Upregulation of nuclear PA28γ expression in cirrhosis and hepatocellular carcinoma.

We previously reported that proteasome activator 28γ (PA28γ) is an oncogenic protein in hepatitis C virus (HCV) core protein transgenic mice. The aim of this study was to determine the role of PA28γ expression at the protein level in the development and progression of human hepatocarcinogenesis and hepatocellular carcinoma (HCC). Samples from tissues representing a wide spectrum of liver disease were analyzed, including histologically normal livers (n=5), HCV-related chronic hepatitis (CH) (n=15) and cirrhosis (n=31). The level of nuclear PA28γ increased with the progression of liver disease from CH to cirrhosis. The majority of cirrhotic livers (68%; 21/31) displayed high nuclear PA28γ expression. However, in half of the HCCs (50%; 18/36), little or no nuclear PA28γ expression was observed, while the remaining 50% (18/36) of the cases displayed high levels of nuclear PA28γ expression. A clinicopathological survey demonstrated a significant correlation between nuclear PA28γ expression and capsular invasion in HCC (P=0.026); a striking difference was found between nuclear PA28γ expression in non-tumor tissues and shorter disease-free survival (P<0.01). Moreover, nuclear PA28γ expression in non-tumor tissues correlated with the expression of molecules related to the genesis of hepatic steatosis and HCC, such as sterol regulatory element binding protein-1c mRNA. The findings suggest the involvement of nuclear PA28γ expression in the progression and relapse of HCC, and suggest that nuclear PA28γ is a potentially suitable target for the prevention and/or treatment of HCC.

[Trial of "Huber Plus" in outpatients with chemotherapy by blood port system].

We evaluated the advantages and disadvantages of Huber Plus through three outpatients treated with central venous (CV) port chemotherapy (FOLFOX). One of the three outpatients first received chemotherapy with safety huber (Huber Plus) in this study, and the huber needle was changed from non-safety to a safety huber (Huber Plus) in two of the three outpatients. All three outpatients were taught about needle removal methods and port care. In patients? education, 1) we used a skin model and training CV port, and 2) dressing materials were used as film dressing plus three-point fixation by Fixomull stretch. As a result, the safety system assured zero incidents. Moreover, the evaluation revealed that operability and pain of Huber Plus were not clinical problems. We suggest that Huber Plus is applicable in outpatient chemotherapy and that our care plan with patients? education might become a standard treatment.

[Our experience using "Huber Plus" needles in our infusion center].

We conducted a pilot trial to compare the operability and safety of two huber needles in the infusion center. In the present study, we used huber needles without the safety cover and one huber needle with the safety cover (Huber Plus(R)). Both huber needles were used nine times. The successful puncture rate of the first time puncture and the incidence of needle accidents with both huber needles were 100% and 0%, respectively. The evaluation of pain and uneasiness by VAS (Visual Analogue scale)revealed the superiority of the safety needle over the than non-safety needle(pain: 3.8 vs 2.6, uneasiness: 3.7 vs 0.5). To our knowledge, this is the first report of the safety of the huber needle in Japan. This system may be recommended in Japan to avoid needle stick injuries, patient pain and uneasiness.

CDC25A inhibition suppresses the growth and invasion of human hepatocellular carcinoma cells.

CDC25A is a cell cycle-activating phosphatase that promotes transition from the G1 to S phase. We previously reported that overexpression of CDC25A in human hepatocellular carcinoma (HCC) tissue samples was associated with poor prognosis. In this study, we attempted suppression of CDC25A in HCC cells to elucidate the therapeutic potential of this approach. Administration of CDC25A antisense (AS) oligonucleotide resulted in 25-50% inhibition of cell growth at 48 h, G0-G1 arrest, and significant inhibition of cancer cell invasion. To elucidate the underlying mechanism of the inhibitory effects of HCC cell invasion, we examined several invasion-associated molecules, and we found that membrane-type 3 (MT3)-matrix metalloproteinase (MMP) mRNA was greatly reduced following treatment with AS oligonucleotide to CDC25A or siRNA treatment. Notably, screening of a panel of gastrointestinal cancer cells indicated that MT3-MMP was generally expressed by HCC cells, whereas other cell types did not express this type of matrix metalloproteinase so frequently. We also found that CDC25A facilitated cellular differentiation by increasing albumin expression in the PLC cell line. These results suggest that CDC25A, by inhibiting HCC growth and invasion, may be a feasible therapeutic target for human HCC.

