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Taketo Yamaguchi

Publications and source records attributed to Taketo Yamaguchi.

51 records · Page 3Linked to original sources
PubMed2004

Distinguishing benign from malignant intraductal papillary mucinous tumors of the pancreas by imaging techniques.

OBJECTIVES: It is often difficult to differentiate benign from malignant intraductal papillary mucinous tumors (IPMTs). This study aimed to differentiate them using various imaging techniques. METHODS: Receiver operating characteristic curves were used to establish optimal cutoff values to differentiate benign from malignant tumors in 121 patients with histologically confirmed IPMTs. RESULTS: For branch duct type, accuracy for malignancy was highest using endoscopic ultrasonography (EUS) to measure the cyst diameter, and accuracy was 68.2% at a cutoff value of 33.9 mm. For main duct type, accuracy was highest, 71.1% at a cutoff value of 8.4 mm for main duct diameter, with magnetic resonance cholangiopancreatography. For all imaging techniques and findings, accuracy was highest using EUS, 76.4% at a cutoff value of 5.4 mm for height of protrusion. Each imaging technique had a positive predictive value of 80% if the cut off value for the height of the protruding lesion was met. CONCLUSIONS: Malignancy can be strongly suspected when the height of protrusion exceeds the respective cutoff values. EUS was most effective to differentiate benign IPMTs from malignant tumors by assessing the height of protrusion.

Adenocarcinoma, Mucinous↗
PubMed2004

[Imaging of acute pancreatitis--the role of US, CT and MRI].

Imaging of the pancreas with US and CT plays a major role in the diagnosis and evaluations of patients with acute pancreatitis. In severe acute pancreatitis, dynamic CT is essential to assess the severity of the disease and evaluate the complications. MRI is comparable to CT in its capacity to provide precise information about the severity of acute pancreatitis. MRI has some advantages over CT in being free from ionizing radiation and lower toxity of gadolinium which is used for contrast medium intravenously. The disadvantages of MRI, however, include cost, longer exam duration, limited availability and the practical difficulties of scanning a patient with ICU equipment.

Acute Disease↗
PubMed2003

Induction of systemic immunity by expression of interleukin-23 in murine colon carcinoma cells.

Interleukin-23 (IL-23), a novel cytokine composed of a newly identified p19 molecule and the p40 subunit of IL-12, can stimulate the proliferation in vitro of memory T cells. We examined whether Colon 26 murine colon carcinoma cells that were retrovirally transduced with the p19-linked p40 gene (Colon 26/IL-23) could produce antitumor effects in inoculated mice. The growth of Colon 26/IL-23 tumors developed in immunocompetent mice was significantly retarded and the tumors disappeared thereafter. Spleen cells from the mice that received Colon 26/IL-23 cells produced significant amounts of interferon-gamma, when they were cultured with irradiated Colon 26 but not irrelevant cells. Depletion of CD8(+) T cells suppressed the production of interferon-gamma. The mice that had rejected Colon 26/IL-23 tumors were resistant to subsequent challenge of parent but not irrelevant tumor cells. Colon 26/IL-23 tumors were not rejected in nude mice but the growth was retarded compared to parent tumors. Treatment of nude mice with anti-asialo GM(1) antibody did not influence the growth of Colon 26/IL-23 tumors. These data suggest that expression of IL-23 in tumors produces T cell-dependent antitumor effects and induces systemic immunity.

Animals↗
PubMed2003

Expression of the interleukin-21 gene in murine colon carcinoma cells generates systemic immunity in the inoculated hosts.

Interleukin-21 (IL-21) is a novel cytokine that can induce proliferation of activated T cells and maturation of natural killer (NK) cells. We therefore examined whether expression of the IL-21 gene in tumor cells could generate antitumor responses. Murine colon carcinoma Colon 26 cells that were transduced with the mouse IL-21 gene (Colon 26/IL-21) were rejected in syngeneic mice and the mice subsequently acquired protective immunity. The growth of Colon 26/IL-21 tumors developed in nude mice was retarded compared with that of parent tumors, and this growth suppression was not observed in nude mice that were treated with anti-asialo GM(1) antibody. Spleen cells from the mice that had rejected Colon 26/IL-21 cells showed cytotoxic activity to Colon 26 but not to irrelevant tumor cells, and produced larger amounts of interferon-gamma upon stimulation with irradiated Colon 26 cells. Spleen cells from Colon 26/IL-21-tumor- but not parent-tumor-bearing mice had lytic activity to YAC-1 cells. These data suggest that expression of IL-21 in tumors induces T- and NK-cell-dependent antitumor effects.

Animals↗
PubMed2003

Transduction of the IL-21 and IL-23 genes in human pancreatic carcinoma cells produces natural killer cell-dependent and -independent antitumor effects.

