Evidence map›Paper›PMID 9427766›Full record

ArticleThe EMBO journal1998

Interstitial deletions and intrachromosomal amplification initiated from a double-strand break targeted to a mammalian chromosome.

E Pipiras, A Coquelle, A Bieth, M Debatisse

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
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  3. Stem cell-derived clade F AAVs mediate high-efficiency homologous recombination-based genome editing.Proceedings of the National Academy of Sciences of the United States of America · 2018
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  20. Monosomy 1p36 breakpoints indicate repetitive DNA sequence elements may be involved in generating and/or stabilizing some terminal deletions.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2004
    Article
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

4 authors at 1 institution in 1 country.

E PipirasUnité de Génétique Somatique (URA CNRS 1960), Institut Pasteur, 25 rue du Dr Roux, 75724 Paris Cédex 15, France.
A Coquelle
A Bieth
M Debatisse
Centre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interstitial deletions of tumour suppressor genes and amplification of oncogenes are two major manifestations of chromosomal instability in tumour cells. The development of model systems allowing the study of the events triggering these processes is of major clinical importance. Using the properties of the I-SceI nuclease to introduce a localized double-strand break (DSB) in a mammalian chromosome carrying its target sequence, we demonstrate here that both types of mutations can be initiated by non-conservative DSB repair pathways. In our system, I-SceI activity dissociates a transfected gpt gene from its promoter, allowing the isolation of gpt- clones. Our results show that intrachromatid single-strand annealing events occur frequently, giving rise to interstitial deletions not accompanied by other chromosomal rearrangements. We also observed that, when present in the cells, extrachromosomal DNA molecules are integrated preferentially at the broken locus. Taking advantage of the insertion of the I-SceI recognition sequence telomeric to and close to the dihydrofolate reductase gene, we show that a less frequent outcome of I-SceI activity is the initiation of cycles of intrachromosomal amplification of this marker, from breaks at a site merging with the enzyme target.

Indexed as

ChromosomesDNA DamageGene AmplificationGene DeletionCloning, MolecularDeoxyribonucleases, Type II Site-SpecificHypoxanthine PhosphoribosyltransferaseSaccharomyces cerevisiae ProteinsDeoxyribonucleases, Type II Site-SpecificHypoxanthine PhosphoribosyltransferaseSaccharomyces cerevisiae ProteinsSCEI protein, S cerevisiae

Identifiers

PMID9427766
PMCPMC1170383
OpenAlexW2151163426

What OpenQuestion holds

Textmetadata
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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.