[Incident surveillance in outpatients treated with hepatic arterial infusion (HAI) chemotherapy with infusion pump].

PURPOSE: An incident situation of hepatic arterial infusion (HAI) chemotherapy was investigated, and the improvement methods were evaluated. METHODS: As a result of surveillance, all incidents were observed in patients during five day continuous HAI infusion conditions: 1) Reverse-flow hemorrhage occurred at home by disconnection of the catheter; and 2) hemorrhage by natural withdrawal of the huber needle, were diagnosed. For 1) we further taped the catheter connection area by Tegaderm and changed the dressing material from SILKYPORE DRESSING (10 x 13 cm and 4 x 6.5 cm in absorption part) plus two-person fixation by Fixomull stretch to IV3000 (9 x 12 cm non-absorption part) plus three-person fixation by Fixomull stretch. Moreover, we changed the needle type (subcutaneous adiposus thickness) from 22 G x 3/4 inch to 20 G x 1 inch. RESULTS AND CONCLUSIONS: The incidents were not observed in 72 patients treated with HAI after improvement. We suggest that prevention of hemorrhage by further taping the catheter connection and improved stability of the needle by dressing proved effective. In conclusion, HAI incident surveillance may well be an important way to care for outpatients treated with HAI chemotherapy, and we thus intend to continue the HAI incident surveillance to improve the nursing care.

[Present situation and problems of the ordering system type infusion center].

We examined four problems of the ordering system type infusion center. In this system,regimen is made by chief physician and cared by the staff in the infusion center. 1) In securing of the staff, an upbringing of doctors and IV nurses are important. 2) An evidence-based regimen is necessary in order to minimize the differences of regimen made by each doctor. 3) A facility expansion might reduce an incident risk. 4) As the condition of patient suddenly changes,the chief physician of the patient should be contacted. We suggest that it is particularly important to make these problems clarified and solved by the team within the institution.

Hepatic resection followed by IFN-alpha and 5-FU for advanced hepatocellular carcinoma with tumor thrombus in the major portal branch.

BACKGROUND/AIMS: The prognosis of hepatocellular carcinoma (HCC) invading the major branches of the portal vein (Vp3) is extremely poor. Recently, we reported the efficacy of combination therapy with subcutaneous interferon (IFN)-alpha and intra-arterial 5-FU for intractable HCC with Vp3. In this study, this therapy was applied for resectable advanced HCC (Vp3) as a postoperative adjuvant. METHODOLOGY: Patients with HCC and tumor thrombi either in the major or first branch of portal vein were included (n=30). Fifteen consecutive patients with HCC and Vp3 were treated with at least 3 cycles of a combination therapy consisting of continuous arterial infusion of 5-FU (300 mg/mm3/day, 5 days/week, for the initial 2 weeks) and subcutaneous injection of IFN (5 MIU, 3 times/week, 4 weeks) as a postoperative adjuvant therapy following hepatic resection. Another 15 patients who underwent hepatic resection with no IFN/5-FU chemotherapy acted as controls. RESULTS: The results were as follows in the IFN/5-FU adjuvant treatment group; disease-free survival (n=11, 5-55 months), survival with recurrence (n=2, 9, 48 months), cancer death (n=1, 18 months), death from other causes but no recurrence (n=l, 22 months). The 1-year survival rate was 100% in patients treated with IFN/5-FU, and 41% in those without IFN/5-FU historical controls (n=15). There was a significant difference in disease-free and overall survival rates between the two groups (p = 0.0033 and 0.0031). CONCLUSIONS: Combination therapy with subcutaneous IFN and intra-arterial perfusion of 5-FU seems to be a promising postoperative adjuvant treatment modality for resectable HCC with Vp3.

