Literature DB >> 9872321

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

R M Pitti1, S A Marsters, D A Lawrence, M Roy, F C Kischkel, P Dowd, A Huang, C J Donahue, S W Sherwood, D T Baldwin, P J Godowski, W I Wood, A L Gurney, K J Hillan, R L Cohen, A D Goddard, D Botstein, A Ashkenazi.   

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/Apol/CD95. 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 cells. 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.

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Year:  1998        PMID: 9872321     DOI: 10.1038/25387

Source DB:  PubMed          Journal:  Nature        ISSN: 0028-0836            Impact factor:   49.962


  177 in total

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