ArticleOncogene2002
Loss of the cell cycle inhibitors p21(Cip1) and p27(Kip1) enhances tumorigenesis in knockout mouse models.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 76 citations in OpenAlex.
- Recent Advances in the Role of Autophagy in Endocrine-Dependent Tumors.Endocrine reviews · 2023Review
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- Review
- Circulating Extracellular Vesicles and Particles Derived From Adipocytes: The Potential Role in Spreading MicroRNAs Associated With Cellular Senescence.Frontiers in aging · 2022Article
- Endothelial sprouting, proliferation, or senescence: tipping the balance from physiology to pathology.Cellular and molecular life sciences : CMLS · 2021Review
- p21 in Cancer Research.Cancers · 2019Review
- UBE2T promotes proliferation via G2/M checkpoint in hepatocellular carcinoma.Cancer management and research · 2019Article
- Article
- DNA damage during S-phase mediates the proliferation-quiescence decision in the subsequent G1 via p21 expression.Nature communications · 2017Article
- Article
- p27kip1 expression limits H-Ras-driven transformation and tumorigenesis by both canonical and non-canonical mechanisms.Oncotarget · 2016Article
- TLE3 represses colorectal cancer proliferation by inhibiting MAPK and AKT signaling pathways.Journal of experimental & clinical cancer research : CR · 2016Article
- Combined loss of PUMA and p21 accelerates c-MYC-driven lymphoma development considerably less than loss of one allele of p53.Oncogene · 2016Article
- The non-canonical functions of p27(Kip1) in normal and tumor biology.Cell cycle (Georgetown, Tex.) · 2016Review
- Protein dynamics: tuning disorder propensity in p53.Nature chemical biology · 2014Article
- miR-221/222 promotes S-phase entry and cellular migration in control of basal-like breast cancer.Molecules (Basel, Switzerland) · 2014Article
- Sumoylation is tumor-suppressive and confers proliferative quiescence to hematopoietic progenitors in Drosophila melanogaster larvae.Biology open · 2012Article
- Article
- Quiescent, slow-cycling stem cell populations in cancer: a review of the evidence and discussion of significance.Journal of oncology · 2011Article
- Endocrine dysfunction in p27Kip1 deficient mice and susceptibility to Wnt-1 driven breast cancer.Carcinogenesis · 2009Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Events that contribute to tumor formation include mutations in the ras gene and loss or inactivation of cell cycle inhibitors such as p21(Cip1) and p27(Kip1). In our previous publication, we showed that mice expressing the MMTV/v-Ha-ras transgene developed tumors earlier and at higher multiplicities in the absence than in the presence of p21(Cip1). To further evaluate the combinatorial role of genetic alterations and loss of cell cycle inhibitors in tumorigenesis, we performed two companion studies. In the first study, wild type and p21(Cip1)-null mice were exposed to the chemical carcinogen, urethane. Similar to its effects in v-Ha-ras mice, loss of p21(Cip1) accelerated tumor onset and increased tumor multiplicity in urethane-treated mice. Lung tumors were the predominant tumor type in urethane-treated mice regardless of p21(Cip1) status. In the second study, tumor formation was monitored in v-Ha-ras mice expressing or lacking p27(Kip1). Unlike p21(Cip1), the absence of p27(Kip1) had no effect on the timing or multiplicity of tumor formation, which was largely restricted to mammary and salivary glands. However, once tumors appeared, they grew faster in p27(Kip1)-null mice than in p27(Kip1)-wild type mice. Increases in growth rate were particularly striking for salivary tumors in ras/p27(-/-) mice. Loss of p21(Cip1), on the other hand, had no effect on tumor growth rate in v-Ha-ras mice. Collectively, our data suggest that p21(Cip1) suppresses tumor formation elicited by multiple agents and that p21(Cip1) and p27(Kip1) suppress tumor formation in different ways.
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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.