1999
DOI: 10.1016/s0168-8278(99)80114-7
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Expression and processing of gastrin in hepatocellular carcinoma, fibrolamellar carcinoma and cholangiocarcinoma

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Cited by 49 publications
(44 citation statements)
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“…In support of this hypothesis, recent studies have shown that CCK-B/gastrin receptors are also expressed by human cholangiocarcinoma. 45 Consistent with antiproliferative properties of gastrin on cholangiocytes, preliminary data from our laboratory have shown 46 that gastrin inhibits the growth of cholangiocarcinoma by interacting with CCK-B/gastrin receptors through a transduction pathway involving IP 3 , Ca 2ϩ , and PKC␣. Direct interaction of gastrin with cholangiocytes is further supported by the finding that serum levels of somatostatin or insulin, which have been shown to modulate cholangiocyte proliferation, 4,13-15 do not change after chronic infusion of gastrin to BDL rats.…”
Section: Discussionmentioning
confidence: 69%
“…In support of this hypothesis, recent studies have shown that CCK-B/gastrin receptors are also expressed by human cholangiocarcinoma. 45 Consistent with antiproliferative properties of gastrin on cholangiocytes, preliminary data from our laboratory have shown 46 that gastrin inhibits the growth of cholangiocarcinoma by interacting with CCK-B/gastrin receptors through a transduction pathway involving IP 3 , Ca 2ϩ , and PKC␣. Direct interaction of gastrin with cholangiocytes is further supported by the finding that serum levels of somatostatin or insulin, which have been shown to modulate cholangiocyte proliferation, 4,13-15 do not change after chronic infusion of gastrin to BDL rats.…”
Section: Discussionmentioning
confidence: 69%
“…Gastrin has been demonstrated as the most important trophic factor for gastrointestinal mucosa as well as a promoter for growth of human cancers including gastric cancer [9,10], colon cancer [11,12], pancreatic cancer [13][14][15], liver cancer [16], lung cancer [17] and renal cancer [18] etc. The promotion effect of gastrin on tumor cell growth can be reached by either an autocrine or paracrine manners [19].…”
Section: Introductionmentioning
confidence: 99%
“…The mechanisms involved in the transcriptional regulation of mammalian antral gastrin gene expression have been challenging to study in vitro because of the absence of G cell lines and in vivo because of the lack of appropriate transgenic models. In addition, although numerous reports have suggested that gastrin is upregulated in colon, liver, pancreatic, lung, and ovarian cancer (1,4,5,8,18,39), studies of cell-specific expression of gastrin in the setting of neoplasia have been limited.…”
mentioning
confidence: 99%