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Prawej Mahawithitwong,
Kenoki Ohuchida, Naoki Ikenaga,
Hayato Fujita,
Ming Zhao,
Shingo Kozono,
Koji Shindo,
Takao Ohtsuka,
Shinichi Aishima,
Kazuhiro Mizumoto,
Masao Tanaka
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ABSTRACT: Kindlin-1 is a novel focal adhesion protein that belongs to the kindlin family. Expression of kindlin-1 has recently been reported in lung and colon cancers, but there have been no studies on its expression in pancreatic cancer. This study aimed to investigate the expression and function of kindlin-1 in pancreatic cancer. Quantitative RT-PCR of Kindlin-1 mRNA was performed in various pancreatic cancer cell lines as well as normal pancreatic epithelial cells and fibroblasts. Immunohistochemical analysis of kindlin-1 was performed for pancreatic cancer tissues. The effects of kindlin-1 on the proliferation, migration and invasion of pancreatic cancer cells were investigated using an RNA interference technique. Kindlin-1 mRNA was highly expressed in the pancreatic cancer cell lines, but only slightly expressed in normal pancreatic epithelial cells and fibroblasts. The Kindlin-1 protein was heterogeneously expressed in the cytoplasm and membrane of pancreatic cancer cells, while normal ductal epithelial cells and stromal cells showed no expression. In vitro experiments involving knockdown of kindlin-1 in AsPC-1 and KP-2 cells revealed that the migratory and invasive abilities of the cells were significantly decreased (P<0.001), while the proliferation abilities were not affected. The present findings suggest that kindlin-1 expression is involved in the progression of pancreatic cancer via enhancement of cell migration and invasion.
International Journal of Oncology 04/2013; 42(4):1360-6. · 2.40 Impact Factor
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ABSTRACT: OBJECTIVES: Kindlin-2 is a novel focal adhesion protein reported to be expressed in breast, lung, and gastric cancers. This study aimed to investigate the significance of kindlin-2 expression in pancreatic ductal adenocarcinomas (PDACs). METHODS: We performed immunohistochemical analysis on kindlin-2 on PDAC samples from 95 patients. We investigated the association between kindlin-2 expression and clinicopathological parameters of PDAC and the survival time of patients with PDAC who underwent pancreatectomy. RESULTS: Kindlin-2 was highly expressed in the peritumoral stroma of PDACs. Stromal kindlin-2 expression was related to nodal metastasis (P = 0.03). Univariate analysis showed that patients with positive kindlin-2 expression had significantly shorter survival times than those with negative kindlin-2 expression (P = 0.01). In addition, multivariate analysis revealed that kindlin-2 expression was an independent factor of poor prognosis in patients with PDAC after R0 resection (RR = 2.15; P = 0.04). CONCLUSIONS: Kindlin-2 expression in stromal components is significantly associated with poor prognosis of patients with PDAC, suggesting that kindlin-2 is a prognostic marker for patients with PDAC.
Pancreas 03/2013; · 2.39 Impact Factor
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ABSTRACT: Pancreatic stellate cells (PSCs), which are implicated in desmoplasia in pancreatic cancer, enhance the malignancy of cancer cells and confer resistance to established treatments. We investigated whether the antifibrotic agent pirfenidone can suppress desmoplasia and exert anti-tumor effects against pancreatic cancer. Primary PSCs were established from pancreatic cancer tissue obtained during surgery. In vitro, pirfenidone inhibited the proliferation, invasiveness, and migration of PSCs in a dose-dependent manner. Although supernatants of untreated PSCs increased the proliferation, invasiveness, and migration of pancreatic cancer cells (PCCs), supernatants of pirfenidone-treated PSCs decreased these effects. Exposure to PCC supernatant increased the production of platelet-derived growth factor-A, hepatic growth factor, collagen type I, fibronectin, and periostin in PSCs, which was significantly reduced by pirfenidone. Mice were subcutaneously implanted with PCCs (SUIT-2 cells) and PSCs into the right flank and PCCs alone into the left flank. Oral administration of pirfenidone to these mice significantly reduced tumor growth of co-implanted PCCs and PSCs, but not of PCCs alone. Pirfenidone also decreased the proliferation of PSCs and the deposition of collagen type I and periostin in tumors. In mice with orthotopic tumors consisting of PCCs co-implanted with PSCs, pirfenidone suppressed tumor growth, reduced the number of peritoneal disseminated nodules, and reduced the incidence of liver metastasis. Pirfenidone in combination with gemcitabine more effectively suppressed orthotopic tumor growth compared with pirfenidone or gemcitabine alone. In conclusion, our findings indicate that pirfenidone is a promising antitumor agent for pancreatic cancer, owing to its suppression of desmoplasia through regulating PSCs.
