ArticleCellscience2009
Roles of retrotransposons in benign and malignant hematologic disease.
Article in Cellscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Investigating the Physiological Regulation of Transposable Elements In Vivo: Nuclei Preparation from Primary Mouse Tissues for Epigenomic Analyses and Computational Approaches to Interrogate the Repeat Genome.Methods in molecular biology (Clifton, N.J.) · 2026Article
- MIR retrotransposons link the epigenome and the transcriptome of coding genes in acute myeloid leukemia.Nature communications · 2022Article
- Fuel source shift or cost reduction: Context-dependent adaptation strategies in closely relatedZoological research · 2022Article
- Inter-Strain Differences in LINE-1 DNA Methylation in the Mouse Hematopoietic System in Response to Exposure to Ionizing Radiation.International journal of molecular sciences · 2017Article
- The cancer-associated CTCFL/BORIS protein targets multiple classes of genomic repeats, with a distinct binding and functional preference for humanoid-specific SVA transposable elements.Epigenetics & chromatin · 2016Article
- Article
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
Abstract
Nearly half of our genomes are repetitive sequences derived from retrotransposons. These repeats have accumulated by a 'copy-and-paste' mechanism whereby: (i.) a genomic template sequence is transcribed to RNA, (ii.) the RNA is reverse-transcribed, and (iii.) the DNA copy is inserted at a new location in the host genome. As we remain susceptible to new retrotransposition events, many of these insertions are highly polymorphic. Transposons are of interest since insertions into both coding and non-coding gene regions have been associated with a wide variety of functional sequelae and because transposable elements can be involved in genomic rearrangements in transformed cells. In this review, we highlight how expression of retrotransposons, de novo and polymorphic transposon insertions, and genomic rearrangements that these repeats potentiate contribute to both benign and neoplastic hematopoietic diseases.
Identifiers
20200603PMC2830787What 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.