ReviewGenes & genomics2023
Emerging role for R-loop formation in hepatocellular carcinoma.
Review in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- SRSF3-TRIM28-MDC1 prevents DNA damage caused by R-loops in fatty liver disease in mice.JCI insight · 2026Article
- R‑loops in hepatocellular carcinoma: Bridging genomic instability and therapeutic opportunity (Review).Molecular medicine reports · 2026Review
- R-loops: a key driver of inflammatory responses in cancer.Experimental & molecular medicine · 2025Review
- The hidden architects of the genome: a comprehensive review of R-loops.Molecular biology reports · 2024Review
- R-loop and diseases: the cell cycle matters.Molecular cancer · 2024Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC.
Indexed as
Identifiers
36635460What 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.