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1 ive assessment of the proximal versus distal bile duct cancer.
2 lliation and survival in nonresectable hilar bile duct cancer.
3 for gallbladder cancer, 97% of extrahepatic bile duct cancer, 91% of ampula of Vater cancer, 96% of
4 able for both toxicity and response: 11 with bile duct cancer and four with gall-bladder carcinoma.
5 m of the secretin receptor in pancreatic and bile duct cancers and developed a dual antibody sandwich
6 ampula of Vater cancer, 96% of intrahepatic bile duct cancer, and 94% of hepatocellular carcinoma.
7 ) arose in the ampulla, 30 (12%) were distal bile duct cancers, and 17 (7%) were duodenal cancers.
8 g a risk factor for developing an aggressive bile duct cancer, cholangiocarcinoma, in chronically inf
12 colorectal, liver, pancreas, and gallbladder/bile duct cancers) in 69,310 nonsmoking and non-alcohol-
13 mation, a risk factor for the development of bile duct cancer, induces inducible nitric oxide synthas
15 mpullary cancer (n = 70; 11%), distal common bile duct cancer (n = 65; 10%), duodenal cancer (n = 26;
16 tail of pancreas, cancer of the extrahepatic bile duct, cancer of the gallbladder, and cancer of the
19 rs1126580), was associated with the risk of bile duct cancer (P = 0.003) and biliary stones (P = 0.0
20 oporfin-PDT can safely be delivered to hilar bile duct cancer patients and results in prolonged paten
21 for independent prognostic variables of age, bile duct cancer, poor tumor differentiation, and positi
24 range 47-88] years) with nonresectable hilar bile duct cancer were treated with T-PDT (median 1 [rang
25 hepatic cholangiocarcinoma (iCCA) is a fatal bile duct cancer with dismal prognosis and limited thera
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