ArticleMolecular and cellular biology2014
p19Ink4d is a tumor suppressor and controls pituitary anterior lobe cell proliferation.
Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- CIP/KIP and INK4 families as hostages of oncogenic signaling.Cell division · 2024Review
- p18INK4C and BRCA1 inhibit follicular cell proliferation and dedifferentiation in thyroid cancer.Cell cycle (Georgetown, Tex.) · 2023Article
- Article
- Preclinical Models of Neuroendocrine Neoplasia.Cancers · 2022Review
- PUMILIO proteins promote colorectal cancer growth via suppressing p21.Nature communications · 2022Article
- The 3PAs: An Update on the Association of Pheochromocytomas, Paragangliomas, and Pituitary Tumors.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2019Review
- Regulation of proliferation in developing human tooth germs by MSX homeodomain proteins and cyclin-dependent kinase inhibitor p19Organogenesis · 2017Article
- Cell cycle-independent roles of p19Chinese journal of cancer · 2017Article
- Article
- Sulforaphane inhibits proliferation and invasive activity of everolimus-resistant kidney cancer cells in vitro.Oncotarget · 2016Article
- p16INK4a suppresses BRCA1-deficient mammary tumorigenesis.Oncotarget · 2016Article
- Rescue from early-onset hearing loss in a mouse model lacking the cyclin-dependent kinase inhibitor p19Ink4d.Cell death & disease · 2016Article
- Animal models of pituitary neoplasia.Molecular and cellular endocrinology · 2016Review
- Pituitary adenoma with paraganglioma/pheochromocytoma (3PAs) and succinate dehydrogenase defects in humans and mice.The Journal of clinical endocrinology and metabolism · 2015Article
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
Abstract
Pituitary tumors develop in about one-quarter of the population, and most arise from the anterior lobe (AL). The pituitary gland is particularly sensitive to genetic alteration of genes involved in the cyclin-dependent kinase (CDK) inhibitor (CKI)-CDK-retinoblastoma protein (Rb) pathway. Mice heterozygous for the Rb mutation develop pituitary tumors, with about 20% arising from the AL. Perplexingly, none of the CKI-deficient mice reported thus far develop pituitary AL tumors. In this study, we show that deletion of p19(Ink4d) (p19), a CKI gene, in mice results in spontaneous development of tumors in multiple organs and tissues. Specifically, more than one-half of the mutant mice developed pituitary hyperplasia or tumors predominantly in the AL. Tumor development is associated with increased cell proliferation and enhanced activity of Cdk4 and Cdk6 and phosphorylation of Rb protein. Though Cdk4 is indispensable for postnatal pituitary cell proliferation, it is not required for the hyperproliferative pituitary phenotype caused by p19 loss. Loss of p19 phosphorylates Rb in Cdk4(-/-) pituitary AL cells and mouse embryonic fibroblasts (MEFs) and rescues their proliferation defects, at least partially, through the activation of Cdk6. These results provide the first genetic evidence that p19 is a tumor suppressor and the major CKI gene that controls pituitary AL cell proliferation.
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