Rinako Kawamura

Phosphorylated Smad2 and Smad3 signaling: Shifting between tumor suppression and fibro-carcinogenesis in chronic hepatitis C.

Insight into hepatic fibrogenesis and carcinogenesis (fibro‐carcinogenesis) caused by hepatitis C virus (HCV) infection has come from recent analyses of transforming growth factor (TGF)‐β signaling. TGF‐β type I receptor and pro‐inflammatory cytokine‐activated kinases differentially phosphorylate Smad2 and Smad3 to create C‐terminally (C), linker (L) or dually (L/C) phosphorylated (p) isoforms. This study aimed to elucidate how HCV infection affected hepatic fibro‐carcinogenesis, particularly via phospho‐Smad signaling.

CHARACTERISTIC INTRADUCTAL ULTRASONOGRAPHIC FEATURES OF PORTAL BILIOPATHY

The term ‘portal biliopathy’ is used to describe cholangiographic abnormalities seen in patients with extrahepatic portal vein obstruction. Portal biliopathy is mainly composed of extrinsic compression of the bile duct caused by enlarged venous collaterals. Herein we report a case of asymptomatic portal biliopathy caused by idiopathic extrahepatic portal vein obstruction. In the present case, intraductal ultrasonography showed normal anatomic layers of the distal common bile duct wall, surrounded by numerous tubular structures which were suspected to be collateral vessels. We suggest that intraductal ultrasonography may be a helpful imaging procedure for detection of this pathological condition.

S-1 monotherapy in a patient with cholangiolocellular carcinoma: A case report

A 71-year-old man with alcoholic cirrhosis was found to have multiple hypervascular lesions in the liver on enhanced computed tomography. An ultrasound-guided biopsy of the lesion was performed. Immunohistochemical analysis for hepatocyte paraffin 1 expression was negative; cytokeratin (CK) 7, CK19, epithelial cell adhesion molecule and epithelial membrane antigens were positive; mucicarmine staining was negative. The tumor was thus histologically diagnosed as cholangiolocellular carcinoma (CoCC). The tumor was inoperable due to the associated advanced liver disease. In addition, the patient preferred systemic chemotherapy using only orally administered agents. Thus, S-1 monotherapy was recommended. S-1 was initially administered orally at a dose of 80 mg/day. Although the levels of tumor marker (prothrombin induced by vitamin K absence/antagonist-II and carbohydrate antigen 19-9) levels were marginally elevated, their values did not change over the entire course. The patient achieved a partial response according to the Response Evaluation Criteria In Solid Tumors (RECIST) and modified RECIST 1 year after chemotherapy initiation. In conclusion, S-1 monotherapy exhibited promising efficacy against unresectable CoCC.