Cancer Research 01/2013; · 7.86 Impact Factor
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ABSTRACT: BACKGROUND: Pancreatic cancer (PC), a hypovascular tumor, thrives under hypoxic conditions. Pancreatic stellate cells (PSCs) promote PC progression by secreting soluble factors, but their functions in hypoxia are poorly understood. This study aimed to clarify the effects of hypoxic conditions on the interaction between PC cells and PSCs. METHODS: We isolated human PSCs from fresh pancreatic ductal adenocarcinomas and analyzed functional differences in PSCs between normoxia (21% O(2)) and hypoxia (1% O(2)), including expression of various factors related to tumor-stromal interactions. We particularly analyzed effects on PC invasiveness of an overexpressed molecule-connective tissue growth factor (CTGF)-in PSCs under hypoxic conditions, using RNA interference techniques. RESULTS: Conditioned media from hypoxic PSCs enhanced PC cell invasiveness more intensely than that from normoxic PSCs (P < 0.01). When co-cultured with PSCs, PC cell invasion was more enhanced under hypoxia than under normoxia (P < 0.05). Among various soluble factors, which were related to invasiveness, CTGF was one of the overexpressed molecules in hypoxic PSCs. A higher level of CTGF expression was also found in supernatant of hypoxic PSCs than in supernatant of normoxic PSCs. PC cell invasiveness was reduced by CTGF knockdown in hypoxic PSCs co-cultured with PC cells (P < 0.05). CONCLUSION: Hypoxia induces PSCs' secretion of CTGF, leading to enhancement of PC invasiveness. CTGF derived from hypoxia-stimulated PSCs may be a new therapeutic target for pancreatic cancer.
Journal of Surgical Research 07/2012; · 2.25 Impact Factor
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ABSTRACT: Solitary necrotic nodule of the liver is a rare nonmalignant lesion of unknown etiology. It is defined as a nodule with a
completely necrotic core enclosed by a hyalinized fibrotic capsule containing elastic fiber. We report a 74-year-old woman
with a solitary necrotic nodule of the liver that mimicked metastasis from a previous rectal adenocarcinoma. She was referred
to us for an asymptomatic liver nodule in segment 8 that had increased in diameter from 5 to 15mm over the past 8months.
Ultrasonography showed a well-defined, oval, hypoechoic mass, and computed tomography showed a hypodense area without contrast
enhancement except for a ring-like enhancement during hepatic arteriography. Magnetic resonance imaging revealed a mass that
was hypointense on T1-weighted imaging and slightly hyperintense on T2-weighted imaging. The patient underwent hepatectomy
of segment 8. The resected specimen contained an oval nonencapsulated nodule with firm and gritty consistency and a well-defined
margin. Histologic findings were compatible with those of solitary necrotic nodule. Clinicians should recognize the existence
of this lesion as one of the differential diagnoses of metastatic liver nodule. Solitary necrotic nodules can change size,
and when enlarged, differentiation from metastasis is extremely difficult.
KeywordsNecrotic nodule-Liver-Metastasis
Clinical Journal of Gastroenterology 04/2012; 2(5):355-360.
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ABSTRACT: A 41-year-old man without clinical symptoms was referred for treatment of an enlarging retroperitoneal tumor. Enhanced computed
tomography showed a well-defined and heterogeneously enhanced tumor, 4cm in size, in the dorsal portion of the pancreas.
