Overexpression of Fas ligand (FasL) during malignant transformation in the large bowel and in Barrett's metaplasia of the esophagus

Younes, Mamoun; Schwartz, Mark R.; Finnie, Delia; Younes, Anas

doi:10.1016/s0046-8177(99)90061-8

Cited by 41 publications

(22 citation statements)

References 16 publications

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Section: Discussionmentioning

confidence: 99%

“…However, FasL expression is not fundamentally a proper event in carcinoma tissue and might be extant in precancerous lesions including adenoma [24, 27, 31]. FasL upregulation might possibly be an early event in the adenoma-carcinoma sequence of colonic carcinogenesis [24, 31]. According to the report presented by Younes et al [24], about 90% of normal colonic mucosa did not express FasL, increased FasL expression paralleled the increase in villous morphology of adenoma, and overexpression was more frequent with progression toward adenocarcinomas.…”

Section: Discussionmentioning

confidence: 99%

“…FasL upregulation might possibly be an early event in the adenoma-carcinoma sequence of colonic carcinogenesis [24, 31]. According to the report presented by Younes et al [24], about 90% of normal colonic mucosa did not express FasL, increased FasL expression paralleled the increase in villous morphology of adenoma, and overexpression was more frequent with progression toward adenocarcinomas. They concluded that FasL expression is essential at an early stage of malignant transformation in colonic mucosa.…”

Section: Discussionmentioning

confidence: 99%

“…The sections were incubated with TBS including 1% bovine serum albumin for 20 min to block nonspecific binding of the immunoreagents. After washing in TBS, the sections were incubated with 1:100 diluted rabbit anti-human polyclonal FasL antibody (Q-20: sc-956, Santa Cruz Biotechnologies, Santa Cruz, Calif., USA), which has been used to determine FasL expression in previous studies of O’Connell et al [23]and Younes et al [24]. All incubations proceeded overnight at 4°C.…”

Section: Methodsmentioning

confidence: 99%

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Fas Ligand Expression Is Correlated with Metastasis in Colorectal Carcinoma

et al. 2003

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The Fas/Fas ligand (FasL) system is one apoptotic pathway through which malignant tumors can evade immune surveillance. While FasL is expressed in malignant tumors, Fas is conversely downregulated to escape host immune attack, resulting in tumor invasion. The aim of the current study was to find out further clinicopathological significance of FasL expression in carcinoma of the colon and rectum. FasL expression was investigated using immunohistochemical staining in 143 consecutive patients with primary colorectal carcinomas. Seventy-nine carcinomas (55.2%) expressed FasL. The incidence of lymph node and distant metastases in carcinomas expressing FasL was significantly higher than in carcinomas that did not express FasL (p = 0.031 and p = 0.0003, respectively). Although univariate analysis showed that survival in patients with carcinomas expressing FasL was significantly poorer than that in patients with carcinomas without FasL expression (p = 0.001), only Dukes’ stage was an independent prognosticator by multivariate analysis. FasL expression was found to be correlated with lymph node involvement and distant metastases in colorectal carcinoma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Fas Ligand Expression Is Correlated with Metastasis in Colorectal Carcinoma

et al. 2003

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“…Other changes previously described in Barrett's lesions include ampli®cation of the HER-2/neu, micro-satellite instability, Rb deletion, rare APC mutations, low expression of E-cadherin, high Src-speci®c activity, and increased expression of Bcl-2, cyclin D1, Fas ligand, TGF-alpha and PCNA (Sherr, 1994;Gimenez et al, 1999;Brien et al, 2000;Younes et al, 1999;Reid et al, 1993;Redd et al, 1994;Flejou et al, 1994;Bilir et al, 1994;Finkel et al, 1994;Kim et al, 1992;Arber et al, 1996a).…”

Section: Introductionmentioning

confidence: 99%

Proton pump inhibitors reduce cell cycle abnormalities in Barrett's esophagus

Umansky

W²,

Hallak

et al. 2001

Oncogene

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Neoplastic progression in Barrett's esophagus is a multistep process in which the metaplastic columnar epithelium sequentially evolves through a metaplasia-dysplasiacarcinoma sequence. The expression and DNA copy number of key cell cycle regulatory genes in paired normal and Barrett's esophagus samples was evaluated. Protein levels were evaluated in 60 formalin-®xed, para n-embedded human tissues by immunohistochemistry. DNA copy number from 20 fresh tissue pairs was analysed by Southern blot analysis. All normal mucosal samples expressed the p27 kip1 protein, but did not display appreciable nuclear staining for p16 kip4 , p21 cip1 or cyclins D1 and E. Barrett's metaplastic specimens displayed increased expression levels of p16 kip4 (74%), p21 cip1 (89%) and cyclins D1 (43%) and E (37%). p27 protein was absent in three cases. There was a signi®cant correlation between the expression of p16 kip4 and cyclin E, and p21 cip1 and p27 kip4 with cyclin D1. DNA analysis did not reveal any ampli®cation or deletion of these genes. Acid suppression, however, was associated with signi®cantly lower expression levels of key cell cycle proteins. Increased expression of key cell cycle regulatory genes appears to occur early in the neoplastic progression associated with Barrett's esophagus. Treatment with proton pump inhibitors appears to alter this increased expression. Oncogene (2001) 20, 7987 ± 7991.

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