tyrosine Kinase Complex Signaling Transduction: Challenges to Overcome Resistance in Chronic Myeloid Leukemia.Pharmaceutics · 2022Review
- DNA methyltransferase inhibitors combination therapy for the treatment of solid tumor: mechanism and clinical application.Clinical epigenetics · 2021Review
- Development of a New Highly Selective Monoclonal Antibody against Preferentially Expressed Antigen in Melanoma (PRAME) and Identification of the Target Epitope by Bio-Layer Interferometry.International journal of molecular sciences · 2021Article
- Preferentially expressed antigen in melanoma as a novel diagnostic marker differentiating thymic squamous cell carcinoma from thymoma.Scientific reports · 2020Article
- The role of the cancer testis antigen PRAME in tumorigenesis and immunotherapy in human cancer.Cell proliferation · 2020Review
- Epigenetic therapy in immune-oncology.Nature reviews. Cancer · 2019Review
- Pattern Recognition Receptors and the Host Cell Death Molecular Machinery.Frontiers in immunology · 2018Review
- BCR-ABL1-induced downregulation of WASP in chronic myeloid leukemia involves epigenetic modification and contributes to malignancy.Cell death & disease · 2017Article
- Immunological off-target effects of imatinib.Nature reviews. Clinical oncology · 2016Review
- The Philadelphia chromosome in leukemogenesis.Chinese journal of cancer · 2016Review
- Somatic Copy Number Amplification and Hyperactivating Somatic Mutations of EZH2 Correlate With DNA Methylation and Drive Epigenetic Silencing of Genes Involved in Tumor Suppression and Immune Responses in Melanoma.Neoplasia (New York, N.Y.) · 2016Article
- Therapeutic applications of TRAIL receptor agonists in cancer and beyond.Pharmacology & therapeutics · 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
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor-related apoptosis-inducing ligand-TNFSF10 (TRAIL), a member of the TNF-α family and a death receptor ligand, was shown to selectively kill tumor cells. Not surprisingly, TRAIL is downregulated in a variety of tumor cells, including BCR-ABL-positive leukemia. Although we know much about the molecular basis of TRAIL-mediated cell killing, the mechanism responsible for TRAIL inhibition in tumors remains elusive because (a) TRAIL can be regulated by retinoic acid (RA); (b) the tumor antigen preferentially expressed antigen of melanoma (PRAME) was shown to inhibit transcription of RA receptor target genes through the polycomb protein, enhancer of zeste homolog 2 (EZH2); and (c) we have found that TRAIL is inversely correlated with BCR-ABL in chronic myeloid leukemia (CML) patients. Thus, we decided to investigate the association of PRAME, EZH2 and TRAIL in BCR-ABL-positive leukemia. Here, we demonstrate that PRAME, but not EZH2, is upregulated in BCR-ABL cells and is associated with the progression of disease in CML patients. There is a positive correlation between PRAME and BCR-ABL and an inverse correlation between PRAME and TRAIL in these patients. Importantly, knocking down PRAME or EZH2 by RNA interference in a BCR-ABL-positive cell line restores TRAIL expression. Moreover, there is an enrichment of EZH2 binding on the promoter region of TRAIL in a CML cell line. This binding is lost after PRAME knockdown. Finally, knocking down PRAME or EZH2, and consequently induction of TRAIL expression, enhances Imatinib sensibility. Taken together, our data reveal a novel regulatory mechanism responsible for lowering TRAIL expression and provide the basis of alternative targets for combined therapeutic strategies for CML.
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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.