Evidence map›Paper›PMID 15531914›Full record

ArticleOncogene2005

Smad4 deficiency in cervical carcinoma cells.

Stephan E Baldus, Elisabeth Schwarz, Claudia Lohrey, Marc Zapatka, Stephanie Landsberg, Stephan A Hahn, Dietmar Schmidt, Hans Peter Dienes, Wolff H Schmiegel, Irmgard Schwarte-Waldhoff

Abstract read
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In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
–field-weighted citation impact
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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. HPV-mediated regulation of SMAD4 modulates the DNA damage response in head and neck cancer.Journal of experimental & clinical cancer research : CR · 2022
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Transforming growth factor-β1 in carcinogenesis, progression, and therapy in cervical cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

10 authors.

Stephan E BaldusInstitute of Pathology, University of Cologne, D-50931 Cologne, Germany.
Elisabeth Schwarz
Claudia Lohrey
Marc Zapatka
Stephanie Landsberg
Stephan A Hahn
Dietmar Schmidt
Hans Peter Dienes
Wolff H Schmiegel
Irmgard Schwarte-Waldhoff

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Squamous cell carcinoma of the uterine cervix is one of the most frequent cancers affecting women worldwide. Carcinomas arise from cervical intraepithelial lesions, in which infection with high-risk human papillomavirus types has led to deregulated growth control through the actions of the viral E6 and E7 oncoproteins. The molecular mechanisms underlying progression to invasive tumor growth are poorly understood. One important feature, however, is the escape from growth inhibition by transforming growth factor beta (TGF-beta). Loss of chromosomal arm 18q is among the most frequent cytogenetic alterations in cervical cancers and has been associated with poor prognosis. Since the TGF-beta response is mediated by Smad proteins and the tumor suppressor gene Smad4 resides at 18q21, we have analysed the Smad4 gene for cervical cancer-associated alterations in cell lines and primary carcinomas. Here, we report Smad4 deficiency in four out of 13 cervical cancer cell lines which is due to an intronic rearrangement or deletions of 3' exons. All cell lines, however, showed either absent or moderate responsiveness to TGF-beta irrespective of their Smad4 status. In 41 primary squamous cervical carcinomas analysed, 10 samples showed loss of Smad4 protein expression and 26 samples a reduced expression. Altogether, our results strongly suggest that Smad4 gene alterations are involved in cervical carcinogenesis.

Indexed as

Chromosomes, Human, Pair 18Loss of HeterozygosityBase SequenceCell DivisionCell Line, TumorChromosome MappingDNA-Binding ProteinsDNA PrimersFemaleGenes, Tumor SuppressorHumansReverse Transcriptase Polymerase Chain ReactionSmad4 ProteinTrans-ActivatorsTransforming Growth Factor betaUterine Cervical NeoplasmsDNA-Binding ProteinsDNA PrimersSmad4 ProteinSMAD4 protein, humanTrans-ActivatorsTransforming Growth Factor beta

Identifiers

PMID15531914

What OpenQuestion holds

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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.