Evidence map›Paper›PMID 14724156›Full record

ArticleGut2004

Molecular targets for tumour progression in gastrointestinal stromal tumours.

N Koon, R Schneider-Stock, M Sarlomo-Rikala, J Lasota, M Smolkin, G Petroni, A Zaika, C Boltze, F Meyer, L Andersson and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 135 citations in OpenAlex.

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  13. SOCS1 gene therapy has antitumor effects in imatinib-resistant gastrointestinal stromal tumor cells through FAK/PI3 K signaling.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2018
    Article
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  20. TSG101 Silencing Suppresses Hepatocellular Carcinoma Cell Growth by Inducing Cell Cycle Arrest and Autophagic Cell Death.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

13 authors at 5 institutions in 3 countries.

N KoonDigestive Health Center of Excellence, University of Virginia Health System, PO Box 800708, Charlottesville, VA 22908-0708, USA.
R Schneider-Stock
M Sarlomo-Rikala
J Lasota
M Smolkin
G Petroni
A Zaika
C Boltze
F Meyer
L Andersson
S Knuutila
M Miettinen
W El-Rifai
University of Virginia Health System · USOtto-von-Guericke University Magdeburg · DEHelsinki University Hospital · FIUnited States Army · USUniversity of Helsinki · FI

Funding

Targets of Gene Overexpression at 17q in Gastric Tumorigenesis: Darpp32R01CA093999 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI EL-RIFAI, WAEL · 2002 to 2017
$4.5M
NCI NIH HHS 1R01 CA 93999-01NCI NIH HHS R01 CA093999
6 · The paper itself

Abstract

BACKGROUND AND

aimsThe distinction between benign and malignant gastrointestinal stromal tumours (GISTs) is often unclear at the clinical and histopathology levels. GISTs are believed to arise from the stem cells of Cajal. In order to define genetic biomarkers and identify target genes related to GIST progression, we analysed and compared benign and malignant GISTs with verified follow up data using cDNA expression arrays.

methodsEight genes were frequently overexpressed in malignant GISTs and their overexpression was confirmed using quantitative real time reverse transcription-polymerase chain reaction. These genes included ezrin (villin 2 (VIL2)), collagen 8 alpha 1 subunit (COL8A1), G2/mitotic specific cyclin B1 (CCNB1), high mobility group protein (HMG2), TSG101 tumour susceptibility protein, CENP-F kinetochore protein, protein tyrosine kinase 2 (FAK), and protein kinase DYRK2. To test these genes in a clinical setting, we obtained diagnostic samples of 16 additional GISTs that were classified at diagnosis as benign, malignant, and uncertain malignant potential (UMP).

resultsThere was remarkable gene overexpression in all malignant GISTs. Statistical analyses revealed significant correlations between overexpression of several gene pairs in malignant GISTs. We found the strongest correlations (rho>0.70) among the significant correlations (p<0.01) between CCNB1-CENP-F (rho = 0.87) and CCNB1-FAK (rho = 0.73). Gene expression of the UMP GISTs suggested two different groups. Three UMP GISTs had gene expression consistent with malignant tumours and their follow up data revealed that indeed these patients had recurrences later on. On the other hand, UMP GISTs that had low gene expression levels continued free of disease for several years.

conclusionsThese results provide insight into the oncogenesis of GISTs and suggest that testing the expression profile of a number of genes may segregate GISTs into groups of different tumour behaviour.

Indexed as

Oligonucleotide Array Sequence AnalysisChromosomal Proteins, Non-HistoneCollagen Type VIIICytoskeletal ProteinsDNA-Binding ProteinsDyrk KinasesEndosomal Sorting Complexes Required for TransportEzrinFocal Adhesion Kinase 2Gastrointestinal NeoplasmsGene ExpressionGenetic MarkersHMGB2 ProteinHumansMicrofilament ProteinsNeoplasm Proteinscentromere protein FChromosomal Proteins, Non-HistoneCollagen Type VIIICytoskeletal ProteinsDNA-Binding ProteinsDyrk KinasesEndosomal Sorting Complexes Required for TransportEzrinFocal Adhesion Kinase 2Genetic MarkersHMGB2 ProteinMicrofilament ProteinsNeoplasm ProteinsPhosphoproteinsProtein Serine-Threonine KinasesProtein-Tyrosine KinasesPTK2B protein, humanTranscription FactorsTsg101 Protein

Identifiers

PMID14724156
PMCPMC1774925
OpenAlexW2168672282

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.