@article{ref1,
title="Fas ligand: A potential target for therapeutic induction of apoptosis and enhancing immunotherapy in cancer",
journal="Expert Opinion on Therapeutic Targets",
year="1999",
author="O'Connell, J.",
volume="3",
number="4",
pages="601-611",
abstract="Fas (CD95/APO-1) is a cell surface receptor which mediates a potent apoptotic death signal upon engagement by its ligand, FasL. Since tumour cells frequently co-express Fas and FasL, the prospect of therapeutically stimulating autocrine suicide of cancer cells via the Fas pathway is tantalising. To achieve this, mechanisms of acquired resistance to Fas-mediated apoptosis, inherent in cancers, must be overcome. Indeed, expression of FasL by Fas-resistant tumours appears to enhance malignancy by triggering apoptosis of Fas-sensitive antitumour immune effector cells. Therapeutic inhibition of this &quot;Fas counterattack&quot; against antitumour immune responses might improve immunotherapeutic approaches. Although restoring the Fas-sensitivity of tumours and inhibiting FasL-mediated counterattack against antitumour lymphocytes have been achieved experimentally in vitro, transferring such approaches to in vivo therapy represents an enormous challenge. © 1999 Ashley Publications Ltd.<p /><p>Language: en</p>",
language="en",
issn="1744-7631",
doi="10.1517/14728222.3.4.601",
url="http://dx.doi.org/10.1517/14728222.3.4.601"
}