Evidence map›Paper›PMID 11526514›Full record

ArticleOncogene2001

Identification of homozygous deletions at chromosome 16q23 in aflatoxin B1 exposed hepatocellular carcinoma.

M C Yakicier, P Legoix, C Vaury, L Gressin, E Tubacher, F Capron, J Bayer, C Degott, C Balabaud, J Zucman-Rossi

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2001. 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
4.1field-weighted citation impact, top 6% 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, 53 citations in OpenAlex.

  1. Article
  2. Frontiers in oncology · 2018
    Review
  3. Article
  4. Article
  5. Alteration of WWOX in human cancer: a clinical view.Experimental biology and medicine (Maywood, N.J.) · 2015
    Review
  6. Article
  7. Article
  8. Article
  9. WWOX expression in colorectal cancer--a real-time quantitative RT-PCR study.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2011
    Article
  10. Loss of WWOX expression in human extrahepatic cholangiocarcinoma.Journal of cancer research and clinical oncology · 2009
    Article
  11. Article
  12. Tumor suppressor and hepatocellular carcinoma.World journal of gastroenterology · 2008
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
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

10 authors at 4 institutions in 1 country.

M C YakicierINSERM U434, CEPH 27 Rue Juliette Dodu 75010 Paris, France.
P Legoix
C Vaury
L Gressin
E Tubacher
F Capron
J Bayer
C Degott
C Balabaud
J Zucman-Rossi
Inserm · FRHôpital Antoine-Béclère · FRHôpital Beaujon · FRHôpital Saint-André · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Loss of heterozygosity (LOH) represents the most frequent genetic alteration observed in hepatocellular carcinoma (HCC). Chromosome 16q is of particular interest as it exhibits LOH in 29% of HCC tumors and is frequently lost in breast, prostate, ovarian and gastric carcinomas. We genotyped 157 HCC tumors for 17 microsatellite markers distributed on chromosome 16q and determined a common region of LOH localized between the markers D16S518 and D16S504. By refining the boundaries of two interstitial LOH and two homozygous deletions, the critical region was delimited to 180 kb between D16S3096 and D16S3029. This region is located in intron 8 of the WWOX/FOR gene, but a search for mutations in all coding exons of this gene in 27 HCC tumors and cell lines did not reveal any tumor somatic alterations. Furthermore, by RT-PCR, no abnormal transcripts of this WWOX/FOR gene was detected in nine HCC cell lines. Finally, analysis of the p53 gene mutations with the clinical parameters of all tumors revealed that the two homozygous deletions have occurred in tumors presenting a R249S mutation. Our data revealed a relationship between chromosome 16q homozygous deletions and R249S p53 mutations in tumors where the patient had been exposed to aflatoxin B1 (P=0.002). These results are consistent with a role of aflatoxin B1 in the instability of chromosome 16q at the fragile site FRA16D. However, the nature of the specific gene that is altered during hepatocarcinogenesis remains to be elucidated.

Indexed as

Aflatoxin B1CarcinogensChromosome DeletionChromosomes, Human, Pair 16HomozygoteAllelesCarcinoma, HepatocellularChromosome MappingExonsFlow CytometryGenes, p53GenotypeHumansLiver NeoplasmsLoss of HeterozygosityMicrosatellite RepeatsAflatoxin B1CarcinogensRNA, Messenger

Identifiers

PMID11526514
OpenAlexW2077211615

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.