ReviewAmerican journal of hematology2025
Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.
Review in American journal of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed.
- Retroelement Hypomethylation Links Hypoxia Signaling, Immune Phenotypes, and Survival in Clear Cell Renal Cell Carcinoma.bioRxiv : the preprint server for biology · 2026Article
- Transposable elements in hematopoietic stem cells upon aging and myeloid malignancies.Mobile DNA · 2026Review
- Overcoming Immune Therapy Resistance in Cancer Through Innate Immune Reprogramming.International journal of molecular sciences · 2025Review
- HERV-derived epitopes represent new targets for T-cell-based immunotherapies in ovarian cancer.Journal for immunotherapy of cancer · 2025Article
- Transposable elements as genome regulators in normal and malignant haematopoiesis.Blood cancer journal · 2025Review
- Cancer cells' chamber of secrets: the link between micronuclei, chromothripsis and malignancy.Open biology · 2025Review
- Endogenous retroelements in hematological malignancies: From epigenetic dysregulation to therapeutic targeting.American journal of hematology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endogenous retroelements (EREs), which comprise half of the human genome, play a pivotal role in genome dynamics. Some EREs retained the ability to encode proteins, although most degenerated or served as a source for novel genes and regulatory elements during evolution. Despite ERE repression mechanisms developed to maintain genome stability, widespread pervasive ERE activation is observed in cancer including hematological malignancies. Challenging the perception of noncoding DNA as "junk," EREs are underestimated contributors to cancer driver mechanisms as well as antitumoral immunity by providing innate immune ligands and tumor antigens. This review highlights recent progress in understanding ERE co-option events in cancer and focuses on the controversial debate surrounding their causal role in shaping malignant phenotype. We provide insights into the rapidly evolving landscape of ERE research in hematological malignancies and their clinical implications in these cancers.
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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.