Evidence map›Paper›PMID 22432062›Full record

ArticleAmerican journal of blood research2011

Premature transcript termination, trans-splicing and DNA repair: a vicious path to cancer.

Eric Kowarz, Jennifer Merkens, Michael Karas, Theo Dingermann, Rolf Marschalek

Open access · greenAbstract read
In one paragraph

Article in American journal of blood research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.3field-weighted citation impact, top 43% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. RNA exon editing: Splicing the way to treat human diseases.Molecular therapy. Nucleic acids · 2024
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  7. Trans-spliced long non-coding RNA: an emerging regulator of pluripotency.Cellular and molecular life sciences : CMLS · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Eric Kowarz
Jennifer Merkens
Michael Karas
Theo Dingermann
Rolf Marschalek

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

So far, about 800 different chromosomal translocations have been characterized in hemato-malignant and solid tumors. Chromosomal translocations mostly result in the expression of chimeric fusion proteins associated with enhanced proliferation and/or malignant transformation. Here, we demonstrate that genes frequently involved in such genetic rearrangements exhibit a unique feature: premature transcriptional termination. These early-terminated RNA molecules have an abundance of 10-20% when compared to their cognate full-length transcripts. They exhibit an unsaturated splice donor site that gives rise to trans-splicing events, leading to RNAs displaying exon repetitions or chimeric fusion RNAs. These arbitrary fusion RNAs mimic the presence of a chromosomal translocation in genetically unaffected cells. Based on our and published data, we propose the hypothesis that these artificial "chimeric fusion transcripts" may influence DNA repair processes, resulting in the generation of de novo chromosomal translocations. This idea provides a rational explanation why different individuals suffer from nearly identical genetic rearrangements.

Indexed as

Acute leukemiachromosomal translocationsDNA repairearly-terminated transcriptsRNA-templated DNA repairtranssplicing

Identifiers

PMID22432062
PMCPMC3301421
OpenAlexW1500134050

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.