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We read with interest the article of Bennett et al,1 showing that the coexpression of Fas–Fas ligand (FasL) did not elicit increased apoptosis in colonic tumour cells. They suggested that colonocytes acquire resistance to Fas mediated apoptosis early in the transformation process. The Cork Group has greatly contributed to unravelling the riddle of the mechanism(s) behind the (CD95/APO1) receptor (Fas)–FasL system, which enables apoptosis to occur in neoplastic tissues.
Using a rat neu transgenic (rNeu-TG) mouse model, Céfai et al demonstrated that the FasL mediated escape from immune rejection of breast tumours correlated with the apoptosis of infiltrating T cells.2
During studies of similar colorectal lesions as those reported by Bennett et al, we investigated the occurrence of infiltrating lymphocytes.3 In that study, intraepithelial lymphocytes (IELs) were recorded in 70% of 102 hyperplastic polyps and tubular adenomas, in > 80% of 75 villous and serrated adenomas, in 14 of 28 incipient adenocarcinomas, and in only nine of 50 advanced carcinomas. IELs were CD3 positive but major histocompatibility …