Evidence map›Paper›PMID 10377436›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Cancer-specific chromosome alterations in the constitutive fragile region FRA3B.

K Mimori, T Druck, H Inoue, H Alder, L Berk, M Mori, K Huebner, C M Croce

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

39 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Replication fork recovery and regulation of common fragile sites stability.Cellular and molecular life sciences : CMLS · 2014
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Common fragile sites: genomic hotspots of DNA damage and carcinogenesis.International journal of molecular sciences · 2012
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Replication stress induces tumor-like microdeletions in FHIT/FRA3B.Proceedings of the National Academy of Sciences of the United States of America · 2008
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

K MimoriKimmel Cancer Institute, Jefferson Medical College, Philadelphia, PA 19107, USA.
T Druck
H Inoue
H Alder
L Berk
M Mori
K Huebner
C M Croce
Sidney Kimmel Cancer Center · USKyushu University · JP

Funding

VIROLOGY AND GENETICS OF CANCERP01CA021124 · NCI · WISTAR INSTITUTE · PI KOPROWSKI, HILARY · 1985 to 1999
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GENTEICS OF HUMAN HEMATOPOIETIC NEOPLASIASR35CA039860 · NCI · WISTAR INSTITUTE · PI CROCE, CARLO M · 1985 to 1998
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NCI NIH HHS CA21124NCI NIH HHS CA39860
6 · The paper itself

Abstract

We have sequenced 870 kilobases of the FHIT/FRA3B locus, from FHIT intron 3 to intron 7. The locus is AT rich (61.5%) and Alu poor (6. 2%), and it apparently does not harbor other genes. In a detailed analysis of the 308-kilobase region between FHIT exon 5 and the telomeric end of intron 3, a region known to encompass a human papillomavirus-16 integration site and two clusters of aphidicolin-induced chromosome 3p14.2 breakpoints, we have precisely mapped 10 deletion and translocation endpoints in cancer-derived cell lines relative to positions of specific repetitive elements, regions of high genome flexibility and aphidicolin-induced breakpoints. Conclusions are (i) that aphidicolin-induced breakpoint clusters fall close to high-flexibility sequences, suggesting that these sequences contribute directly to aphidicolin-induced fragility; (ii) that 9 of the 10 FHIT allelic deletions in cancer cell lines resulted in loss of exons, with 7 deletion endpoints near long interspersed nuclear elements or long terminal repeat elements; and (iii) that cancer-specific deletions encompass multiple high-flexibility genomic regions, suggesting that fragile breaks may occur at these regions, whereas repair of the breaks involves homologous pairing of flanking sequences with concomitant deletion of the damaged fragile sequence.

Indexed as

Acid Anhydride HydrolasesBiomarkers, TumorGenetic MarkersBis(5'-adenosyl)triphosphataseChromosome FragilityHumansMolecular Sequence DataNeoplasm ProteinsNeoplasmsProteinsSequence DeletionTranslocation, GeneticTumor Cells, CulturedAcid Anhydride HydrolasesBiomarkers, TumorBis(5'-adenosyl)triphosphataseGenetic MarkersNeoplasm ProteinsProteins

Identifiers

PMID10377436
PMCPMC22107
OpenAlexW1970474771

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.