SynthesisFrontiers in cell and developmental biology2022
Disrupting Mechanisms that Regulate Genomic Repeat Elements to Combat Cancer and Drug Resistance.
Synthesis in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 14 citations in OpenAlex.
- USP24 is a cross-reactive DUB targeting MOV10 to regulate IFN-I production.Nature communications · 2026Article
- Review
- KDM5 demethylases suppress R-loop-mediated 'viral mimicry' and DNA damage in breast cancer cells.eLife · 2025Article
- Deciphering the code of resistance: a genomic and transcriptomic exploration of the Cystoisospora suis Holland-I strain.Scientific reports · 2025Article
- Article
- A multi-omics integrative approach unravels novel genes and pathways associated with senescence escape after targeted therapy in NRAS mutant melanoma.Cancer gene therapy · 2023Article
- The role of transposable elements in aging and cancer.Biogerontology · 2023Review
- Review
- Repeat Element Activation-Driven Inflammation: Role of NFκB and Implications in Normal Development and Cancer?Biomedicines · 2022Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite advancements in understanding cancer pathogenesis and the development of many effective therapeutic agents, resistance to drug treatment remains a widespread challenge that substantially limits curative outcomes. The historical focus on genetic evolution under drug "pressure" as a key driver of resistance has uncovered numerous mechanisms of therapeutic value, especially with respect to acquired resistance. However, recent discoveries have also revealed a potential role for an ancient evolutionary balance between endogenous "viral" elements in the human genome and diverse factors involved in their restriction in tumor evolution and drug resistance. It has long been appreciated that the stability of genomic repeats such as telomeres and centromeres affect tumor fitness, but recent findings suggest that de-regulation of other repetitive genome elements, including retrotransposons, might also be exploited as cancer therapy. This review aims to present an overview of these recent findings.
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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.