ReviewMolecular and cellular endocrinology2010
PRKAR1A and the evolution of pituitary tumors.
Review in Molecular and cellular endocrinology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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
12 citing papers in PubMed, 40 citations in OpenAlex.
- Analysis of differentially expressed proteins in lymph fluids related to lymphatic metastasis in a breast cancer rabbit model guided by contrast‑enhanced ultrasound.Oncology letters · 2024Article
- Pituitary Tumorigenesis-Implications for Management.Medicina (Kaunas, Lithuania) · 2023Review
- The Spectrum of Familial Pituitary Neuroendocrine Tumors.Endocrine pathology · 2023Review
- Bilateral Adrenal Hyperplasia: Pathogenesis and Treatment.Biomedicines · 2021Review
- Corticotropinoma as a Component of Carney Complex.Journal of the Endocrine Society · 2017Article
- Animal models of pituitary neoplasia.Molecular and cellular endocrinology · 2016Review
- A Histopathological Study of Multi-hormone Producing Proliferative Lesions in Estrogen-induced Rat Pituitary Prolactinoma.Acta histochemica et cytochemica · 2014Article
- The role of genetic and epigenetic changes in pituitary tumorigenesis.Neurologia medico-chirurgica · 2014Review
- Familial isolated pituitary adenomas (FIPA) and the pituitary adenoma predisposition due to mutations in the aryl hydrocarbon receptor interacting protein (AIP) gene.Endocrine reviews · 2013Review
- The genetic heterogeneity and mutational burden of engineered melanomas in zebrafish models.Genome biology · 2013Article
- Novel Mutation in PRKAR1A in Carney Complex.Korean journal of pathology · 2012Article
- Familial isolated pituitary adenomas: from genetics to therapy.Clinical and translational science · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Carney complex (CNC) is an inherited tumor predisposition associated with pituitary tumors, including GH-producing pituitary adenomas and rare reports of prolactinomas. This disease is caused by mutations in PRKAR1A, which encodes the type 1A regulatory subunit of the cAMP-dependent protein kinase, PKA. Loss of PRKAR1A causes enhanced PKA signaling, which leads to pituitary tumorigenesis. Mutations in the gene have not been detected in sporadic pituitary tumors, but there is some data to suggest that non-genomic mechanisms may cause loss of protein expression. Unlike CNC patients, mice heterozygous for Prkar1a mutations do not develop pituitary tumors, although complete knockout of the gene in the Pit1 lineage of the pituitary produces GH-secreting pituitary adenomas. These data indicate that complete loss of Prkar1a/PRKAR1A is able to cause pituitary tumors in mice and men. The pattern of tumors is likely related to the signaling pathways employed in specific pituitary cell types.
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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.