Successful treatment of multiple hepatocellular carcinoma with tumor thrombi in the major portal branches by intraarterial 5-fluorouracil perfusion chemotherapy combined with subcutaneous interferon-alpha and hepatectomy.

We experienced a patient who received successful treatment for multiple hepatocellular carcinoma (HCC) nodules, with tumor thrombi in the major portal branches, with intraarterial 5-fluorouracil perfusion chemotherapy combined with subcutaneous interferon-alpha administration. The patient was a 50-year-old man with hepatitis C virus and HCC. The tumors consisted of a 5-cm main nodule in the right lobe (segment 8) and multiple intrahepatic metastases. The tumor also involved portal vein thrombosis throughout the right portal branch. After two cycles of interferon-alpha/5-fluorouracil combination chemotherapy, tumor markers demonstrated a decreasing tendency. Nine months after the initiation of this therapy, the tumors were limited to the right lobe and were surgically removed by S8 subsegmentectomy, S5 partial hepatectomy, and portal thrombectomy. The serum levels of both alpha-fetoprotein and protein induced by vitamin K absence II fell to normal levels after hepatic resection. Fifty-eight months after the first treatment, he is alive with several recurrent nodules in the liver. In conclusion, the interferon-alpha/5-fluorouracil combination therapy is a useful treatment for HCC in patients who have multiple intrahepatic metastases and portal vein thrombosis. In addition to this therapy, combined modality therapy including, for example, surgical resection, can sometimes have a dramatic therapeutic effect, shown by tumor markers reverting to normal levels.

Overexpression of MT3-MMP in hepatocellular carcinoma correlates with capsular invasion.

BACKGROUND/AIMS: Extracellular matrix-degrading matrix metalloproteinases (MMPs) are invariably up-regulated in epithelial cancers and are key agonists of angiogenesis, invasion and metastasis. Recent studies have shown high levels of various MMPs, including MT1-MMP, MMP-1, MMP-2 and MMP-9, and their involvement in tumor progression in human hepatocellular carcinoma (HCC). However, the expression and role of MT3-MMP in HCC remains unclear. METHODOLOGY: We examined the immunohistochemical expression of MT3-MMP in surgically resected HCCs (n=58), hepatitis C virus (HCV) and hepatitis B virus (HBV)-related chronic hepatitis (n=34) and cirrhosis (n=24). RESULTS: MT3-MMP expression was observed in all non-cancerous liver tissues. In HCCs, 52% (30/58) of patients showed high MT3-MMP expression while the remaining 48% (28/58) of patients showed low expression. A clinicopathological survey demonstrated a significant correlation between high MT3-MMP expression and capsular invasion of carcinoma (p = 0.034) although there was no correlation between high MT3-MMP expression in HCC and overall survival or disease-free survival. CONCLUSIONS: MT3-MMP was expressed not only in chronic hepatitis and liver cirrhosis, but also in HCC, and high MT3-MMP expression correlated significantly with capsular invasion of carcinoma.

Stronger growth-inhibitory effect of interferon (IFN)-beta compared to IFN-alpha is mediated by IFN signaling pathway in hepatocellular carcinoma cells.

