ArticleBiochemical and biophysical research communications2008
Induction of follistatin precedes gastric transformation in gastrin deficient mice.
Article in Biochemical and biophysical research communications, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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.
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.
Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Genetically engineered mouse models in gastric precancerous lesions research.World journal of gastrointestinal surgery · 2025Review
- Morphogen Signals Shaping the Gastric Glands in Health and Disease.International journal of molecular sciences · 2022Review
- Recapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.Advances in experimental medicine and biology · 2016Review
- Inflammation and Gli2 suppress gastrin gene expression in a murine model of antral hyperplasia.PloS one · 2012Article
- Gastric tuft cells express DCLK1 and are expanded in hyperplasia.Histochemistry and cell biology · 2011Article
- Nucleolar follistatin promotes cancer cell survival under glucose-deprived conditions through inhibiting cellular rRNA synthesis.The Journal of biological chemistry · 2010Article
- Inducible activation of Cre recombinase in adult mice causes gastric epithelial atrophy, metaplasia, and regenerative changes in the absence of "floxed" alleles.American journal of physiology. Gastrointestinal and liver physiology · 2010Article
- Hedgehog signaling and gastrointestinal cancer.Biochimica et biophysica acta · 2010Review
- Article
- Clinical and Therapeutic Implications of Follistatin in Solid Tumours.Cancer genomics & proteomicsReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We previously showed that antral gastric tumors develop in gastrin-deficient (Gas(-/-)) mice. Therefore Gas(-/-) mice were studied sequentially over 12 months to identify molecular mechanisms underlying gastric transformation. Fundic atrophy developed by 9 months in Gas(-/-) mice. Antral mucosal hyperplasia developed coincident with the focal loss of TFF1 and Muc5AC. Microarray analysis of 12 month Gas(-/-) tumors revealed an increase in follistatin, an activin/BMP antagonist. We found that elevated follistatin expression occurred in the proliferative neck zone of hyperplastic antrums, in antral tumors of Gas(-/-) mice, and also in human gastric cancers. Follistatin induced cyclin D1 and the trefoil factors TFF1 and TFF2 in a gastric cancer cell line. We concluded that antral hyperplasia in Gas(-/-) mice involves amplification of mucous cell lineages due to follistatin, suggesting its role in the development of antral gastric tumors.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.