Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo
Year: 1998
Type: preprint
Abstract: Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.
Source: Genes & Development
Institutions: National Institutes of Health, The University of Texas MD Anderson Cancer Center, Harvard University, National Institute of Environmental Health Sciences, Dana-Farber Cancer Institute, National Cancer Institute, Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology
Language: English
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
OpenAlex ID: W2107570915