Taiichi Nakagawa

Combination therapy with transcatheter arterial chemoembolization and percutaneous microwave coagulation therapy for hepatocellular carcinoma.

A small number of microwave electrode insertions and microwave irradiations were used to obtain complete tumor necrosis in hepatocellular carcinomas (HCC) measuring > 2.0 cm but ≤ 3.0 cm in greatest dimension. The efficacy of combining transcatheter arterial chemoembolization (TACE) with subsequent percutaneous microwave coagulation therapy (PMCT) was assessed in this study.

Down-regulation of TGF-β receptors in human colorectal cancer : implications for cancer development

Many colorectal cancer cells are resistant to the anti-proliferative effects of transforming growth factor-β (TGF-β). TGF-β also acts as paracrine factor from cancer cells on their mesenchymal cells. The aim of this study was to examine the expression of TGF-β and its receptors in human colorectal cancer tissue and determine any relationship with cancer growth. In situ hybridization and Northern blot hybridization detection of TGF-β1, type I and type II receptor mRNA and immunohistochemical staining of TGF-β1 were performed using 11 human colorectal adenomas, 22 colorectal cancers and ten normal colorectal mucosas as control. TGF-β receptor mRNAs were expressed mainly by normal colorectal epithelial cells and adenoma. However, mRNAs for TGF-β receptors were only faintly, if at all, expressed in eight of 22 human colorectal cancers. In addition, intense signals of TGF-β1 mRNA and the protein were detected in all colorectal cancers. TGF-β receptor mRNAs and TGF-β1 protein were also distributed in fibroblasts and endothelial cells in the interstitium. Moreover, Smad 4 protein was translocated to nucleus in primarily cultured adenoma cells, but not in cancer cells after TGF-β stimulation. The escape of human colon cancer from TGF-β -mediated growth inhibition by down-regulation of TGF-β receptors as well as the effects of TGF-β on stroma formation and angiogenesis indicate a possible role for TGF-β in the progression of colon cancer in an intact host.

Rapid progression of hepatocellular carcinoma after transcatheter arterial chemoembolization and percutaneous radiofrequency ablation in the primary tumour region.

We report one patient who showed rapid progression of hepatocellular carcinoma (HCC) after undergoing transcatheter arterial chemoembolization (TACE) and percutaneous radiofrequency ablation (PRFA) for a small HCC measuring 2.5 cm in diameter. Enhanced magnetic resonance imaging (MRI) following treatment showed complete tumour necrosis and did not reveal the presence of a tumour around the treated area. Furthermore, the serum alpha-fetoprotein (AFP) level decreased at the completion of therapy. However, the HCC advanced in a very short time. Numerous tumours around the treated area were observed on enhanced computed tomography (CT) 50 days after PRFA. It is strongly suspected that the tumour was disseminated through the portal system because of the presence pattern of tumours. We believe this to be the first case illustrating a hepatic cancer that progressed rapidly following TACE and PRFA.

Percutaneous microwave coagulation therapy for solitary metastatic liver tumors from colorectal cancer: a pilot clinical study

Objective:Percutaneous microwave coagulation therapy (PMCT) was performed for metachronous small solitary liver tumors measuring ≤3.0 cm in diameter that had metastasized from colorectal cancer. PMCT was used for local control of the lesions, and the efficacy of this treatment was assessed.Methods:In 15 patients, a microwave electrode (specially designed for this purpose, 25 cm long and 2.0 mm thick) was inserted percutaneously into the tumor area under ultrasonic guidance. Microwaves at 80 watts were used to irradiate the tumor and the surrounding area.Results:Thirteen of the 15 metastatic tumors were radically ablated by 3–10 applications of microwave irradiation. Although the follow-up period was short (9–37 months), 10 patients survived. No recurrence has been detected in the treated area (except two foci where PMCT was insufficient), and no serious side effects or complications were encountered during or after the PMCT. In four of the five nonsurviving patients, death was due to metastases to the bone, brain, lung, or other areas of the liver despite complete local tumor control by PMCT.Conclusion:PMCT is a safe and effective treatment for metachronous small liver tumors that have metastasized from colorectal cancer.

Hepatic infarction following percutaneous ethanol injection therapy for hepatocellular carcinoma

We report on two patients who developed hepatic infarction after undergoing percutaneous ethanol injection therapy (PEIT) for hepatocellular carcinoma (HCC). In both cases, liver function parameters deteriorated immediately after the ethanol injection, and enhanced computed tomography images showed a wedge-shaped avascular low-density area due to hepatic infarction. In one patient, PEIT was performed for a nodule treated with transcatheter arterial infusion (TAI) using a suspension of styrene maleic acid neocarzinostatin (SMANCS) 4 weeks before. In the other patient, TAI with SMANCS had been carried out 14 months previously for a different nodule in the same segment where the nodule treated with PEIT was located. When PEIT is used for patients with HCC who have previously undergone TAI, especially with SMANCS, PEIT may induce hepatic infarction.

Usefulness of the high sensitivity PIVKA-II measurement method in diagnosis of hepatocellular carcinoma: A comparison with the conventional method

Abstract We investigated a new PIVKA-II assay kit (Eizai, ED-008) that incorporates the use of an improved secondary antibody compared with the conventional EIA method, and is highly sensitive to PIVKA-II (sensitivity: 0,0125 AU/ml). Using this new kit, we measured plasma PIVKA-II levels in 76 subjects in whom the conventional PIVKA-II assay was negative (≤ 0.0625 AU/ml). There were 30 patients with HCC, 14 patients with liver cirrhosis (six with α-fetoprotein ≥ 50 ng/ml), 11 patients with chronic active hepatitis C, 11 patients with chronic inactive hepatitis C, and ten healthy volunteers. The new assay kit detected PIVKA-II (≥ 0.0125 AU/ml) in 11 patients with HCC (36.7%), and one patient with liver cirrhosis (7.1%), but was negative in the patients with chronic active or inactive hepatitis C and the controls. Among the 11 HCC patients positive for PIVKA-II, the plasma α-fetoprotein level was greater than 100 ng/ml in two patients (18.2%), while it was above this level in three of the 19 patients negative for PIVKA-II. The mean size of the main tumor in the patients positive and negative for PIVKA-II was 2.16 + 0.87 cm and 2.62 + 1.50 cm, respectively, with no significant difference between the groups (P = 0.47). However, in seven patients positive for PIVKA-II, the tumor size was less than 2 cm. This assay also showed a high specificity for HCC (0.98). We concluded that this assay may allow PIVKA-II to be used as a more effective indicator of HCC.