ArticleCell cycle (Georgetown, Tex.)2007
Differential gene expression of p27Kip1 and Rb knockout pituitary tumors associated with altered growth and angiogenesis.
Article in Cell cycle (Georgetown, Tex.), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Cyclooxygenase-2 negatively regulates osteogenic differentiation in murine bone marrow mesenchymal stem cells via the FOXO3a/p27kip1 pathway.Bone & joint research · 2025Article
- The miR-106a~363Oncotarget · 2017Article
- In Vivo Mouse Intervertebral Disc Degeneration Model Based on a New Histological Classification.PloS one · 2016Article
- Pituitary adenoma with paraganglioma/pheochromocytoma (3PAs) and succinate dehydrogenase defects in humans and mice.The Journal of clinical endocrinology and metabolism · 2015Article
- Roles of tumor suppressors in regulating tumor-associated inflammation.Cell death and differentiation · 2014Review
- Genetic characterization of p27(kip1) and stathmin in controlling cell proliferation in vivo.Cell cycle (Georgetown, Tex.) · 2014Article
- Cyclin D1 and cdk4 mediate development of neurologically destructive oligodendroglioma.Cancer research · 2011Article
- p27(Kip1) is required to maintain proliferative quiescence in the adult cochlea and pituitary.Cell cycle (Georgetown, Tex.) · 2011Article
- Cooperation between cyclin E and p27(Kip1) in pituitary tumorigenesis.Molecular endocrinology (Baltimore, Md.) · 2010Article
- Mouse models of endocrine tumours.Best practice & research. Clinical endocrinology & metabolism · 2010Review
- Cancer models in Caenorhabditis elegans.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Review
- The function of p27 KIP1 during tumor development.Experimental & molecular medicine · 2009Review
- Cellular mechanisms of tumour suppression by the retinoblastoma gene.Nature reviews. Cancer · 2008Review
- Targeting prostate cancer based on signal transduction and cell cycle pathways.Cell cycle (Georgetown, Tex.) · 2008Review
- Experimental models of hepatocellular carcinoma.Journal of hepatology · 2008Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Mice lacking the p27Kip1 Cdk inhibitor, like mice lacking Rb, develop pituitary tumors involving pars intermedia melanotrophs, yet p27(Kip1) tumors are genetically distinct from Rb derived tumors as they exhibit haploid insufficiency. We compared tumors from mice with p27( Kip1) constitutive and tissue specific null mutations to tumors arising in tissue specific Rb knockout mice with the aim of determining whether they are distinguished by quantitative or qualitative differences. The rate of p27Kip1 knockout tumor development was strongly influenced by strain background due to polygenic strain modifiers in the C57BL/6J versus 129S4 strains but, unlike a prior report of Rb mutants, this impacted tumor incidence but not the tumor spectrum. p27Kip1 tumors were oligoclonal or polyclonal based on studies of X-chromosomal inactivation of Dock11. In contrast, Rb null tissue developed monoclonal neoplasms even in the absence of a requirement for Rb mutant clonal selection. Rb null tumors exhibited a higher proliferation rate and developed ischemic necrosis associated with an aberrant vasculature. p27Kip1 null tumors maintained normal vascular density, through a tumor cell dependent mechanism, but were more often hemorrhagic. Gene expression profiles distinguished p27Kip1 from Rb null tumors including significant differences in expression of Rb and E2F signature genes. Rb null tumors expressed higher levels of VEGF which, in other systems, is associated with dilated vessels, ineffective perfusion and tissue hypoxia. Mouse models lacking p27Kip1 and Rb may help us better understand the pathophysiology of MEN syndromes, retinoblastoma and other cancers that disrupt these important cell cycle inhibitors.
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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.