We examined whether novel cytokines, interleukin (IL)-21 and IL-23, that were expressed in tumors could produce antitumor effects in the inoculated mice. Human pancreatic cancer AsPC-1 cells were retrovirally transduced with murine IL-21 or IL-23 (p19-linked p40) gene (AsPC-1/IL-21, AsPC-1/IL-23) and were injected into nude or severe combined immunodeficiency (SCID) mice. Although the proliferation in vitro of the transduced cells remained the same as that of parent cells, growth of AsPC-1/IL-21 and AsPC-1/IL-23 tumors developed in nude mice was retarded compared with that of parent tumors. Treatment of nude mice with anti-asialo GM(1) antibody temporally abrogated the growth retardation of AsPC-1/IL-21, but not AsPC-1/IL-23 tumors; however, the growth of AsPC-1/IL-21 tumors came to be retarded thereafter with the regeneration of natural killer (NK) cells. The growth of AsPC-1/IL-21 tumors developed in SCID mice was also retarded compared with parent tumors and the growth retardation was abrogated by treatment with anti-asialo GM(1) antibody. The growth of AsPC-1/IL-23 tumors in SCID mice was not different from that of parent tumors. Cytotoxic activity and secretion of interferon-gamma in response to AsPC-1 cells were induced in spleen cells of the mice bearing AsPC-1/IL-21 or AsPC-1/IL-23 tumors. When nude mice were injected with a mixed population of AsPC-1/IL-21 and AsPC-1/IL-23 cells, no synergistic effects were observed. These data collectively suggest that expression of IL-21 and IL-23 in tumors can produce NK cell-dependent and -independent antitumor effects in an alpha beta T cell-defective condition, respectively.

Animals↗
PubMed2003

Survival regulation in pancreatic cancer cells by c-Jun.

Over 90% of human pancreatic cancers harbor an activating point mutation in the K-ras gene at codon 12. However, it is not clear whether all downstream K-ras are activated and which downstream contributes to the cell survival and proliferation of pancreatic cancer cells. MEK kinase 1 (MEKK1)-c-Jun N-terminal kinase (JNK)-c-Jun pathway has an important role in cell proliferation, survival and apoptosis in various cells. We previously demonstrated that the dominant negative form of MEKK1 (DN-MEKK) inhibits the survival of human pancreatic cancer cell lines. In this study we investigated whether JNK-c-Jun, the downstream pathway of DN-MEKK, affects the survival of human pancreatic cancer cell lines. Colony formation assays indicated that c-Jun failed to inhibit the survival of pancreatic cancer cells, whereas c-Jun remarkably inhibited the cell survival of non-pancreatic cancer cells. Reporter gene assays using Gal4-c-Jun and gel retardation assays indicated that c-Jun functions were activated in growing pancreatic cancer cells. These results revealed that c-Jun activation does not prevent the cell survival of pancreatic cancer cells in contrast to non-pancreatic cancer cells. It appears that MEKK1-JNK-c-Jun pathway fails to act as a negative regulator for the cell survival of pancreatic cancer cells. Greater understanding of these mechanisms may be helpful in the treatment of pancreatic cancer.

Apoptosis↗
PubMed2002

Endoscopic internal biliary drainage in a child with malignant obstructive jaundice caused by neuroblastoma.

We describe a 13-year-old girl who underwent insertion of a Flexima biliary stent for obstructive jaundice due to compression of the extrahepatic bile duct by an enlarged lymph node secondary to neuroblastoma. This novel endoscopic internal biliary drainage procedure was safe and effective even for a child, and improved her quality of life. We further review other treatment options available for malignant obstructive jaundice in children.

Bile Ducts, Intrahepatic↗
PubMed2002

Dominant negative MEKK1 inhibits survival of pancreatic cancer cells.

Human pancreatic cancers harbor mutations in the K-ras gene, and these mutations convert the gene oncogenic and constitutively active forms. However, in pancreatic cancer cells little is known about the activation of the downstream pathways of Ras, MEK-ERK and MEKK1-JNK, and their roles in cell survival and proliferation. An analysis of nine pancreatic cancer tissues revealed JNK activation in all tumor samples and ERK activation in three tumor samples. Colony formation assays by transfection of dominant negative mutants of Ras, ERK or MEKK1 into pancreatic cancer cell lines (BxPC-3, PANC-1, MIAPaCa-2 and AsPC-1) and an amnion-derived cell line (FL) revealed that DN-MEKK strongly inhibits the survival of colonies in pancreatic cancer cells, but not in FL cells. In vitro kinase assays and luciferase assays using the Gal4c-Jun system revealed that in pancreatic cancer cells DN-MEKK fails to inhibit JNK activation. In PANC-1 cells, c-Jun was found to be a major component of protein component binding to AP-1 site and CRE, but not in FL cells. The inhibitory effect of DN-MEKK in PANC-1 cells was thought to be the result of the inhibition of c-Jun DNA-binding. The difference of suppression in pancreatic cancer cells and non-pancreatic cancer cells suggested that the MEKK1 pathway mainly contributes to cell survival in pancreatic cancer cells and may provide an advantage for the gene therapy of pancreatic cancers using DN-MEKK expression vectors.

