ArticleReproductive biology and endocrinology : RB&E2010
Genetic evidence that SMAD2 is not required for gonadal tumor development in inhibin-deficient mice.
Article in Reproductive biology and endocrinology : RB&E, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 11 citations in OpenAlex.
- SMAD3 Activation: A Converging Point of Dysregulated TGF-Beta Superfamily Signaling and Genetic Aberrations in Granulosa Cell Tumor Development?Biology of reproduction · 2016Review
- Insights into granulosa cell tumors using spontaneous or genetically engineered mouse models.Clinical and experimental reproductive medicine · 2016Review
- Mouse models of adrenocortical tumors.Molecular and cellular endocrinology · 2016Review
- Betaglycan alters NFκB-TGFβ2 cross talk to reduce survival of human granulosa tumor cells.Molecular endocrinology (Baltimore, Md.) · 2013Article
- Two sides of the story? Smad4 loss in pancreatic cancer versus head-and-neck cancer.FEBS letters · 2012Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundInhibin is a tumor-suppressor and activin antagonist. Inhibin-deficient mice develop gonadal tumors and a cachexia wasting syndrome due to enhanced activin signaling. Because activins signal through SMAD2 and SMAD3 in vitro and loss of SMAD3 attenuates ovarian tumor development in inhibin-deficient females, we sought to determine the role of SMAD2 in the development of ovarian tumors originating from the granulosa cell lineage.
methodsUsing an inhibin alpha null mouse model and a conditional knockout strategy, double conditional knockout mice of Smad2 and inhibin alpha were generated in the current study. The survival rate and development of gonadal tumors and the accompanying cachexia wasting syndrome were monitored.
resultsNearly identical to the controls, the Smad2 and inhibin alpha double knockout mice succumbed to weight loss, aggressive tumor progression, and death. Furthermore, elevated activin levels and activin-induced pathologies in the liver and stomach characteristic of inhibin deficiency were also observed in these mice. Our results indicate that SMAD2 ablation does not protect inhibin-deficient females from the development of ovarian tumors or the cachexia wasting syndrome.
conclusionsSMAD2 is not required for mediating tumorigenic signals of activin in ovarian tumor development caused by loss of inhibin.
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