CYFRA 21-1 concentrations differed according to the tumour size and vascular invasion, but not according to the number of tumours or nodal status. These results suggested that CYFRA 21-1 should be Sorafenib VEGFR-2 useful for disease staging and monitoring in patients with ICC. In conclusion, serum CYFRA 21-1 should be a useful diagnostic test for ICC given its outstanding sensitivity. Serum CYFRA 21-1 concentrations reflected differences in ICC tumour burden, so this marker also could be applied to staging and monitoring. Prospective studies should be performed to evaluate the real impact of serum CYFRA 21-1 as a marker for ICC.
Gastrin was originally described as a gastrointestinal (GI) regulatory peptide whose principal function was to stimulate postprandial gastric acid secretion.

However, in addition to its recognised role in the physiological regulation of acid secretion, another biological property attributed to gastrin is its trophic effects. A prospective study by Thorburn et al (1998) suggested that hypergastrinemia is associated with an increased risk for colorectal cancer (CRC), and numerous studies have demonstrated that gastrin stimulates the growth of malignant colorectal adenocarcinomas (Wang et al, 1996; Malecka-Panas et al, 1997; Baldwin & Shulkes, 1998; Nakata et al, 1998; Koh et al, 1999; Stepan et al, 1999; Smith & Watson, 2000). Transgenic mice overexpressing progastrin and glycine-extended gastrin demonstrate enhanced colonic proliferation (Wang et al, 1996; Koh et al, 1999), and conversely, gastrin-deficient mice manifest decreased colonic proliferation (Koh et al, 1997).

Repression of the gastrin gene in human colon cancer cells by antisense gastrin RNA yields a significant growth inhibition of these cells, suggesting that gastrin expression may be required for colon tumour progression (Singh et al, 1996). Although these studies all suggest a role for gastrin in the pathogenesis of CRC, little is known regarding the factors and mechanisms involved in mediating the trophic properties of this important peptide. Overwhelming evidence derived from studies involving Anacetrapib primary colon tumours of both hereditary and sporadic origin has implicated aberrations of the adenomatous polyposis coli (APC) tumour suppressor gene and ��-catenin oncogene in the pathogenesis of CRC (Kinzler & Vogelstein, 1996; Mirabelli-Primdahl et al, 1999; Miyaki et al, 1999; Samowitz et al, 1999). Although multiple mechanisms may induce the neoplastic growth of colorectal tumours, ��-catenin appears to play a pivotal role in this process.