Increased Susceptibility to Tumor Initiation and Metastasis in TNF-Related Apoptosis-Inducing Ligand-Deficient Mice1
By E. Cretney, K. Takeda, H. Yagita, M. Glaccum, J. Peschon, M. Smyth. Journal of Immunology, 2002
671 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/4f8f1e99a12b96ca22cf2154be06e3148ea1e68b
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In Cancer Research
In Immunology
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- Shulin Wang
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In Molecular Biology
Citations in the corpus
- Phenotypic diversity and plasticity in circulating neutrophil subpopulations in cancer. (2015, background): “%) had increased expression of TRAIL (Figure S2) raising the possibility that this LDN subpopulation may play a role in antitumor immunity (Cretney et al., 2002).”
- How Do Cytotoxic Lymphocytes Kill Cancer Cells? (2015, background): “This effect was originally shown using transplanted syngeneic cell lines (11, 54, 60, 61) and later confirmed in a more physiologic model of spontaneous metastasis during chemically induced carcinomas (62).”
- Apo2L/TRAIL and its death and decoy receptors (2003, result): “Cretney et al.71 confirmed many of these results in Apo2L/ TRAIL-deficient mice.”
- TRAIL and apoptosis induction by TNF-family death receptors (2003, background): “Mouse gene knockout studies indicate that TRAIL has an important role in antitumor surveillance by immune cells (Cretney et al., 2002; Smyth et al., 2003), and mediates thymocyte apoptosis and is important in the induction of autoimmune diseases (Lamhamedi-Cherradi et al., 2003).”
- Apo2L/TRAIL: apoptosis signaling, biology, and potential for cancer therapy. (2003, background): “Apo2L/TRAIL knockout mice are viable, fertile and have no obvious haematological defects [104,105], suggesting this death ligand does not have an essential developmental function.”