ArticleJournal of experimental & clinical cancer research : CR2015
Hematopoietic neoplasms in Prkar2a-deficient mice.
Article in Journal of experimental & clinical cancer research : CR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Genome-Wide Protein Interaction Analysis in Parasitic Gyrodactylus Flatworms-Fish Hosts System and Drug Target Identification.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Downregulation of NCL attenuates tumor formation and growth in HeLa cells by targeting the PI3K/AKT pathway.Cancer medicine · 2022Article
- A Novel Platelet-Related Gene Signature for Predicting the Prognosis of Triple-Negative Breast Cancer.Frontiers in cell and developmental biology · 2021Article
- Prkar1a haploinsufficiency ameliorates the growth hormone excess phenotype in Aip-deficient mice.Human molecular genetics · 2020Article
- The Molecular Basis for Specificity at the Level of the Protein Kinase a Catalytic Subunit.Frontiers in endocrinology · 2018Review
- PKA regulatory IIα subunit is essential for PGD2-mediated resolution of inflammation.The Journal of experimental medicine · 2016Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundProtein kinase A (PKA) is a holoenzyme that consists of a dimer of regulatory subunits and two inactive catalytic subunits that bind to the regulatory subunit dimer. Four regulatory subunits (RIα, RIβ, RIIα, RIIβ) and four catalytic subunits (Cα, Cβ, Cγ, Prkx) have been described in the human and mouse genomes. Previous studies showed that complete inactivation of the Prkar1a subunit (coding for RIα) in the germline leads to embryonic lethality, while Prkar1a-deficient mice are viable and develop schwannomas, thyroid, and bone neoplasms, and rarely lymphomas and sarcomas. Mice with inactivation of the Prkar2a and Prkar2b genes (coding for RIIα and RIIβ, respectively) are also viable but have not been studied for their susceptibility to any tumors.
methodsCohorts of Prkar1a (+/-) , Prkar2a (+/-) , Prkar2a (-/-) , Prkar2b (+/-) and wild type (WT) mice have been observed between 5 and 25 months of age for the development of hematologic malignancies. Tissues were studied by immunohistochemistry; tumor-specific markers were also used as indicated. Cell sorting and protein studies were also performed.
resultsBoth Prkar2a (-/-) and Prkar2a (+/-) mice frequently developed hematopoietic neoplasms dominated by histiocytic sarcomas (HS) with rare diffuse large B cell lymphomas (DLBCL). Southern blot analysis confirmed that the tumors diagnosed histologically as DLBCL were clonal B cell neoplasms. Mice with other genotypes did not develop a significant number of similar neoplasms.
conclusionsPrkar2a deficiency predisposes to hematopoietic malignancies in vivo. RIIα's likely association with HS and DLBCL was hitherto unrecognized and may lead to better understanding of these rare neoplasms.
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