A low-density nodule was detected in the left adrenal gland, 10mm in diameter. Retroperitoneal sarcoma and nonfunctional
left adrenal tumor were suspected, and surgical treatment was performed. During excision of the retroperitoneal tumor, blood
pressure was extremely elevated when the tumor was compressed. Blood pressure normalized after excision of the tumor; thus,
a diagnosis of paraganglioma was favored over that of retroperitoneal sarcoma. The left adrenal gland was resected together
with the adrenal tumor. Microscopically, the tumor cells of the retroperitoneum had round to oval nuclei, and abundant granular
amphophilic cytoplasm proliferated in nest-like fashion. Extra-adrenal retroperitoneal paraganglioma was considered, and the
adrenal tumor was diagnosed as cortical adenoma. In patients with retroperitoneal tumor, even in the absence of clinical symptoms,
we should keep in mind the possibility of extra-adrenal paraganglioma.
Clinical Journal of Gastroenterology 04/2012; 3(1):13-17.
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Nihon Naika Gakkai Zasshi 01/2012; 101(1):4-6.
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ABSTRACT: Extracellular matrix (ECM) remodeling is predominantly mediated by fibroblasts using intracellular and extracellular pathways. Although it is well known that extracellular degradation of the ECM by proteases derived from cancer cells facilitates cellular invasion, the intracellular degradation of ECM components by cancer cells has not been clarified. The aim of this study was to characterize collagen internalization, which is the initial step of the intracellular degradation pathway in pancreatic cancer cells, in light of epithelial-mesenchymal transition (EMT).
We analyzed the function of collagen internalization in two pancreatic cancer cell lines, SUIT-2 and KP-2, and pancreatic stellate cells (PSCs) using Oregon Green 488-gelatin. PSCs had a strong ability for collagen uptake, and the pancreatic cancer cells also internalized collagen although less efficiently. The collagen internalization abilities of SUIT-2 and KP-2 cells were promoted by EMT induced by human recombinant transforming growth factor β1 (P<0.05). Expression of Endo180, a collagen uptake receptor, was high in mesenchymal pancreatic cancer cell lines, as determined by EMT marker expression (P<0.01). Quantitative RT-PCR and western blot analyses showed that Endo180 expression was also increased by EMT induction in SUIT-2 and KP-2 cells. Endo180 knockdown by RNA interference attenuated the collagen uptake (P<0.01) and invasive abilities (P<0.05) of SUIT-2 and KP-2 cells.
Pancreatic cancer cells are capable of collagen internalization, which is enhanced by EMT. This ECM clearance system may be a novel mechanism for cellular invasion and a potential therapeutic target in pancreatic cancer.
PLoS ONE 01/2012; 7(7):e40434. · 4.09 Impact Factor
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Kenji Fujiwara,
Kenoki Ohuchida,
Kazuhiro Mizumoto,
Koji Shindo,
Daiki Eguchi,
Shingo Kozono, Naoki Ikenaga,
Takao Ohtsuka,
Shunichi Takahata,
Shinichi Aishima,
Masao Tanaka
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ABSTRACT: Pancreatic stellate cells (PSCs) play a crucial role in the aggressive behavior of pancreatic cancer. Although heterogeneity of PSCs has been identified, the functional differences remain unclear. We characterized CD271(+) PSCs in human pancreatic cancer. Immunohistochemistry for CD271 was performed for 31 normal pancreatic tissues and 105 pancreatic ductal adenocarcinomas (PDACs). We performed flow cytometry and quantitative RT-PCR, and assessed CD271 expression in PSCs isolated from pancreatic tissues and the changes in CD271 expression in PSCs cocultured with cancer cells. We also investigated the pattern of CD271 expression in a SCID mouse xenograft model. In the immunohistochemical analyses, the CD271-high staining rates in pancreatic stroma in normal pancreatic tissues and PDACs were 2/31 (6.5%) and 29/105 (27.6%), respectively (p = 0.0069). In PDACs, CD271(+) stromal cells were frequently observed on the edge rather than the center of the tumors. Stromal CD271 high expression was associated with a good prognosis (p = 0.0040). Flow cytometric analyses demonstrated CD271-positive rates in PSCs were 0-2.1%. Quantitative RT-PCR analyses revealed that CD271 mRNA expression was increased in PSCs after coculture with pancreatic cancer cells. However, the level of CD271 mRNA expression subsequently decreased after the transient increase. Furthermore, CD271 mRNA expression was decreased in PSCs migrating toward pancreatic cancer cells through Matrigel. In the xenograft model, CD271(+) PSCs were present at tumor margins/periphery and were absent in the tumor core. In conclusion, CD271 was expressed in PSCs around pancreatic tumors, but not in the center of the tumors, and expression decreased after long coculture with pancreatic cancer cells or after movement toward pancreatic cancer cells. These findings suggest that CD271(+) PSCs appear at the early stage of pancreatic carcinogenesis and that CD271 expression is significantly correlated with a better prognosis in patients with PDAC.
