Evidence map›Paper›PMID 12802290›Full record

ArticleOncogene2003

Upregulation of c-MYC in WT1-mutant tumors: assessment of WT1 putative transcriptional targets using cDNA microarray expression profiling of genetically defined Wilms' tumors.

Malini Udtha, Sang-Joon Lee, Rita Alam, Kevin Coombes, Vicki Huff

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. HtrA2, taming the oncogenic activities of WT1.Cell cycle (Georgetown, Tex.) · 2010
    Article
  8. Article
  9. An integrated genome screen identifies the Wnt signaling pathway as a major target of WT1.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Differential gene expression in stromal cells of human giant cell tumor of bone.Virchows Archiv : an international journal of pathology · 2004
    Article
  16. Article
  17. 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

5 authors at 2 institutions in 1 country.

Malini UdthaDepartment of Molecular Genetics/Cancer Genetics, The University of Texas MD Anderson Cancer Center, Houston 77030, USA.
Sang-Joon Lee
Rita Alam
Kevin Coombes
Vicki Huff
Cancer Genetics (United States) · USThe University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
TRANSCRIPTIONAL REGULATION OF WT-1P01CA034936 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI STRONG, LOUISE C · 1985 to 2010
$26.4M
MOLECULAR INVESTIGATION OF FAMILIAL WILMS TUMORR01CA078257 · NCI · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI HUFF, VICKI · 1999 to 2003
$1.4M
NCI NIH HHS CA16672NCI NIH HHS CA34936NCI NIH HHS CA78257
6 · The paper itself

Abstract

The Wilms' tumor suppressor gene, WT1, functions as a transcriptional regulator that represses or activates the expression of a variety of putative target genes. However, it is not clear which genes are the biological targets of WT1, nor which cellular pathway(s) is critically altered in tumors as a result of WT1 mutation. To investigate in vivo the role of WT1 as a transcription factor in Wilms' tumors, we used cDNA microarrays to compare the expression of putative WT1 target genes in a set of 15 primary Wilmstumors carrying WT1-inactivating mutations versus a set of 16 tumors with no WT1 mutations. We hypothesized that the expression of direct downstream targets of WT1 that are relevant to tumor development would differ between these two genetically distinct sets of tumors. Using the Atlas Human Cancer 1.2 cDNA arrays to quantitate gene expression in the 31 tumors, we found that the expression of one WT1 putative target gene, c-MYC, statistically significantly differed between the two sets of tumors and was upregulated in WT1-mutant tumors. This increase of relative gene expression for c-MYC was confirmed using real-time reverse transcription-polymerase chain reaction. The differential expression of another putative target gene, EGR1, approached significance and was also upregulated in WT1-mutant tumors. These data, in addition to the coexpression of c-MYC and WT1 in embryonic renal mesenchyme, strongly suggest that c-MYC is a biologically relevant target of WT1 in Wilmstumors.

Indexed as

Gene Expression Regulation, NeoplasticGenes, mycTranscription, GeneticGene Expression ProfilingHumansKidney NeoplasmsMutationOligonucleotide Array Sequence AnalysisUp-RegulationWilms TumorWT1 ProteinsWT1 Proteins

Identifiers

PMID12802290
OpenAlexW2064722919

What OpenQuestion holds

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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.