Biomedical subjects

Toshio Kokuryo

Publications and source records attributed to Toshio Kokuryo.

3 recordsLinked to original sources

PubMed2005

Tumor necrosis factor alpha promotes invasiveness of cholangiocarcinoma cells via its receptor, TNFR2.

We studied the effect of TNF-alpha stimulation on a cholangiocarcinoma cell line, CCKS1. CCKS1 expressed only one type TNF receptor, TNFR2. Treatment of CCKS1 with TNF-alpha substantially activated NFkappaB, MAPK and Akt signalings which in turn activated matrix metalloproteinase-9 (MMP-9) secretion and in vitro invasiveness of CCKS1. Pretreatment of cells with anti-TNFR2 neutralizing antibody inhibited the TNF-alpha-dependent signaling and MMP-9 secretion and subsequently blocked invasion in vitro. Moreover, an inhibitor for matrix metalloproteinase, Galardin, suppressed the invasion in a dose-dependent manner. Similarly, pharmacological inhibition of signaling clearly suppressed the TNF-alpha dependent MMP-9 secretion. These results strongly suggest that TNF-alpha-TNFR2 signaling plays an important role to convert the cholangiocarcinoma cells to be more aggressive one.

Cholangiocarcinoma↗

PubMed2003

Profiling of gene expression associated with hepatolithiasis by complementary DNA expression array.

By use of cDNA expression array method, we compared the expression profiles of genes in hepatolithiasis tissues with those of paired normal tissues. Expression of 1176 cancer related genes that include 33 tumor suppressor genes, 100 proto-oncogenes and 37 DNA damage repair genes were examined in this study. We found that expression of tumor suppressor genes and proto-oncogenes was systemically activated in hepatholithiasis tissues, suggesting that expression of genes controlling cell growth becomes unstable in liver lobe of hepatolithiasis. In contrast, expression of DNA damage repair genes were not activated but rather remained unchanged in hepatholithiasis tissues, suggesting that repair process is not strongly activated but rather impaired in hepatholithiasis tissues.

Calculi↗

PubMedDate not supplied

Biliary stricture with hepatolithiasis as a late complication of retrograde transhepatic biliary drainage.

A 63-year-old man was admitted to a community hospital complaining of fever and epigastric pain. He had undergone cholecystectomy and choledocholithotomy with retrograde transhepatic biliary drainage 7 years previously. Referred to our hospital after demonstration of hepatolithiasis by computed tomography, he underwent further imaging that showed a dilated left lateral anterior segmental bile duct (B3) with hepatolithiasis. After he underwent percutaneous transhepatic biliary drainage via the B3 segmental bile duct, cholangiography performed through the drainage catheter revealed a biliary stricture at the confluence of B3 associated with intrahepatic stones. percutaneous transhepatic cholangioscopy showed a stricture and a cholangioscopic biopsy specimen contained no malignant cells. After performing cholangioscopic lithotomy, an endoprosthesis was inserted and connected to a subcutaneously placed reservoir. Repeat percutaneous transhepatic cholangioscopy 10 months later demonstrated a decreased degree of the stricture, so the endoprosthetic catheter could be removed. Retrospective review of computed tomography images obtained just after the first operation indicated that the retrograde transhepatic biliary drainage catheter had passed close to the B3, and that intrahepatic bile duct dilation was not present. Therefore, we suspect that biliary stricture was caused by an old bile duct injury due to retrograde transhepatic biliary drainage catheter placement. Percutaneous transhepatic cholangioscopy effectively managed this stricture and associated hepatolithiasis.

Bile Ducts, Intrahepatic↗