Adenocarcinoma↗
PubMed2002

Immunohistochemical analysis and in situ hybridization of cyclooxygenase-2 expression in intraductal papillary-mucinous tumors of the pancreas.

BACKGROUND: The objective of this study was to investigate COX-2 expression in intraductal papillary-mucinous tumor of the pancreas (IPMT) using immunohistochemical staining (IH) and in situ hybridization (ISH). METHODS: Immunohistochemical staining of COX-2 was performed using samples from 42 patients with IPMT (hyperplasia, 10; adenoma, 13; noninvasive adenocarcinoma, 13; invasive adenocarcinoma, 6) and from 10 patients with ductal pancreatic adenocarcinoma, 10 with chronic pancreatitis, and 6 normal pancreatic tissues as controls. Also, COX-2 was determined in five patients with IPMT noninvasive adenocarcinoma, in whom all histologic types, hyperplasia, adenoma, and adenocarcinoma were observed in the same excised specimens. Furthermore, IH of proliferating cell nuclear antigen (PCNA) was performed, and the labeling index (LI) was calculated to investigate the correlation with COX-2. To confirm COX-2 mRNA, the authors performed ISH in 20 IPMT patients. RESULTS: COX-2 was positive in 0%, 0%, and 10% of pancreatic duct epithelial cells from normal pancreatic tissue, chronic pancreatitis, and IPMT hyperplasia, respectively. Whereas it was positive in 69%, 77%, 67%, and 80% of IPMT adenoma, IPMT noninvasive adenocarcinoma, IPMT invasive adenocarcinoma, and ductal pancreatic adenocarcinoma, respectively, showing significant differences between IPMT hyperplasia and IPMT adenoma or IPMT adenocarcinoma (noninvasive and invasive adenocarcinoma). In the same patient, COX-2 was negative in the hyperplasia region but positive in adenoma and adenocarcinoma regions, showing results reflecting the progression of the disease. In the COX-2 negative group, PCNA-LI was 19.2 +/- 17.9%, and 33.5 +/- 15.7% in the positive group, a significant difference. On ISH, COX-2 mRNA was expressed in three of four and seven of eight COX-2 positive patients with IPMT adenoma and adenocarcinoma, respectively. CONCLUSIONS: COX-2 was highly expressed in adenoma and adenocarcinoma in IPMT, showing a relation to the histologic grade of IPMT.

Adenocarcinoma↗
PubMed2002

Peroral cholangioscopic treatment of hepatolithiasis: Long-term results.

BACKGROUND: Peroral cholangioscopic lithotomy is an effective treatment for extrahepatic bile duct stones. However, an evaluation of the usefulness and long-term results of peroral cholangioscopic lithotomy for hepatolithiasis has not been reported. The aim of this study was to evaluate the usefulness and long-term results of peroral cholangioscopic lithotomy for hepatolithiasis. METHODS: From August 1987 to July 1998, 36 consecutive patients underwent peroral cholangioscopic lithotomy for hepatolithiasis; 34 were followed for a mean of 93 months (range, 14 to 164 months). RESULTS: The rate of complete stone removal was 64%; the morbidity rate was 2.8%. The recurrence rate for patients in whom stones were completely removed was 21.7%. Two patients (5.9%) had cholangiocarcinoma develop during follow-up. CONCLUSION: Although incomplete stone removal and recurrence are common, peroral cholangioscopic lithotomy is a sufficiently safe and effective method for the treatment of hepatolithiasis.

Adult↗
PubMed2002

Diagnosis and patient management of intraductal papillary-mucinous tumor of the pancreas by using peroral pancreatoscopy and intraductal ultrasonography.

BACKGROUND & AIMS: Intraductal papillary-mucinous tumor (IPMT) of the pancreas has attracted increasing interest because of its unique presentation. The differential diagnosis between malignant and benign tumors is extremely important in the determination of the therapy for IPMT. The aims of this study are to determine the usefulness of peroral pancreatoscopy (POPS) and intraductal ultrasonography (IDUS) in IPMT for the differentiation of malignant from benign disease, and to evaluate the significance of these techniques as new preoperative examinations. METHODS: Sixty histopathologically confirmed patients with IPMT underwent POPS and/or IDUS preoperatively. POPS was perfomed in all patients, and IDUS in 40. Findings of POPS and IDUS were compared with histopathology of resected specimens. The postoperative follow-up data were analyzed. RESULTS: Protruding lesions were detected by POPS in 40 patients. They were classified into 5 groups. Fish-egg-like type with vascular images, villous type, and vegetative type were considered to be malignant. By IDUS, lesions protruding 1 mm or more were observed in 36 patients. Of the lesions protruding 4 mm or more, 88% were malignant. Combination of POPS and IDUS improved the differential diagnosis between benign and malignant IPMT. The 3-year cumulative survival rate and disease-free survival rate were extremely high at 95% and 93%, respectively. CONCLUSIONS: The combination of POPS and IDUS results in a considerably improved differential diagnosis between malignant and benign IPMT and is useful for determining an effective therapeutic approach. These new techniques can contribute to improvements in postoperative results.