PLoS ONE 01/2012; 7(12):e52682. · 4.09 Impact Factor
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Kohei Nakata,
Kenoki Ohuchida,
Kazuhiro Mizumoto,
Tadashi Kayashima, Naoki Ikenaga,
Hiroshi Sakai,
Cui Lin,
Hayato Fujita,
Takao Otsuka,
Shinichi Aishima,
Eishi Nagai,
Yoshinao Oda,
Masao Tanaka
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ABSTRACT: MicroRNAs (miRNAs) have been gaining attention as new, key molecules that contribute to carcinogenesis. In pancreatic cancer, previous profiling analyses of miRNA expression have shown that several miRNAs are differently expressed in normal and cancerous tissues. Several pancreatic cancer-specific miRNAs differed, however, in each analysis.
We investigated the miRNA expression profiles of the pancreatic cancer cell lines CAPAN-1 and CFPAC1 and an immortalized human normal pancreatic ductal epithelial cell line (HPDE) using a high-throughput, TaqMan, qRT-PCR array analysis. We also analyzed the expression levels of this miRNA in microdissected (n = 15) and formalin-fixed, paraffin-embedded (FFPE) (n = 115) samples from pancreatic cancers by quantitative RT-PCR. Finally, we investigated the effects of this miRNA on the invasiveness of pancreatic cancer cells.
Based on the microarray analysis, miR-372, miR-146a, miR-204, miR-10a, and miR-10b showed particularly large differences (>10-fold changes) between both pancreatic cell lines and HPDE cells. Thirteen of the 15 pancreatic cancer cell lines showed 2.1- to 36.4-fold (median, 15.3-fold) greater levels of miR-10b than HPDE cells. Microdissection analysis revealed that miR-10b exhibited greater expression levels in pancreatic cancer cells (n = 5) than in normal pancreatic ductal cells (n = 10) (P < .020). Analysis of FFPE samples showed that high miR-10b expression was associated with a lesser overall survival (P = .014). Furthermore, miR-10b correlated with the invasiveness of pancreatic cancer cells (P < .01).
miR-10b is overexpressed in pancreatic cancer and may be involved in the invasiveness in pancreatic cancer cells, thereby leading to a poor prognosis.
Surgery 11/2011; 150(5):916-22. · 3.10 Impact Factor
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ABSTRACT: Detection of aberrant microRNA (miR) expression may contribute to diagnosis and prognosis of various cancers. The aim of this study is to evaluate the correlation between miR-203 expression and prognosis of patients with pancreatic adenocarcinoma after curative resection.
A total of 113 formalin-fixed paraffin-embedded tissue samples of pancreatic adenocarcinoma, 20 samples of chronic pancreatitis, and 8 samples of normal pancreas were obtained. We investigated the association of miR-203 expression measured by quantitative reverse-transcription polymerase chain reaction assays with clinicopathological parameters and survival times.
miR-203 was overexpressed in pancreatic adenocarcinoma samples compared with chronic pancreatitis (P < 0.001) and normal pancreas (P = 0.001) samples. An association between miR-203 expression and clinicopathological factors of pancreatic adenocarcinoma was not observed. On univariate analysis, the high-miR-203 group and the subgroup (20%) of cases with the highest miR-203 overexpression had significantly shorter survival time (P = 0.048 and P = 0.024, respectively). Multivariate analysis revealed that miR-203 expression was an independent predictor of poor prognosis in cases with no residual tumor (relative risk 2.298, P = 0.027).
miR-203 expression is a new prognostic marker in pancreatic adenocarcinoma patients.
