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

被引：657

作者：

Pitti, RM

Marsters, SA

Lawrence, DA

Roy, M

Kischkel, FC

Dowd, P

Huang, A

Donahue, CJ

Sherwood, SW

Baldwin, DT

Godowski, PJ

Wood, WI

Gurney, AL

Hillan, KJ

Cohen, RL

Goddard, AD

Botstein, D

Ashkenazi, A

机构：

[1] Genentech Inc, Dept Mol Oncol, S San Francisco, CA 94080 USA

[2] Genentech Inc, Dept Mol Biol, S San Francisco, CA 94080 USA

[3] Genentech Inc, Dept Immunol, S San Francisco, CA 94080 USA

[4] Stanford Univ, Dept Genet, Stanford, CA 94305 USA

来源：

NATURE | 1998年 / 396卷 / 6712期

关键词：

D O I：

10.1038/25387

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

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 Fast and Fas is to mediate immune-cytotoxic killing of cells that are potentially harmful to the organism, such as virus-infected or tumour cells(1). Here we report the discovery of a soluble decoy receptor, termed decoy receptor 3 (DcR3), that binds to Fast and inhibits Fast-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.

引用

页码：699 / 703

页数：5

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