ArticleOncogene2004
A dynamic switch in Rb+/- mediated neuroendocrine tumorigenesis.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Sprouting Angiogenesis in Human Pituitary Adenomas.Frontiers in oncology · 2022Article
- Phenotypical and Pharmacological Characterization of Stem-Like Cells in Human Pituitary Adenomas.Molecular neurobiology · 2017Article
- Novel retinoblastoma mutation abrogating the interaction to E2F2/3, but not E2F1, led to selective suppression of thyroid tumors.Cancer science · 2014Article
- Genetic and epigenetic mutations of tumor suppressive genes in sporadic pituitary adenoma.Molecular and cellular endocrinology · 2014Review
- Sca1⁺ murine pituitary adenoma cells show tumor-growth advantage.Endocrine-related cancer · 2014Article
- Genetically engineered mouse models of pituitary tumors.Frontiers in oncology · 2014Review
- The role of Cdk5 in neuroendocrine thyroid cancer.Cancer cell · 2013Article
- Mouse models of endocrine tumours.Best practice & research. Clinical endocrinology & metabolism · 2010Review
- Skp2 is required for survival of aberrantly proliferating Rb1-deficient cells and for tumorigenesis in Rb1+/- mice.Nature genetics · 2010Article
- Senescence mediates pituitary hypoplasia and restrains pituitary tumor growth.Cancer research · 2007Article
- Differential gene expression of p27Kip1 and Rb knockout pituitary tumors associated with altered growth and angiogenesis.Cell cycle (Georgetown, Tex.) · 2007Article
- Visualizing dynamic E2F-mediated repression in vivo.Molecular and cellular biology · 2006Article
- Exploring the tumors of multiple endocrine neoplasia type 1 in mouse models for basic and preclinical studies.International journal of endocrine oncologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Rb+/- mice develop a complex spectrum of neuroendocrine tumors on a mixed genetic (129Sv x C57BL/6) background. To understand how the 129Sv and C57BL/6 contributions affect Rb+/- tumorigenesis, we serially backcrossed Rb+/- animals to the 129Sv or C57BL/6 strain, and analysed their pathological profiles. Strikingly, the length of survival and the penetrance, severity and multiplicity of neuroendocrine tumors switch dramatically between Rb+/- animals from the two genetic backgrounds. In fact, the 129Sv background significantly enhances both the initiation and progression of tumorigenesis in the intermediate lobe of the pituitary (ILP) in Rb+/- animals. This is due to the surprising fact that ILPs from wild-type 129Sv animals are inherently abnormal, and thus greatly predisposed to neoplasia. This is likely to explain the high incidence of ILP tumors, an otherwise rare tumor type in wild-type mice, in numerous knockout studies performed on the 129Sv strain, and raises the intriguing possibility that the classic Rb+/- neuroendocrine tumors may fade away in another as of yet unidentified inbred strain. Finally, we have increased the utility of the Rb+/- tumor model, since Rb+/- animals on the C57BL/6 background develop high-penetrance tumors of the anterior lobe of the pituitary, a class of tumors estimated to occur in 20-25% of humans.
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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.