Annals of Surgical Oncology 12/2010; 17(12):3120-8. · 4.17 Impact Factor
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ABSTRACT: CD24 is a molecule involved in cell adhesion and tumor metastasis. The aims of this study were (1) to evaluate the association between CD24 expression and the progression of intraductal papillary mucinous neoplasms of the pancreas and (2) to investigate the association between CD24 expression in pancreatic cancer and the prognosis of patients who underwent curative pancreatectomy. Immunohistochemical analysis of CD24 was performed for 95 intraductal papillary mucinous neoplasms of the pancreas and 83 pancreatic cancers. We investigated the association between CD24 expression and the histologic grade of intraductal papillary mucinous neoplasms of the pancreas, the clinicopathologic parameters of pancreatic cancers, and the survival time of pancreatic cancer patients who underwent pancreatectomy. The positive rates of CD24 expression in intraductal papillary mucinous adenoma, borderline intraductal papillary mucinous neoplasm, noninvasive intraductal papillary mucinous carcinoma, and invasive intraductal papillary mucinous carcinoma were 5 (20%) of 24, 12 (48%) of 25, 10 (43%) of 23, and 15 (65%) of 23, respectively. The CD24-positive rates were significantly higher in borderline intraductal papillary mucinous neoplasm and intraductal papillary mucinous carcinoma compared with intraductal papillary mucinous adenoma (P = .046 and P = .007, respectively). The staining scores, which were determined from the percentage of stained cells and the staining intensity, were significantly higher in invasive intraductal papillary mucinous carcinoma than in noninvasive intraductal papillary mucinous carcinoma (P = .043). In the pancreatic cancers, higher tumor stage (P = .007), nodal metastasis (P = .021), and higher-grade tumors (P < .001) were more frequent in the CD24-positive group compared with the CD24-negative group. CD24 expression was associated with shorter survival in univariate analysis (P = .028) However, based on the multivariate analysis, the CD24 expression was not associated with survival. In conclusion, CD24 is involved in the progression of intraductal papillary mucinous neoplasms of the pancreas and in the malignant behavior of pancreatic cancers.
Human pathology 10/2010; 41(10):1466-74. · 3.03 Impact Factor
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ABSTRACT: Pancreatic stellate cells (PSCs) promote the progression of pancreatic cancer by producing extracellular matrix and soluble factors. However, the functional heterogeneity of PSCs has not been identified until now. Detailed characterization of the PSCs in human pancreatic cancer would provide a set of potential targets for stroma-directed therapy.
We isolated PSCs from fresh pancreatic ductal adenocarcinoma tissue and sorted them by flow cytometry according to cell surface expression of CD10, which is a stromal prognostic marker for various tumors. We analyzed the functional differences between CD10(+) PSCs and CD10(-) PSCs.
Immunohistochemical analysis showed that the frequency of CD10 expression by PSCs was markedly higher in tumor tissue than in normal tissue (33.7% vs 0%, respectively, P = .028). In pancreatic ductal adenocarcinoma, CD10 expression by PSCs was associated with positive nodal metastases (P = .011) and a shorter survival time (P < .001). In vitro coculture experiments showed that CD10(+) PSCs promoted the invasiveness of pancreatic cancer cell lines, SUIT-2 and Panc-1 cells more intensively than CD10(-) PSCs. CD10(+) PSCs significantly increased the tumor growth and invasiveness of SUIT-2 cells in a murine cotransplantation model. CD10(+) PSCs secreted higher levels of matrix metalloproteinase 3 than CD10(-) PSCs, and knockdown of matrix metalloproteinase 3 in cocultured PSCs reduced the invasion of SUIT-2 and Panc-1 cells.
CD10(+) PSCs enhance the progression of pancreatic cancer cells. CD10(+) PSCs may be a candidate for selective therapeutic targeting in the treatment of pancreatic cancer.
Gastroenterology 09/2010; 139(3):1041-51, 1051.e1-8. · 11.68 Impact Factor
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ABSTRACT: Recently, cancer stem cells have been reported as a new therapeutic target in pancreatic cancer as well as other cancers, but the specific role of these cells is unknown.
The authors investigated the functional roles of CD133+ cells, 1 of the putative cancer stem cell candidates in pancreatic cancer. CD133 expression was assessed in human pancreatic cancer and cancer cell lines by quantitative real-time reverse transcriptase polymerase chain reaction and flow cytometry. Next, they compared the ability of CD133+ and CD133- cells to proliferate, migrate, and invade using 2 pancreatic cancer cell lines. In particular, they evaluated the relationship between CD133+ cells and primary pancreatic stromal cells.
