ArticleScientific reports2017
Suppression of Transposable Elements in Leukemic Stem Cells.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 30 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Disrupting Mechanisms that Regulate Genomic Repeat Elements to Combat Cancer and Drug Resistance.Frontiers in cell and developmental biology · 2022Pooled it
- Article
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- Transposable elements shape stemness in normal and leukemic hematopoiesis.Nature genetics · 2026Article
- MORC2 promotes acute myeloid leukemia by silencing LINE-1 retrotransposon.Functional & integrative genomics · 2026Article
- Article
- Revisiting Clonal Evolution Through the Light of Retrotransposons.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- How to drug a leukemic stem cell: deciphering heterogeneity for better specificity.Blood neoplasia · 2025Review
- Hypomethylating agents increase L1 retroelement expression without inducing novel insertions in myeloid malignancies.Molecular oncology · 2025Article
- Chronic Myelomonocytic Leukemia Microenvironment in Disease Progression and Therapy: Focus on Stepwise Reconfiguring of Myeloid-Immune Cell Interactions Driving Immune Tolerance.Current hematologic malignancy reports · 2025Review
- Dysregulation of transposable elements and PIWI-interacting RNAs in myelodysplastic neoplasms.Biomarker research · 2025Article
- Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.American journal of hematology · 2025Review
- Targeting heterochromatin eliminates chronic myelomonocytic leukemia malignant stem cells through reactivation of retroelements and immune pathways.Communications biology · 2024Article
- The role of transposable elements in aging and cancer.Biogerontology · 2023Review
- Repeat Element Activation-Driven Inflammation: Role of NFκB and Implications in Normal Development and Cancer?Biomedicines · 2022Review
- MIR retrotransposons link the epigenome and the transcriptome of coding genes in acute myeloid leukemia.Nature communications · 2022Article
- Controlled variable selection in Weibull mixture cure models for high-dimensional data.Statistics in medicine · 2022Article
- HERVs characterize normal and leukemia stem cells and represent a source of shared epitopes for cancer immunotherapy.American journal of hematology · 2022Article
- Endogenous Retroviruses (ERVs): Does RLR (RIG-I-Like Receptors)-MAVS Pathway Directly Control Senescence and Aging as a Consequence of ERV De-Repression?Frontiers in immunology · 2022Review
- Repeat to gene expression ratios in leukemic blast cells can stratify risk prediction in acute myeloid leukemia.BMC medical genomics · 2021Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genomic transposable elements (TEs) comprise nearly half of the human genome. The expression of TEs is considered potentially hazardous, as it can lead to insertional mutagenesis and genomic instability. However, recent studies have revealed that TEs are involved in immune-mediated cell clearance. Hypomethylating agents can increase the expression of TEs in cancer cells, inducing 'viral mimicry', causing interferon signalling and cancer cell killing. To investigate the role of TEs in the pathogenesis of acute myeloid leukaemia (AML), we studied TE expression in several cell fractions of AML while tracking its development (pre-leukemic haematopoietic stem cells, leukemic stem cells [LSCs], and leukemic blasts). LSCs, which are resistant to chemotherapy and serve as reservoirs for relapse, showed significant suppression of TEs and interferon pathways. Similarly, high-risk cases of myelodysplastic syndrome (MDS) showed far greater suppression of TEs than low-risk cases. We propose TE suppression as a mechanism for immune escape in AML and MDS. Repression of TEs co-occurred with the upregulation of several genes known to modulate TE expression, such as RNA helicases and autophagy genes. Thus, we have identified potential pathways that can be targeted to activate cancer immunogenicity via TEs in AML and MDS.
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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.