ArticleMolecular endocrinology (Baltimore, Md.)2008
Pituitary-specific knockout of the Carney complex gene Prkar1a leads to pituitary tumorigenesis.
Article in Molecular endocrinology (Baltimore, Md.), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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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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.
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Who cites it
32 citing papers in PubMed, 75 citations in OpenAlex.
- Familial isolated pituitary adenoma is independent ofHeliyon · 2024Article
- Preclinical Models of Neuroendocrine Neoplasia.Cancers · 2022Review
- The cAMP-signaling cancers: Clinically-divergent disorders with a common central pathway.Frontiers in endocrinology · 2022Review
- Pituitary neuroendocrine tumors: a model for neuroendocrine tumor classification.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2021Review
- Genomics and Epigenomics of Pituitary Tumors: What Do Pathologists Need to Know?Endocrine pathology · 2021Review
- Prkar1a haploinsufficiency ameliorates the growth hormone excess phenotype in Aip-deficient mice.Human molecular genetics · 2020Article
- Modulation of polycystic kidney disease by G-protein coupled receptors and cyclic AMP signaling.Cellular signalling · 2020Review
- MicroRNA-200b inhibits pituitary tumor cell proliferation and invasion by targeting PKCα.Experimental and therapeutic medicine · 2017Article
- Corticotropinoma as a Component of Carney Complex.Journal of the Endocrine Society · 2017Article
- Adipocyte Versus Somatotrope Leptin: Regulation of Metabolic Functions in the Mouse.Endocrinology · 2016Article
- Animal models of pituitary neoplasia.Molecular and cellular endocrinology · 2016Review
- Review
- Genomic approaches to problems in pituitary neoplasia.Endocrine pathology · 2014Review
- A Histopathological Study of Multi-hormone Producing Proliferative Lesions in Estrogen-induced Rat Pituitary Prolactinoma.Acta histochemica et cytochemica · 2014Article
- Genetically engineered mouse models of pituitary tumors.Frontiers in oncology · 2014Review
- The role of genetic and epigenetic changes in pituitary tumorigenesis.Neurologia medico-chirurgica · 2014Review
- The molecular pathogenesis of pituitary adenomas: an update.Endocrinology and metabolism (Seoul, Korea) · 2013Review
- cAMP/PKA signaling defects in tumors: genetics and tissue-specific pluripotential cell-derived lesions in human and mouse.Molecular and cellular endocrinology · 2013Review
- Thyroid-specific ablation of the Carney complex gene, PRKAR1A, results in hyperthyroidism and follicular thyroid cancer.Endocrine-related cancer · 2012Article
- Genetic predisposition to peripheral nerve neoplasia: diagnostic criteria and pathogenesis of neurofibromatoses, Carney complex, and related syndromes.Acta neuropathologica · 2012Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Carney complex (CNC) is an inherited neoplasia syndrome characterized by spotty skin pigmentation, myxomas, endocrine tumors, and schwannomas. Among the endocrine tumors that comprise the syndrome, GH-producing pituitary tumors are seen in approximately 10% of patients, although biochemical abnormalities of the GH axis are much more common. To explore the role of loss of the CNC gene PRKAR1A on pituitary tumorigenesis, we produced a tissue-specific knockout (KO) of this gene in the mouse. For these studies, we generated a mouse line expressing the cre recombinase in pituitary cells using the rat GHRH receptor promoter. These mice were then crossed with Prkar1a conditional null animals to produce tissue-specific KOs. Although prolactinomas were observed in KO and control mice, the KO mice exhibited a significantly increased frequency of pituitary tumors compared with wild-type or conventional Prkar1a(+/-) mice. Characterization of the tumors demonstrated they were composed of cells of the Pit1 lineage that stained for GH, prolactin, and TSH. At the biochemical level, levels of GH in the serum of KO animals were markedly elevated compared with controls, regardless of the presence of a frank tumor. These data indicate that complete loss of Prkar1a is sufficient to allow the formation of pituitary tumors and abnormalities of the GH axis, in close analogy to human patients with CNC.
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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.