CD133 was expressed in primary human pancreatic cancer tissues and some cancer cell lines, whereas there was little expression in primary normal pancreatic epithelial cells and primary pancreatic stromal cells. CD133+ cells, isolated by flow cytometry, showed increased cell proliferation under anchorage-independent conditions (P<.01), and enhanced migration and invasion, particularly when cocultured with primary pancreatic stromal cells (P<.001). Chemokine-related receptor-4 (CXCR4), markedly overexpressed in CD133+ cells, may be responsible for the increased invasive ability of the cells cocultured with pancreatic stromal cells, which express stromal derived factor-1, the ligand to CXCR4.
These data suggest that CD133+ cells exhibit more aggressive behavior, such as increased cell proliferation, migration, and invasion, especially in the presence of pancreatic stromal cells. The targeting therapy for the interaction between CD133+ cancer cells and stromal cells may be a new approach for the treatment of pancreatic cancer.
Cancer 07/2010; 116(14):3357-68. · 4.77 Impact Factor
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ABSTRACT: The aim of this study is to evaluate the clinical significance of S100A4 mRNA expression in pancreatic cancer.
We obtained invasive ductal carcinoma (IDC) cells from ten lesions, intraductal papillary mucinous neoplasm (IPMN) cells from 20 lesions, and normal ductal cells from 20 normal pancreatic tissues by laser microdissection of frozen tissues. S100A4 expression was examined in the microdissected cells and in formalin-fixed paraffin-embedded (FFPE) samples of 87 pancreatic cancers by quantitative reverse transcription-polymerase chain reaction.
IDC cells expressed higher levels of S100A4 than IPMN cells (P = 0.002) and normal ductal cells (P < 0.001), although the difference between IPMN cells and normal ductal cells was not statistically significant (P = 0.070). Analysis of FFPE samples revealed that high S100A4 expression was significantly associated with a shorter overall survival (P = 0.023). In immunohistochemical analysis, the extent of S100A4 mRNA expression was significantly correlated with the expression of S100A4 protein (P = 0.028).
S100A4 could be a marker for malignancy in pancreatic tumors and for poor prognosis in patients with pancreatic cancer.
Journal of Gastrointestinal Surgery 08/2009; 13(10):1852-8. · 2.83 Impact Factor
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ABSTRACT: An 80-year-old woman who had undergone both a cholecystectomy and an appendectomy presented with intermittent abdominal pain. Computed tomography (CT) revealed an encapsulated circumscribed cluster of jejunal loops in the left upper quadrant. The hernia orifice was adjacent to the left side of the superior mesenteric artery and vein. An upper gastrointestinal series also revealed a cluster of jejunal loops, suggesting the possibility of an internal hernia. Laparoscopic surgery was performed. The hernia orifice was found to be caused by abnormal adhesion between the transverse mesocolon and the jejunum mesentery. An adhesiotomy reduced the jejunum entrapped in the hernia. The hernia space was a large mesocolic fossa composed of transverse mesocolon and mesentery, continuing to the splenic flexure. The hernia was classified as a variant of paraduodenal hernia.
Surgery Today 02/2009; 39(6):533-5. · 1.22 Impact Factor
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ABSTRACT: To clarify the characteristics of hepatocellular carcinoma (HCC) with bile duct invasion, we retrospectively analyzed clinical features and surgical outcome of HCC with bile duct invasion (b(+) group, n = 15) compared to those without bile duct invasion (b(-) group, n = 256). In the b(+) group, four patients (27%) showed obstructive jaundice, and a diagnosis of bile duct invasion was obtained preoperatively in seven patients (47%). The levels of serum bilirubin and carbohydrate antigen 19-9 were significantly higher in the b(+) group. Macroscopically, confluent multinodular type and infiltrative type were predominant in the b(+) group (P = 0.002). Microscopically, capsule infiltration (P = 0.040) and intrahepatic metastasis (P = 0.013) were predominant in the b(+) group. Portal vein invasion was associated significantly with the b(+) group (P = 0.004); however, the frequency of hepatic vein invasion was similar (P = 0.096). The median survival after resection was significantly shorter in the b(+) group than in the b(-) group (11.4 vs. 56.1 months, P = 0.002), and eight of 11 intrahepatic recurrences in the b(+) group occurred within 3 months after surgery. HCC with bile duct invasion has an infiltrative nature and a high risk of intrahepatic recurrence, resulting in poor prognosis.
