Evidence map›Paper›PMID 8887655›Full record

ArticleMolecular and cellular biology1996

Clonal analysis of delayed karyotypic abnormalities and gene mutations in radiation-induced genetic instability.

A J Grosovsky, K K Parks, C R Giver, S L Nelson

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Origin of Cancer: An Information, Energy, and Matter Disease.Frontiers in cell and developmental biology · 2016
    Article
  5. Article
  6. Article
  7. What mechanisms/processes underlie radiation-induced genomic instability?Cellular and molecular life sciences : CMLS · 2012
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Radiation-induced mutations in unirradiated DNA.Proceedings of the National Academy of Sciences of the United States of America · 1999
    Article
  19. 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 2 countries.

A J GrosovskyBiomedical Sciences, Graduate Program, University of California, Riverside, USA. Grosovsk@mail.ucr.edu
K K Parks
C R Giver
S L Nelson
University of California, Riverside · US

Funding

RADIATION MUTAGENESIS OF HUMAN CELLSR01CA055659 · NCI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI GROSOVSKY, ANDREW J. · 1992 to 1995
–
NCI NIH HHS R01-CA55659
6 · The paper itself

Abstract

Many tumors exhibit extensive chromosomal instability, but karyotypic alterations will be significant in carcinogenesis only by influencing specific oncogenes or tumor suppressor loci within the affected chromosomal segments. In this investigation, the specificity of chromosomal rearrangements attributable to radiation-induced genomic instability is detailed, and a qualitative and quantitative correspondence with mutagenesis is demonstrated. Chromosomal abnormalities preferentially occurred near the site of prior rearrangements, resulting in complex abnormalities, or near the centromere, resulting in deletion or translocation of the entire chromosome arm, but no case of an interstitial chromosomal deletion was observed. Evidence for chromosomal instability in the progeny of irradiated cells also included clonal karyotypic heterogeneity. The persistence of instability was demonstrated for at least 80 generations by elevated mutation rates at the heterozygous, autosomal marker locus tk. Among those TK- mutants that showed a loss of heterozygosity, a statistically significant increase in mutation rate was observed only for those in which the loss of heterozygosity encompasses the telomeric region. This mutational specificity corresponds with the prevalence of terminal deletions, additions, and translocations, and the absence of interstitial deletions, in karyotypic analysis. Surprisingly, the elevated rate of TK- mutations is also partially attributable to intragenic base substitutions and small deletions, and DNA sequence analysis of some of these mutations is presented. Complex chromosomal abnormalities appear to be the most significant indicators of a high rate of persistent genetic instability which correlates with increased rates of both intragenic and chromosomal-scale mutations at tk.

Indexed as

Chromosome AberrationsChromosome DisordersChromosome MappingBase SequenceB-LymphocytesCell LineChromosome DeletionChromosomes, Human, Pair 17Clone CellsFrameshift MutationGamma RaysGene RearrangementHumansHypoxanthine PhosphoribosyltransferaseKaryotypingMutagenesisHypoxanthine PhosphoribosyltransferaseThymidine Kinase

Identifiers

PMID8887655
PMCPMC231628
OpenAlexW2137125319

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.