Adenoma↗
PubMed2002

Evaluation of the Helicobacter pylori stool antigen test for monitoring eradication therapy.

OBJECTIVE: We aimed to clarify the time course of the Helicobacter pylori stool antigen (HpSA) level during and after eradication therapy and to determine the appropriate time of measurement of HpSA to evaluate eradication. METHODS: The subjects were 47 patients who were positive for H. pylori. The patients underwent a 1-wk regimen of triple therapy. The outcome of the eradication therapy was judged by urea breath test, culture, and histology 6 wk after the end of treatment. The HpSA level was serially measured nine times from before therapy until 12 wk after the end of therapy. RESULTS: In the group with successful eradication, HpSA became negative immediately after the end of therapy and the negativity persisted. In contrast, in the noneradication group HpSA became negative immediately after therapy, but became positive again within 2 wk after the end of therapy. The mean absorbance value of the HpSA test on the 4th day after the initiation of eradication therapy was significantly higher in the noneradication group than in the group with successful eradication. The diagnostic accuracy of the HpSA test increased to > or = 90% 2 wk after therapy and thereafter. Comparison of the diagnostic accuracy at 4 wk after the end of therapy showed no significant differences with that at 2, 6, 8, and 12 wk after the end of therapy. CONCLUSIONS: The course of the HpSA levels during and after eradication therapy in patients with successful eradication was quite different from that in noneradication patients. Measurement of HpSA was useful to evaluate eradication, and the appropriate evaluation of the outcome of treatment could be made as early as 2 wk after the end of therapy.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMedDate not supplied

A promoter region of midkine gene can activate transcription of an exogenous suicide gene in human pancreatic cancer.

We examined a possible application of regulatory regions of the midkine (MK) gene for suicide gene therapy of pancreatic cancer. The expression of MK has been demonstrated in human pancreatic cancer tissues but scarcely in normal adult tissues. Northern blot analysis confirmed that human pancreatic cancer cell lines expressed the MK gene. A 609-bp genomic fragment in the 5'-regulatory region of the MK gene, when transfected into human pancreatic cancer cells, activated the transcription of a fused reporter gene to an extent greater than the SV40 promoter. In contrast, the 609-bp fragment-mediated promoter activity tested in fibroblast cells was significantly weak. Human pancreatic cancer cells (AsPC-1) that were transduced with the herpes simplex virus-thymidine kinase gene linked with the 609-bp promoter markedly increased their sensitivity to a prodrug, ganciclovir, compared with untransduced cells. The present study suggests that preferential cytotoxic effects for pancreatic tumors can be achieved by using the MK promoter.

Carrier Proteins↗
PubMedDate not supplied

Successful treatment for ampullary submucosal bleeding-induced pancreatitis: a rare sequla of hereditary hemorrhagic telangiectasia.

Hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease) is clinically characterized by the triad of mucocutaneous telangiectasia, recurrent epistaxis, and a familial history. We describe a 68-year-old woman with hereditary hemorrhagic telangiectasia undergoing transduodenal papillectomy for ampullary submucosal bleeding-induced pancreatitis. When she was 63 years old, she presented with abdominal pain due to acute pancreatitis, and from the age of 68, frequency of the symptom increased a couple of times a month. Gastrofiberscopy showed enlarged ampulla of Vater. Doppler ultrasonography showed rich and tortuous signals of bloodstream at submucosal region of the ampulla. Arteriogram revealed that hypervascular staining was fed by the inferior pancreaticoduodenal artery. Microcoil embolization was attempted and hypervascular staining disappeared. However, one week later, endoscopic papillotomy was unable to be performed due to risk of uncontrollable bleeding since Doppler ultrasonography showed signals of bloodstream at submucosal region of the ampulla again. Finally, she underwent open transduodenal papillectomy. She had an uneventful postoperative course, and has been free of pancreatitis for 20 months after surgery. We also review the literature and discuss the surgical indication for gastrointestinal and hepato-biliary-pancreatic involvement with hereditary hemorrhagic telangiectasia. To our knowledge, this is the first reported case of successful surgical treatment for pancreatitis due to sequla of hereditary hemorrhagic telangiectasia.

Aged↗