Journal of Gastrointestinal Surgery 12/2008; 13(3):492-7. · 2.83 Impact Factor
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ABSTRACT: A 77-year-old woman with a complaint of itching was shown to have an elevated serum bilirubin level. She had no history of liver disease. Computed tomography and magnetic resonance cholangiopancreatography revealed a 17-mm-diameter cystic lesion obstructing the main hepatic duct at the hepatic hilum. Drip infusion cholangiographic computed tomography and endoscopic retrograde cholangiography showed that the cyst did not communicate with the biliary tree; thus, a peribiliary cyst was diagnosed. Cystectomy was performed, and the jaundice resolved. Peribiliary cysts are generally asymptomatic and rarely cause obstructive jaundice. They are usually multiple and caused by an underlying liver disorder with a poor prognosis. Our case suggests that peribiliary cysts can arise in healthy liver and cause symptoms. Cystectomy is the treatment of choice if the cyst is solitary.
Journal of Gastrointestinal Surgery 01/2008; 13(1):174-6. · 2.83 Impact Factor
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ABSTRACT: Several studies have revealed the diagnostic value of fluorodeoxyglucose-positron emission tomography for breast carcinomas. However, breast carcinomas display considerable variation in 18F-labeled 2-fluoro-2-deoxy-D-glucose uptake, and few papers have reported the clinical utility of the standardized uptake values (SUV). The purpose of this study is to investigate the relationship between SUV assessed by positron emission tomography (PET) and the clinicopathological characteristics of breast carcinoma. We reviewed 52 breast carcinomas of 45 patients presented at our department between January 2004 and July 2005. We compared the histopathological findings of the breast carcinomas with the preoperative SUV. Of the 52 breast carcinomas, 49 (94%) were detected by preoperative PET. A positive correlation was found between the SUV and tumor size (P < 0.01), histological grade (P < 0.01), the expression of the estrogen receptor (P < 0.001), progesterone receptor (P < 0.01), and p53 (P < 0.01). The number of metastatic axillary lymph nodes (r = 0.73; P < 0.0001) and the MIB-1 labeling rates (r = 0.5; P < 0.01) correlated with the SUV of the breast carcinomal. No relationship existed between the SUV and the following: histological tumor types (P = 0.07), human epidermal growth factor receptor-2 status (P = 0.10), and the presence of metastatic lymph nodes (P = 0.10). The SUV of the breast carcinomas correlate with several histopathological and immunohistochemical prognostic factors. We can obtain information on the degree of malignancy of the carcinoma and prognostic factors by preoperative PET examination.
The American surgeon 11/2007; 73(11):1151-7. · 1.28 Impact Factor
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ABSTRACT: To investigate whether laparoscopically assisted distal gastrectomy (LADG) contributes to long-term quality of life as compared to open gastrectomy in patients with early-stage gastric cancer.
Quality of life was self-reported using a 15-item questionnaire with five options for each question. The responses obtained from 47 LADG patients and 33 conventional open gastrectomy patients were compared. All patients underwent Billroth I gastrectomy for early gastric cancer between September 1999 and October 2002.
Patients who underwent LADG showed better results than those who underwent the open procedure with regard to satisfaction with the operation (87.2% vs. 57.6%; P < 0.01). However, the rate of late complications such as delayed gastric emptying was higher in the LADG group than in the open group (40.4% vs. 18.2%; P < 0.05). No differences were observed between the LADG and open groups with regard to appetite loss, heartburn, diarrhea, or difficulty in swallowing.
LADG has an equivocal effect on long-term quality of life. Satisfaction with the surgical procedure was greater in patients who underwent the LADG method; however, complications that impaired the quality of life were also seen. The usefulness of LADG should be assessed in view of the immediate and relatively short-term outcomes and their effect on long-term quality of life.
Journal of Laparoendoscopic & Advanced Surgical Techniques 05/2006; 16(2):119-23. · 1.40 Impact Factor
