Evidence map›Paper›PMID 11531255›Full record

ArticleBritish journal of cancer2001

Frequent genomic imbalances suggest commonly altered tumour genes in human hepatocarcinogenesis.

F Niketeghad, H J Decker, W H Caselmann, P Lund, F Geissler, H P Dienes, P Schirmacher

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.3field-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

17 citing papers in PubMed, 64 citations in OpenAlex.

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  13. Chronic hepatitis B in hepatocarcinogenesis.Postgraduate medical journal · 2006
    Review
  14. Article
  15. Article
  16. Review
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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

7 authors at 4 institutions in 1 country.

F NiketeghadInstitute of Pathology, University of Cologne, Joseph Stelzmann Str. 9, Cologne, D-50931, Germany.
H J Decker
W H Caselmann
P Lund
F Geissler
H P Dienes
P Schirmacher
University of Cologne · DEJohannes Gutenberg University Mainz · DELeipzig University · DEUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocellular carcinoma (HCC) is one of the most frequent-occurring malignant tumours worldwide, but molecular changes of tumour DNA, with the exception of viral integrations and p53 mutations, are poorly understood. In order to search for common macro-imbalances of genomic tumour DNA, 21 HCCs and 3 HCC-cell lines were characterized by comparative genomic hybridization (CGH), subsequent database analyses and in selected cases by fluorescence in situ hybridization (FISH). Chromosomal subregions of 1q, 8q, 17q and 20q showed frequent gains of genomic material, while losses were most prevalent in subregions of 4q, 6q, 13q and 16q. Deleted regions encompass tumour suppressor genes, like RB-1 and the cadherin gene cluster, some of them previously identified as potential target genes in HCC development. Several potential growth- or transformation-promoting genes located in chromosomal subregions showed frequent gains of genomic material. The present study provides a basis for further genomic and expression analyses in HCCs and in addition suggests chromosome 4q to carry a so far unidentified tumour suppressor gene relevant for HCC development.

Indexed as

Chromosome DeletionTranslocation, GeneticCarcinoma, HepatocellularFemaleGenes, Tumor SuppressorHumansIn Situ Hybridization, FluorescenceKaryotypingLiver NeoplasmsMaleTumor Cells, Cultured

Identifiers

PMID11531255
PMCPMC2364116
OpenAlexW2078943507

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.