ArticleEndocrine pathology2009
No evidence for WT1 involvement in a beta-catenin-independent activation of the Wnt signaling pathway in pituitary adenomas.
Article in Endocrine pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
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6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The overexpression of Wilms' tumor gene product WT1, which acts as a tumor suppressor or oncogene, has been reported in various malignancies. Recent studies have shown that the interaction partner Wnt-4 is upregulated in pituitary adenomas dependent on the Pit-1 lineage (somatotrophs, lactotrophs, and thyrotrophs). However, no data on WT1 expression in nontumorous pituitary tissue or pituitary adenomas is available to date. We investigated WT1 expression in 90 paraffin-embedded pituitary adenomas, including eight atypical adenomas, and in 28 nontumorous pituitary glands by immunohistochemistry. WT1 is absent in epithelial cells of all nontumorous pituitary glands and in 87 out of 90 pituitary adenomas. Only two GHomas (including one atypical adenoma) and one gonadotropin-producing adenoma expressed WT1 in the cytoplasm of single tumor cells without nuclear staining. There is no evidence that WT1 does regulate the Wnt-4/beta-catenin-independent pathway which is activated in the Pit-1-expressing subset of pituitary adenomas.
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