Interferon (IFN) is a promising drug for prevention and treatment of hepatocellular carcinoma (HCC) in combination with chemotherapeutic agents. We previously reported that the spectra of antiproliferative activity and synergistic effect of IFN-beta when combined with anticancer drugs are more potent than those of IFN-alpha in HCC cells. However, the mechanism of the diverse antitumor effects of the IFNs is not understood yet. We studied the expression of IFN alpha receptor 2 (IFNAR2), STATs, and IFN-alpha, IFN-beta's growth-inhibitory effect, signal transduction and binding to IFNAR2 on three HCC cell lines and a tumor xenografted mouse model (12 animals/group). From the results, IFN-beta showed a significantly stronger growth-inhibitory effect than IFN-alpha on the HuH7 cell line (expressing low IFNAR2), however it was similarly high on PLC/PRF/5 and weak on HLE. In the nude mouse tumor xenograft model, IFN-beta injection significantly suppressed tumor volume relative to vehicle injection, while IFN-alpha showed weaker growth-inhibition. IFN signal transduction (phosphorylated-STAT1, 3) induced by IFN-beta was higher than that by IFN-alpha in HuH7 and tumor xenografts. Pretreatment of hepatoma cells with anti-IFNAR2 antibody blocked the IFN signaling, more for IFN-alpha. IFN-alpha's antiproliferative effect was reduced by the antibody in lower concentrations compared to that of IFN-beta. Taken together, the HCC cells that express low IFNAR2 and are resistant to IFN-alpha were sensitive to the growth-inhibitory effect of IFN-beta, which might be mediated by stronger IFN signal transduction and distinct binding to IFNAR compared to IFN-alpha.

Expression of type I interferon receptor as a predictor of clinical response to interferon-alpha therapy of gastrointestinal cancers.

Interferon (IFN) is used in the treatment of many malignancies and viral disorders. We recently reported a significant correlation between the efficacy of IFN-alpha combined with chemotherapy in the treatment of advanced hepatocellular carcinoma (HCC) and IFN-alpha/type I IFN receptor (IFNAR2) expression. It is possible that the expression of IFNAR2 in gastrointestinal cancerous tissue, apart from HCC, may predict the efficacy of IFN-alpha combination therapy. We investigated the expression of IFNAR2 in 100 gastrointestinal cancerous tissues. IFNAR2 expression was examined using immunohistochemistry, in surgically resected tissue samples (20 esophageal, 20 gastric, 20 colorectal, 20 cholangiocarcinoma, and 20 pancreatic samples). The expression rate of IFNAR2 was 35.0% (7/20), 25.0% (5/20), 20.0% (4/20), 45.0% (9/20), and 25.0% (5/20) in esophageal, gastric cancer, colorectal, cholangiocarcinoma and pancreatic cancer samples, respectively. In our previous report, the expression rate of IFNAR2 in HCC samples was 64.8% (59/91). Thus, the expression rates of IFNAR2 in the five types of gastrointestinal cancers tested here were low, compared with HCC. The clinical efficacy of IFN-alpha mono- or combination therapies in patients with gastrointestinal neoplasms is expected to be lower than in patients with HCC based on the expression level of IFNAR2.

Expression pattern of angiogenic factors and prognosis after hepatic resection in hepatocellular carcinoma: importance of angiopoietin-2 and hypoxia-induced factor-1 alpha.

BACKGROUND: Hepatocellular carcinoma (HCC) is a hypervascular tumor and angiogenesis plays an important role in its progression. Angiogenesis is regulated by a balance between pro and antiangiogenic molecules. The aim of this study was to investigate the expressions of angiogenic factors and elucidate their roles in angiogenesis in HCC. METHODS: We investigated immunohistochemical expression of vascular endothelial growth factor (VEGF), angiopoietins (Ang-1 and Ang-2), hypoxia-induced factor-1alpha (HIF-1alpha) and thrombospondin-1 (TSP-1) in 60 specimens of surgically resected HCC. We investigated the relationship between their expressions and clinicopathological factors or prognosis. RESULTS: Ang-2 staining had a significant correlation with the grade of differentiation of HCC cells (P=0.0082). VEGF and Ang-2 expression correlated positively with microvessel density (MVD) (P=0.0061 and 0.0374, respectively). MVD of well-differentiated HCC were significantly lower than those of moderately and poorly differentiated HCC. The disease-free survival time of patients with high Ang-2 and/or HIF-1alpha expression was significantly shorter than that of the low expression group (P=0.0278 and 0.0374, respectively). CONCLUSION: Our study showed that the expression of VEGF and Ang-2 correlated with MVD. Strong Ang-2 expression and/or high nuclear expression of HIF-1alpha is a significant predictive factor for recurrence after curative resection in HCC patients.

