Evidence map›Paper›PMID 12096341›Full record

ArticleOncogene2002

Novel colon cancer cell lines leading to better understanding of the diversity of respective primary cancers.

Beatrix Vécsey-Semjén, Karl-Friedrich Becker, Alexandra Sinski, Elizabeth Blennow, Ilja Vietor, Kurt Zatloukal, Hartmut Beug, Ernst Wagner, Lukas A Huber

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 62 citations in OpenAlex.

  1. Review
  2. TheCancers · 2021
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  16. Involvement of members of the cadherin superfamily in cancer.Cold Spring Harbor perspectives in biology · 2009
    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

9 authors at 6 institutions in 3 countries.

Beatrix Vécsey-SemjénIMP, Research Institute of Molecular Pathology, Vienna, Austria.
Karl-Friedrich Becker
Alexandra Sinski
Elizabeth Blennow
Ilja Vietor
Kurt Zatloukal
Hartmut Beug
Ernst Wagner
Lukas A Huber
Research Institute of Molecular Pathology · ATBoehringer Ingelheim (Austria) · ATKarolinska University Hospital · SETechnical University of Munich · DEUniversität Innsbruck · ATUniversity of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major obstacle to obtaining more detailed insights into the diversity of phenotypic and molecular changes occurring in colon cancer cells is the lack of low-passage colon cancer cell lines, which would still closely reflect the phenotype of the colon cancer cells in vivo. Here, we characterize eight novel, low passage number human colon carcinoma cell lines, originating from colorectal cancers extensively characterized in the clinics. All cell lines closely resemble the original tumors with respect to phenotype, markers and detectable genetic changes. Cell morphology and marker expression is highly variable, ranging from fully polarized cells correctly expressing all basolateral epithelial markers, to cells with mesenchymal characteristics and a complete loss of polarity due to delocalization or loss of junction complex proteins. The alterations in phenotype and epithelial marker expression correspond to changes already detectable in the primary tumor in vivo. Seven of the cell lines show chromosomal instability, while one cell line is characterized by microsatellite instability. p53 associated with K-ras mutations were detected in three cell lines. Hitherto non-described E-cadherin mutations were found at both alleles in one cell line whereas in another cell line the E-cadherin protein was down-regulated. A stabilizing beta-catenin mutation (S45F) appears in the same cell line that carried the mutated E-cadherin gene. Six cell lines carried APC mutations, which in five of the lines led to an activated beta-catenin/Tcf/LEF signaling pathway. In accordance with beta-catenin/Tcf/LEF activation, the cell lines show increased migration and invasiveness. Our results show that the characterized, low-passage cell lines mirror the diversity of the individual tumors from which they were derived. Through molecular analyses of these cell lines we demonstrate that tumorgenicity events are much more diverse in human colon cancer than expected, despite the common origin of the tumors from a small patient group with similar tumor grading and clinical prognosis.

Indexed as

Trans-ActivatorsZebrafish ProteinsAdenomatous Polyposis Coli ProteinAdherens JunctionsAgedAnimalsbeta CateninBiomarkers, TumorCadherinsCell DivisionColonic NeoplasmsCytoskeletal ProteinsDNA Mutational AnalysisFemaleGene Expression Regulation, NeoplasticGenes, p53Adenomatous Polyposis Coli Proteinbeta CateninBiomarkers, TumorCadherinsCTNNB1 protein, humanCTNNB1 protein, mouseCytoskeletal ProteinsProto-Oncogene ProteinsTrans-ActivatorsWnt ProteinsZebrafish Proteins

Identifiers

PMID12096341
OpenAlexW2012507614

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.