Evidence map›Paper›PMID 15568039›Full record

ArticleOncogene2004

The human tumor suppressor CEACAM1 modulates apoptosis and is implicated in early colorectal tumorigenesis.

Stefanie Nittka, Juliane Günther, Cornelia Ebisch, Andreas Erbersdobler, Michael Neumaier

Abstract read
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In one paragraph

Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.6field-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

41 citing papers in PubMed, 85 citations in OpenAlex.

  1. Mechanism and function of CEACAM1 splice isoforms.European journal of clinical investigation · 2024
    Review
  2. Structural aspects of CEACAM1 interactions.European journal of clinical investigation · 2024
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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

5 authors at 4 institutions in 1 country.

Stefanie NittkaInstitute for Clinical Chemistry, Medical Faculty Mannheim of the University of Heidelberg, D-68167 Mannheim, Germany.
Juliane Günther
Cornelia Ebisch
Andreas Erbersdobler
Michael Neumaier
Universität Hamburg · DEUniversity Hospital Heidelberg · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity Medical Centre Mannheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Defects in the adenomatous polyposis coli (APC) tumor suppressor pathway are sufficient for neoplastic transformation as the initiating step in colorectal carcinogenesis. In contrast, hyperplastic tumors possess normal APC function, and it is unclear whether they represent significant precursor lesion in cancer development. CEACAM1 is a tumor suppressor whose expression is known to be lost in the great majority of early adenomas and carcinomas. We found that loss of CEACAM1 expression is more common in neoplastic tumors than APC mutations. While APC function was normal in hyperplastic aberrant cypt foci and hyperplastic polyps, loss of CEACAM1 was observed as frequently as in the neoplasias. Moreover, the presence or absence of CEACAM1 expression in the hyperplastic tumors correlates with normal or reduced apoptosis, respectively. In vitro, CEACAM1 acts as a regulator of apoptosis in CEACAM1-transfected Jurkat cells. Finally, in human HT29 colon cancer cells, apoptosis can be specifically restored by induction of CEACAM1 expression. These data suggest an oncodevelopmental link between neoplasia and hyperplasia and demonstrate that CEACAM1 acts as a regulator of apoptosis in the colonic epithelium. Thus, failure of the maturing colon cell to express CEACAM1 is likely to contribute to the development of hyperplastic lesions, which may eventually pave the way to neoplastic transformation and colon cancer development.

Indexed as

Genes, Tumor SuppressorAntigens, CDAntigens, DifferentiationApoptosisBase SequenceCell Adhesion MoleculesColorectal NeoplasmsDNA PrimersGenes, APCHumansIn Vitro TechniquesMutationAntigens, CDAntigens, DifferentiationCD66 antigensCell Adhesion MoleculesDNA Primers

Identifiers

PMID15568039
OpenAlexW1993847375

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.