Genomic amplification of a decoy receptor for Fas ligand in lung and colon cancer

Robert M. Pitti, Scot A. Marsters, David A. Lawrence, Margaret Roy, Frank C. Kischkel, Patrick Dowd, Arthur Huang, Christopher J. Donahue, Steven W. Sherwood, Daryl T. Baldwin, Paul J. Godowski, William I. Wood, Austin L. Gurney, Kenneth J. Hillan, Robert L. Cohen, Audrey D. Goddard, David Botstein and Avi Ashkenazi ()
Additional contact information
Robert M. Pitti: Molecular Biology, and Immunology, Genentech Inc.
Scot A. Marsters: Molecular Biology, and Immunology, Genentech Inc.
David A. Lawrence: Molecular Biology, and Immunology, Genentech Inc.
Margaret Roy: Molecular Biology, and Immunology, Genentech Inc.
Frank C. Kischkel: Molecular Biology, and Immunology, Genentech Inc.
Patrick Dowd: Molecular Biology, and Immunology, Genentech Inc.
Arthur Huang: Molecular Biology, and Immunology, Genentech Inc.
Christopher J. Donahue: Molecular Biology, and Immunology, Genentech Inc.
Steven W. Sherwood: Molecular Biology, and Immunology, Genentech Inc.
Daryl T. Baldwin: Molecular Biology, and Immunology, Genentech Inc.
Paul J. Godowski: Molecular Biology, and Immunology, Genentech Inc.
William I. Wood: Molecular Biology, and Immunology, Genentech Inc.
Austin L. Gurney: Molecular Biology, and Immunology, Genentech Inc.
Kenneth J. Hillan: Molecular Biology, and Immunology, Genentech Inc.
Robert L. Cohen: Molecular Biology, and Immunology, Genentech Inc.
Audrey D. Goddard: Molecular Biology, and Immunology, Genentech Inc.
David Botstein: Stanford University
Avi Ashkenazi: Molecular Biology, and Immunology, Genentech Inc.

Nature, 1998, vol. 396, issue 6712, 699-703

Abstract: Abstract Fas ligand (FasL) is produced by activated T cells and natural killer cells and it induces apoptosis (programmed cell death) in target cells through the death receptor Fas/Apo1/CD95 (ref. 1). One important role of FasL and Fas is to mediate immune-cytotoxic killing of cells that are potentially harmful to the organism, such as virus-infected or tumour cells1. Here we report the discovery of a soluble decoy receptor, termed decoy receptor 3 (DcR3), that binds to FasL and inhibits FasL-induced apoptosis. The DcR3 gene was amplified in about half of 35 primary lung and colon tumours studied, and DcR3 messenger RNA was expressed in malignant tissue. Thus, certain tumours may escape FasL-dependent immune-cytotoxic attack by expressing a decoy receptor that blocks FasL.

Date: 1998
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/25387 Abstract (text/html)
Access to the full text of the articles in this series is restricted.

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:396:y:1998:i:6712:d:10.1038_25387

Ordering information: This journal article can be ordered from
https://www.nature.com/

DOI: 10.1038/25387

Access Statistics for this article

Nature is currently edited by Magdalena Skipper

More articles in Nature from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().