Angiogenesis in cholangiocellular carcinoma: expression of vascular endothelial growth factor, angiopoietin-1/2, thrombospondin-1 and clinicopathological significance.

Angiogenesis in cholangiocellular carcinoma (CCC) has rarely been investigated. The aim of this study was to determine the angiogenesis status of CCC and assess its relationship with angiogenic factors and clinicopathological characteristics. We examined 33 surgically resected CCC specimens. Tumor angiogenesis was assessed by microvessel density (MVD) using the anti-CD34 antibody, and the expression of VEGF, Ang-1, Ang-2, and TSP-1 was determined by immunohistochemistry. The mean (+/- SD) MVD was 87.2+/-52.6/mm2 (range, 0-229/mm2). A total of 75.6% cases were positive for VEGF expression, 36% for Ang-1, 57.6% for Ang-2 and 45.5% for TSP-1. VEGF and Ang-2 expression was associated with a significantly higher level of MVD (p=0.004 and 0.015, respectively). TSP-1 expression was associated with a significantly lower level of MVD (p=0.005) and a higher level of intrahepatic metastasis (46.7% vs. 5.6%, p=0.012). There was no significant correlation between VEGF, Ang-1, Ang-2, and TSP-1 expression and tumor size, capsule formation, infiltration of capsule, portal vein invasion, intrahepatic metastasis or CCC differentiation. There was no significant correlation between MVD levels, VEGF, Ang-1, Ang-2, and TSP-1 expression and postoperative survival. A considerable degree of angiogenesis, comparable to that of other solid tumors, was observed in CCC. VEGF and Ang-2 might play a proangiogenic role, and TSP-1 may play an inhibitory role in CCC. Although TSP-1 may increase intrahepatic CCC metastases, neither MVD levels nor the expression of VEGF, Ang-1, or Ang-2 was associated with clinicopathological factors and prognosis.

TGF-beta1-induced cell growth arrest and partial differentiation is related to the suppression of Id1 in human hepatoma cells.

Transforming growth factor beta 1 (TGF-beta1) is a proposed regulator of Ids (inhibitors of DNA binding/differentiation) gene expression in epithelial cells. We previously reported that Id proteins are variously expressed in human hepatocellular carcinomas (HCC). However, the mechanism of regulation of Ids in HCC remains obscure. Here, we examined the relationship between Id1 and TGF-beta1 in four HCC cell lines, and studied the changes in cell proliferation, cell cycle and differentiation. The four HCC cell lines expressed Id1, TGF-beta1 and their receptors at various levels. TGF-beta1 strongly inhibited the growth of HuH7 cells, while the growth inhibition was moderate in PLC/PRF/5, and was not observed in HLE and HLF cell lines. TGF-beta1-induced growth inhibition in HuH7 cells was associated with cell accumulation in the G1 phase and partial induction of differentiation (with reduction of AFP and AFP-L3). Induction by TGF-beta1 dose-dependently suppressed Id1 expression in HuH7 cells; 1 ng/ml TGF-beta1 inhibited Id1 by 84.0 and 78.6% that of the untreated control at transcriptional and protein levels, respectively. HLE and HLF cells, which did not exhibit a TGF-beta1 growth inhibitory effect, lacked TGF-beta receptors and Id1 expression was not altered. In PLC/PRF/5 cells, Id1 augmentation was not observed in response to TGF-beta1, indicating that TGF-beta1-induced growth inhibition was not related to Id1 in this cell line. Our results suggest that, in some HCC cells, the pathway of suppression of Id1 by TGF-beta1 may be important in TGF-beta1-induced growth inhibition and partial differentiation.

