ArticlePloS one2010
Fas/CD95 deficiency in ApcMin/+ mice increases intestinal tumor burden.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Colorectal cancer murine models: Initiation to metastasis.Cancer letters · 2024Review
- FAS gene expression, prognostic significance and molecular interactions in lung cancer.Frontiers in oncology · 2024Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
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- Ap4 is rate limiting for intestinal tumor formation by controlling the homeostasis of intestinal stem cells.Nature communications · 2018Article
- Vasohibin-2 modulates tumor onset in the gastrointestinal tract by normalizing tumor angiogenesis.Molecular cancer · 2014Article
- Circulating levels of soluble Fas ligand reflect disease progression in multiple myeloma.Medical oncology (Northwood, London, England) · 2014Article
- Down-regulation of BAX gene during carcinogenesis and acquisition of resistance to 5-FU in colorectal cancer.Pathology oncology research : POR · 2014Article
- An apoptosis-independent role of SMAC in tumor suppression.Oncogene · 2013Article
- Recent progress in mouse models for tumor suppressor genes and its implications in human cancer.Clinical Medicine Insights. Oncology · 2013Article
- NF-κB directly regulates Fas transcription to modulate Fas-mediated apoptosis and tumor suppression.The Journal of biological chemistry · 2012Article
- Acute sensitization of colon cancer cells to inflammatory cytokines by prophase arrest.Biochemical pharmacology · 2012Article
- Oncolytic poxvirus armed with Fas ligand leads to induction of cellular Fas receptor and selective viral replication in FasR-negative cancer.Cancer gene therapy · 2012Article
- Deconstructing p53 transcriptional networks in tumor suppression.Trends in cell biology · 2012Review
- Article
- Effect of sulindac sulfide on metallohydrolases in the human colon cancer cell line HT-29.PloS one · 2011Article
- The armadillo repeat domain of Apc suppresses intestinal tumorigenesis.Mammalian genome : official journal of the International Mammalian Genome Society · 2010Article
- Pro-protein convertase subtilisin/kexin type 9 promotes intestinal tumor development by activating Janus kinase 2/signal transducer and activator of transcription 3/SOCS3 signaling in ApcInternational journal of immunopathology and pharmacologyArticle
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
backgroundFas, a member of the tumor necrosis family, is responsible for initiating the apoptotic pathway when bound to its ligand, Fas-L. Defects in the Fas-mediated apoptotic pathway have been reported in colorectal cancer. METHODOLOGY/PRINCIPAL
findingsIn the present study, a variant of the Apc(Min/+) mouse, a model for the human condition, Familial Adenomatous Polyposis (FAP), was generated with an additional deficiency of Fas (Apc(Min/+)/Fas(lpr)) by cross-breeding Apc(Min/+) mice with Fas deficient (Fas(lpr)) mice. One of the main limitations of the Apc(Min/+) mouse model is that it only develops benign polyps. However, Apc(Min/+)/Fas(lpr) mice presented with a dramatic increase in tumor burden relative to Apc(Min/+) mice and invasive lesions at advanced ages. Proliferation and apoptosis markers revealed an increase in cellular proliferation, but negligible changes in apoptosis, while p53 increased at early ages. Fas-L was lower in Apc(Min/+)/Fas(lpr) mice relative to Apc(Min/+) cohorts, which resulted in enhanced inflammation. CONCLUSIONS/SIGNIFICANCE: This study demonstrated that imposition of a Fas deletion in an Apc(Min/+) background results in a more aggressive phenotype of the Apc(Min/+) mouse model, with more rapid development of invasive intestinal tumors and a decrease in Fas-L levels.
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