Evidence map›Paper›PMID 11429425›Full record

ArticleJournal of clinical pathology2001

Expression of transcription factor AP-2 in colorectal adenomas and adenocarcinomas; comparison of immunohistochemistry and in situ hybridisation.

K M Ropponen, J K Kellokoski, R T Pirinen, K I Moisio, M J Eskelinen, E M Alhava, V M Kosma

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Journal of clinical pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 63 citations in OpenAlex.

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  13. Ectopic expression of AP-2α transcription factor suppresses glioma progression.International journal of clinical and experimental pathology · 2014
    Article
  14. Activator protein-2α functions as a master regulator of multiple transcription factors in the mouse liver.Hepatology research : the official journal of the Japan Society of Hepatology · 2011
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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 1 institution in 1 country.

K M RopponenDepartment of Pathology and Forensic Medicine, University of Kuopio, PO Box 1627, FIN 70211, Kuopio University Hospital, Kuopio, Finland.
J K Kellokoski
R T Pirinen
K I Moisio
M J Eskelinen
E M Alhava
V M Kosma
Kuopio University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsTo investigate whether the three different AP-2 isoforms are expressed differently in colorectal adenomas and carcinomas.

methodsThe study comprised 43 randomly selected patients diagnosed and treated at Kuopio University Hospital in 1996 for colorectal adenocarcinoma (n = 30) and colorectal adenoma (n = 13). The expression of AP-2alpha, AP-2beta, and AP-2gamma was analysed by immunohistochemistry (IHC) and the mRNA status of AP-2alpha was determined by in situ hybridisation (ISH) and confirmed by reverse transcription polymerase chain reaction (RT-PCR). AP-2 expression patterns were correlated with clinicopathological variables.

resultsIn adenomas and carcinomas, AP-2beta cytoplasmic positivity was higher than that of AP-2alpha or AP-2gamma. AP-2alpha expression was reduced in advanced Dukes's stage carcinomas. In high grade carcinomas, both AP-2alpha and AP-2gamma expression was reduced. ISH demonstrated increased AP-2alpha values in high grade carcinomas. Seven of 30 carcinoma specimens displayed a moderate or strong mRNA signal, despite being negative for AP-2alpha protein. RT-PCR from AP-2alpha mRNA and protein positive tumours confirmed that the positive signal in ISH originated from the exon 2 of TFAP2A.

conclusionsAP-2alpha was reduced in advanced Dukes's stage adenocarcinomas. Together with reduced AP-2gamma expression in high grade carcinomas, this might contribute to tumour progression. The discrepancy between mRNA and protein expression suggests that post-transcriptional regulatory mechanisms might modify the availability of functional AP-2alpha protein in colorectal carcinoma.

Indexed as

AdenocarcinomaAdenomaAdultAgedAged, 80 and overColorectal NeoplasmsDisease ProgressionDNA-Binding ProteinsFemaleGene ExpressionHumansImmunoenzyme TechniquesIn Situ HybridizationMaleMiddle AgedNeoplasm ProteinsDNA-Binding ProteinsNeoplasm ProteinsRNA, MessengerRNA, NeoplasmTFAP2A protein, humanTFAP2B protein, humanTFAP2C protein, humanTranscription Factor AP-2Transcription Factors

Identifiers

PMID11429425
PMCPMC1731475
OpenAlexW1984253873

What OpenQuestion holds

Textmetadata
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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.