Defective death receptor signaling as a cause of tumor immune escape
- 1 February 2002
- journal article
- review article
- Published by Elsevier in Seminars in Cancer Biology
- Vol. 12 (1) , 51-55
- https://doi.org/10.1006/scbi.2001.0405
Abstract
No abstract availableKeywords
This publication has 30 references indexed in Scilit:
- FAS Engagement Induces the Maturation of Dendritic Cells (Dcs), the Release of Interleukin (Il)-1β, and the Production of Interferon γ in the Absence of IL-12 during Dc–T Cell Cognate InteractionThe Journal of Experimental Medicine, 2000
- Alterations of Fas (Apo-1/CD95) Gene in Cutaneous Malignant MelanomaThe American Journal of Pathology, 1999
- Antitumor effect of allogenic fibroblasts engineered to express Fas ligand (FasL)Gene Therapy, 1998
- Death Receptors: Signaling and ModulationScience, 1998
- Viral FLICE-inhibitory proteins (FLIPs) prevent apoptosis induced by death receptorsNature, 1997
- Apoptosis by Death FactorCell, 1997
- Melanoma Cell Expression of Fas(Apo-1/CD95) Ligand: Implications for Tumor Immune EscapeScience, 1996
- Ras Gene Mutation: A Rare Event in Nonmetastatic Primary Malignant MelanomaJournal of Investigative Dermatology, 1995
- Analysis ofras mutations in human melanocytic lesions: activation of theras gene seems to be associated with the nodular type of human malignant melanomaZeitschrift für Krebsforschung und Klinische Onkologie, 1995
- RAS Mutations in Human Melanoma: A Marker of Malignant ProgressionJournal of Investigative Dermatology, 1994