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1 t and whose dysregulation may play a role in biliary cancer.
2 peutic alternative in patients with advanced biliary cancer.
3 tor have each been shown to have activity in biliary cancer.
4 GFR blockade with erlotinib in patients with biliary cancer.
5  in liver to later-developed mucin-producing biliary cancer.
6 ollow-up, 13 patients (3.3%), presented with biliary cancer.
7  4 adverse effects in patients with advanced biliary cancers.
8 ts of genetic inactivation in pancreatic and biliary cancers.
9                               We included 64 biliary cancers, 122 liver cancers, and 224 age-matched
10 ven the possibility of future development of biliary cancer after CC resection.
11 NPs examined, 14 were related to the risk of biliary cancer and stones.
12  (21%) were performed for primary hepatic or biliary cancers and 161 (9%) for benign disease.
13 differentially up-regulated genes in primary biliary cancers and biliary cancer cell lines and their
14 served in sporadic pulmonary, pancreatic and biliary cancers and melanomas.
15 oup for gallstone disease, susceptibility to biliary cancer, and show variants that alter sterolin fu
16 nt study has not been previously reported in biliary cancers, and represent novel potential screening
17                Cholangiocarcinoma (CCA) is a biliary cancer arising from damaged bile ducts.
18                                              Biliary cancers (BCs) carry a poor prognosis, but target
19 eceptor 1 and ligand expression is common in biliary cancers (BILI) and may be associated with worse
20 genes was confirmed in tissue microarrays of biliary cancers by immunohistochemical analysis (n = 4)
21 ly resected biliary carcinomas (n = 11), and biliary cancer cell lines (n = 9).
22 gulated genes in primary biliary cancers and biliary cancer cell lines and their expression profiles
23  4) or in situ hybridization (n = 1), and in biliary cancer cell lines by reverse transcriptase PCR (
24   MIR1249 expression was increased in CD133+ biliary cancer cells freshly isolated from the stem cell
25   MIR1249 expression was increased in CD133+ biliary cancer cells freshly isolated from the stem nich
26 type: metastatic neuroendocrine (81 months), biliary cancer (cholangiocarcinoma) (63 months), gallbla
27 rchis viverrini, which is a primary cause of biliary cancer (cholangiocarcinoma) and infects 12 milli
28 r with the ability to discriminate pancreato-biliary cancers from non-cancer pancreatitis patients.
29 r CA19-9 for the discrimination of pancreato-biliary cancers from non-cancerous pancreatitis patients
30 plant hepatocellular (HR 2.92, P = 0.001) or biliary cancer (HR 12.7, P < 0.001), glomerular filtrati
31 11/LKB1 in the development of pancreatic and biliary cancer in patients with and without the PJS.
32 al to tumorigenesis were up-regulated in the biliary cancers, including proliferation and cell cycle
33 eukemia or lymphoma, and those with liver or biliary cancer; it was longest for those with chronic lu
34 0), miscellaneous liver metastases (N = 42), biliary cancer (N = 20), and benign tumors (N = 176).
35 cardia gastric cancer, gallbladder and other biliary cancer, ovarian cancer, testicular cancer, anal
36                                              Biliary cancers overexpress epidermal growth factor rece
37 subgroup with native-liver hepatocellular or biliary cancer (P = 0.02).
38 t diagnostics for the detection of pancreato-biliary cancers (PBCs) need to be optimized.
39                               GABA decreases biliary cancer proliferation and reduces the metastatic
40  established from 276 pancreato-duodenal and biliary cancer resections.
41 e allelotype of 82 xenografted pancreatic or biliary cancers using 386 microsatellite markers and spa
42 py in patients with metastatic pancreatic or biliary cancer with homologous recombination deficiency
43 noma (CCA) includes a heterogeneous group of biliary cancers with a dismal prognosis.
44 noma (CCA) includes a heterogeneous group of biliary cancers with poor prognosis.