[Neoadjuvant therapy with imatinib mesilate for gastrointestinal stromal tumor of the stomach before subsequent successful surgical resection].

A 65-year-old man is presented here with a huge mass of 13 cm in diameter in the left upper abdomen. Histopathologic assessment of endoscopic forceps biopsy revealed a c-kit positive gastrointestinal storomal tumor (GIST) of the stomach. Abdominal computed tomography (CT) showed a direct invasion to the pancreas. Imatinib mesilate was administered as neoadjuvant therapy according to the NCCN Guidelines. Imatinib mesilate therapy was stopped within 2 weeks because of adverse events such as Grade 2 of facial edema and dizziness. However, no hematological adverse event was shown. After three months of treatment (relative dose intensity was 87.5%), CT revealed a reduction in tumor diameter of 35.6% and showed no longer a direct invasion to the pancreas. The radical operation was considered feasible and partial gastrectomy was performed. The tumor was well encapsulated and radical surgery was possible without rupture. Adjuvant therapy was not performed. The patient has now been in good health without a recurrence for three months after the surgery.

[A case of an elderly patient with gastric cancer successfully treated with TS-1 considering impaired renal function caused by aging].

A 75-year-old female patient with impaired renal function caused by aging was treated with TS 1 for gastric cancer with extensive multiple liver metastases. TS-1 contains CDHP, which inhibits DPD activity and maintains a high blood concentration of 5-FU. Because CDHP is excreted from the kidney, a careful TS-1 administration is necessary for patients with impaired renal function considering an occurrence of severe adverse events. Based on the result previously reported by us about pharmacokinetic study and recommended administration dosage of TS-1 for patients with impaired renal function, we administered 50 mg/day of TS-1 for four weeks followed by two weeks rest per one course for this patient. The patient's creatinine clearance calculated by the Cockcroft-Gault method was 38 ml/min, and we reduced the administration dosage in consideration of her impaired renal function, although normal dosage of TS-1 calculated from body surface area for this patient was 100 mg/day. As this patient underwent TS-1 treatment, sizes of multiple liver metastases and the blood concentration level of CEA were gradually reduced, and the reductive rate of the former was more than 90% and the level of the latter fell to a normal range after 12 courses of TS 1 treatment. Through all the treatment courses, relative drug intensity was 100% and the performance status of this patient was kept 0 without any grade 3 or more adverse events under ambulatory treatment. A successful treatment for this patient might indicate that it was important to consider the appropriate reduction of the dosage of TS-1 administration for elderly patients with gastric cancer, because there is a reverse correlation between aging and renal function. To clarify this problem, a multicenter prospective phase II study about TS-1 reductive administration depending on the renal function for elderly patients with gastric cancer (OGSG0404) is ongoing in our clinical study group (OGSG; Osaka Gastrointestinal Chemotherapy Study Group).

[A case of complete remission of carcinomatous ascites refractory for TS-1 monotherapy treated with TS-1 plus paclitaxel combined therapy for gastric cancer].

A 38-year-old female patient with gastric cancer, of which histological type was a poorly differenciated adenocarcinoma and a clinical finding was T3N1MO (Stage IIIA), underwent total gastrectomy with D2 lymphadenectomy as the surgical treatment. However, CY1 was detected during the operation and the final finding was T3N1MOHOPOCY1 (Stage IV). Because this surgical treatment ended in curative C, we administered 80 mg/m2/day of TS-1 for four weeks followed by two weeks rest per one course for CY1 after the surgical treatment. After two courses of TS-1 monotherapy, extensive carcinomatous ascites appeared and blood concentration level of CA19-9 increased. We next treated this patient with TS-1+paclitaxel as a second line chemotherapy, because both of them have been reported to migrate to peritoneal very well and to be effective for peritoneal dissemination. The regimen of this combined therapy consisted of four weeks administration of TS-1 (80 mg/m2/day) followed by two weeks rest and injections of paclitaxel (50 mg/m2) at day 1 and 8 for 21 days as one course. When this patient underwent TS-1+paclitaxel combined treatment, the amount of carcinomatous ascites and blood concentration level of CA19-9 were gradually reduced and the former completely disappeared, and the latter fell to a normal range after five courses. Through all treatment courses, a performance status of this patient was kept 0 without a severe adverse event under ambulatory treatment. After 29 courses, the blood concentration level of CA19-9 rose again and local recurrence was detected at the lesion of esophagoenterostomy, though carcinomatous ascites had been kept in complete remission. We treated surgically for this local recurrence because of CY0 at the operation. At the present, 3 years and 8 months have passed since the first treatment started. This patient is still alive without cancer in ambulatory.

