ArticlePloS one2011
Functional interactions between retinoblastoma and c-MYC in a mouse model of hepatocellular carcinoma.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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Who cites it
5 citing papers in PubMed, 14 citations in OpenAlex.
- Targeting Oncoimmune Drivers of Cancer Metastasis.Cancers · 2021Review
- RB loss contributes to aggressive tumor phenotypes in MYC-driven triple negative breast cancer.Cell cycle (Georgetown, Tex.) · 2015Article
- RB tumor suppressive function in response to xenobiotic hepatocarcinogens.The American journal of pathology · 2014Article
- Endoreplication and polyploidy: insights into development and disease.Development (Cambridge, England) · 2013Review
- Identification of RARRES1 as a core regulator in liver fibrosis.Journal of molecular medicine (Berlin, Germany) · 2012Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Inactivation of the RB tumor suppressor and activation of the MYC family of oncogenes are frequent events in a large spectrum of human cancers. Loss of RB function and MYC activation are thought to control both overlapping and distinct cellular processes during cell cycle progression. However, how these two major cancer genes functionally interact during tumorigenesis is still unclear. Here, we sought to test whether loss of RB function would affect cancer development in a mouse model of c-MYC-induced hepatocellular carcinoma (HCC), a deadly cancer type in which RB is frequently inactivated and c-MYC often activated. We found that RB inactivation has minimal effects on the cell cycle, cell death, and differentiation features of liver tumors driven by increased levels of c-MYC. However, combined loss of RB and activation of c-MYC led to an increase in polyploidy in mature hepatocytes before the development of tumors. There was a trend for decreased survival in double mutant animals compared to mice developing c-MYC-induced tumors. Thus, loss of RB function does not provide a proliferative advantage to c-MYC-expressing HCC cells but the RB and c-MYC pathways may cooperate to control the polyploidy of mature hepatocytes.
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Registered trials
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