ArticleCancer research2007
Senescence mediates pituitary hypoplasia and restrains pituitary tumor growth.
Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Correlations of pituitary tumor transforming gene expression with human pituitary adenomas: a meta-analysis.PloS one · 2014Pooled it
- Analysis of senescence in pituitary tumors from different lineages and the potential role of senolytic drugs as targeted therapies.Frontiers in endocrinology · 2026Article
- New insights in cellular senescence: The pituitary model.Journal of neuroendocrinology · 2025Review
- The SASP factor IL-6 sustains cell-autonomous senescent cells via a cGAS-STING-NFκB intracrine senescent noncanonical pathway.Aging cell · 2024Article
- Recent Therapeutic Advances in Pituitary Carcinoma.Journal of immunotherapy and precision oncology · 2023Review
- Clinical Biology of the Pituitary Adenoma.Endocrine reviews · 2022Review
- Article
- Architects of Pituitary Tumour Growth.Frontiers in endocrinology · 2022Review
- Adamantinomatous craniopharyngioma as a model to understand paracrine and senescence-induced tumourigenesis.Cellular and molecular life sciences : CMLS · 2021Review
- BRD4 as a therapeutic target for nonfunctioning and growth hormone pituitary adenoma.Neuro-oncology · 2020Article
- Genistein inhibits proliferation and induces senescence in neonatal mouse pituitary gland explant cultures.Toxicology · 2019Article
- Predicting the regrowth of clinically non-functioning pituitary adenoma with a statistical model.Journal of translational medicine · 2019Article
- Unmasking a new prognostic marker and therapeutic target from the GDNF-RET/PIT1/p14ARF/p53 pathway in acromegaly.EBioMedicine · 2019Article
- Two-Step Senescence-Focused Cancer Therapies.Trends in cell biology · 2018Review
- Response of Myeloid Leukemia Cells to Luteolin is Modulated by Differentially Expressed Pituitary Tumor-Transforming Gene 1 (PTTG1) Oncoprotein.International journal of molecular sciences · 2018Article
- P21Journal of neuro-oncology · 2018Article
- Deciphering the Contributions of CRH Receptors in the Brain and Pituitary to Stress-Induced Inhibition of the Reproductive Axis.Frontiers in molecular neuroscience · 2018Article
- HMGA2 cooperates with either p27Cell cycle (Georgetown, Tex.) · 2018Article
- Autocrine IL-6 mediates pituitary tumor senescence.Oncotarget · 2017Article
- PTTG1 regulated by miR-146a-3p promotes bladder cancer migration, invasion, metastasis and growth.Oncotarget · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Understanding factors subserving pituitary cell proliferation enables understanding mechanisms underlying uniquely benign pituitary tumors. Pituitary tumor-transforming gene (Pttg) deletion results in pituitary hypoplasia, low pituitary cell proliferation rates, and rescue of pituitary tumor development in Rb(+/-) mice. Pttg(-/-) pituitary glands exhibit ARF/p53/p21-dependent senescence pathway activation evidenced by up-regulated p19, cyclin D1, and Bcl-2 protein levels and p53 stabilization. High pituitary p21 levels in the absence of PTTG were associated with suppressed cyclin-dependent kinase 2 activity, Rb phosphorylation, and cyclin A expression, all required for cell cycle progression. Although senescence-associated beta-galactosidase was enhanced in Pttg-deficient pituitary glands, telomere lengths were increased. DNA damage signaling pathways were activated and aneuploidy was evident in the Pttg-deficient pituitary, triggering senescence-associated genes. To confirm the p21 dependency of decreased proliferation and senescence in the Pttg-null pituitary, mouse embryonic fibroblast (MEF) colony formation was tested in wild-type, Pttg(-/-), Rb(+/-), Rb(+/-)Pttg(-/-), and Rb(+/-)Pttg(-/-)p21(-/-) cells. Rb(+/-)Pttg(-/-) MEFs, unlike Rb(+/-) cells, failed to produce colonies and exhibited high levels of senescence. p21 deletion from Rb(+/-)Pttg(-/-) MEFs enhanced anchorage-independent cell growth, accompanied by a marked decrease in senescence. As cell proliferation assessed by bromodeoxyuridine incorporation was higher in Rb(+/-)Pttg(-/-)p21(-/-) relative to Rb(+/-)Pttg(-/-) pituitary glands, p21-dependent senescence provoked by Pttg deletion may underlie pituitary hypoplasia and decreased tumor development in Rb(+/-)Pttg(-/-) mice.
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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.