[A trial of TS-1 administration on the basis of the pharmacokinetic study for an advanced gastric cancer patient with impaired renal function].

TS-1 is an antitumor drug including 5-chloro-2,4 dihydroxypyridine (CDHP), which inhibits dihydriopyrimidine dehydrogenase (DPD) activity selectively in metabolism of 5-FU. However, TS-1 therapy tends to increase adverse events for patients with impaired renal function due to excessively high blood concentration of 5-FU, because CDHP is mainly excreted into the urine. In a 67-year-old male with advanced gastric cancer, renal dysfunction occurred during TS-1 administration as its adverse event. We studied the pharmacokinetics of 5-FU, which were analyzed on the T1/2 value and the AUC (0-infinity) of 5-FU with a single and consecutive TS-1 administration, and estimated an optimal TS-1 administration regimen for this patient. The regimen is 60 mg/body/day given in one divided dose for 28 days consecutively followed by 14 days rest. This regimen enabled a continuation of TS-1 treatment for the patient. In conclusion, individual dose adjustment using pharmacokinetic study of 5-FU might be beneficial to patients with impaired renal function.

[A case of pseudo aneurysm of common hepatic artery related to hepatic arterial infusion chemotherapy].

A 87-year-old male underwent the extended hepatic left lobectomy and the partial hepatectomy (S7, S8) for liver hepatic metastasis from the rectal cancer in March 2003. The reserver was implanted by the GDA-coil method from the right femoral artery, and WHF was enforced 10 times. Epigastric and back pain appeared from January 2004. The pain became strong gradually. MRI and CT scan were examined after hospitalization. These imaging tests showed the pseudo aneurysm of common hepatic artery. Therefore, an emergency angiography was performed, and pseudo aneurysm of the common hepatic artery was embolized with 36 metallic coils. After the embolization, the pain had disappeared suddenly. The patient was discharged the 7th day after embolization. Hepatic arterial infusion chemotherapy is considered safe with respect to blood and non blood toxicity, which was compared with systemic chemotherapy. However, there were also complications like this case, and caution is required.

[A case of peritoneal dissemination disappeared by CPT-11 + TS-1 combination chemotherapy].

A patient is a 35-year-old man. By a diagnosis of descending colon cancer, descending colon ablative operation and D1 lymph node dissection were performed on April 22, 2004. It was P3H0N1SE, Stage IV in perioperative findings. Abdominal CT showed peritoneal dissemination of 1.7 cm at the right under the abdominal wall wound and 1.2 cm in the rectovesical pouch on May 18, 2004. CPT-11 + TS-1 combination chemotherapy was started on June 22nd. In the five weeks of the combination chemotherapy, continuous infusion of CPT-11 (150 mg/body day 1 and 15) was twice administered, and oral administration of TS-1 (120 mg/body/day) was given for 3 weeks (day 1-21). Peritoneal dissemination disappeared after the two-course end, and we judged it as CR. Furthermore, we were certain that we obtained CR after the three course end. The adverse event was only neutropenia of grade 1. The fourth course was not administered, but recurrence has not been observed. Abdominal CT showed no recurrence on March 3, 2005 since the combination chemotherapy ended 6 months ago.