Evidence map›Paper›PMID 10805745›Full record

ArticleMolecular and cellular biology2000

Homologous and nonhomologous recombination resulting in deletion: effects of p53 status, microhomology, and repetitive DNA length and orientation.

D Gebow, N Miselis, H L Liber

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

40 citing papers in PubMed, 98 citations in OpenAlex.

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  15. Mapping the physical and functional interactions between the tumor suppressors p53 and BRCA2.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  16. L1 recombination-associated deletions generate human genomic variation.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
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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

3 authors at 1 institution in 1 country.

D GebowDepartment of Radiation Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.
N Miselis
H L Liber
Massachusetts General Hospital · US

Funding

RADIATION BIOLOGY TRAINING PROGRAMT32CA009078 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI D'ANDREA, ALAN D. · 1985 to 2009
$4.6M
IONIZING RADIATION MUTAGENESIS IN HUMAN CELLSR01CA049696 · NCI · MASSACHUSETTS GENERAL HOSPITAL · PI LIBER, HOWARD L · 1989 to 2004
$1.2M
IONIZING RADIATION MUTAGENESIS IN HUMAN CELLSR55CA049696 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI LIBER, HOWARD L · 1994 to 1994
–
NCI NIH HHS CA09078NCI NIH HHS CA49696NCI NIH HHS R01 CA049696NCI NIH HHS T32 CA009078
6 · The paper itself

Abstract

Repetitive DNA elements frequently are precursors to chromosomal deletions in prokaryotes and lower eukaryotes. However, little is known about the relationship between repeated sequences and deletion formation in mammalian cells. We have created a novel integrated plasmid-based recombination assay to investigate repeated sequence instability in human cells. In a control cell line, the presence of direct or inverted repeats did not appreciably influence the very low deletion frequencies (2 x 10(-7) to 9 x 10(-7)) in the region containing the repeat. Similar to what has been observed in lower eukaryotes, the majority of deletions resulted from the loss of the largest direct repeat present in the system along with the intervening sequence. Interestingly, in closely related cell lines that possess a mutant p53 gene, deletion frequencies in the control and direct-repeat plasmids were 40 to 300 times higher than in their wild-type counterparts. However, mutant p53 cells did not preferentially utilize the largest available homology in the formation of the deletion. Surprisingly, inverted repeats were approximately 10,000 times more unstable in all mutant p53 cells than in wild-type cells. Finally, several deletion junctions were marked by the addition of novel bases that were homologous to one of the preexisting DNA ends. Contrary to our expectations, only 6% of deletions in all cell lines could be classified as arising from nonhomologous recombination.

Indexed as

Recombination, GeneticCell LineDNAHumansSequence DeletionTumor Suppressor Protein p53DNATumor Suppressor Protein p53

Identifiers

PMID10805745
PMCPMC85773
OpenAlexW2103913668

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.