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Biomedical subjects

Masayuki Imamura

Publications and source records attributed to Masayuki Imamura.

At least 55 records · Page 3Linked to original sources
PubMed2004

Weakness of anastomotic site in diabetic rats is caused by changes in the integrity of newly formed collagen.

AIMS: Diabetes mellitus often causes anastomotic leakage leading to severe complications after surgery. The purpose of this study was to determine whether collagen synthesis is correlated with the anastomotic strength in diabetic animals in special reference to collagen type differences. METHODS: Thirty Lewis rats weighing approximately 250 g were made diabetic by tail vein injection of streptozotocin (STZ). Laparotomy was performed through a midline incision under ether anesthesia. A colonic segment 5 cm distal to the ileocecal junction was transected then anastomosed with absorbable suture. Anastomotic strength was measured on days 3, 5, 7 and 14 postoperatively, and compared with normal rats. Collagen type I and type III mRNA together with the total collagen concentration were measured in anastomotic sites. RESULTS: Anastomotic strength in diabetic rats was significantly lower on day 7, but gradually recovered up to day 14. There was no statistical significance between the two groups in hydroxyproline concentrations. Although the expressions of mRNA of collagen type III in both groups were statistically not different, that of collagen type I in the diabetes group merely increased and was clearly less than that of the control group. CONCLUSIONS: Anastomotic integrity in diabetic rats was significantly damaged on day 7 after surgery but recovered by day 14. This is caused not by the total contents of collagen accumulation but by the decrease of newly formed collagen type I contents.

Anastomosis, Surgical↗
PubMed2004

Clinical significance of dysadherin expression in gastric cancer patients.

PURPOSE: Dysadherin, a cancer-associated cell membrane glycoprotein, has been reported to down-regulate E-cadherin expression and promote metastasis. To evaluate the role of dysadherin in gastric cancer, we examined dysadherin and E-cadherin expression in gastric cancer patients. EXPERIMENTAL DESIGN: Dysadherin and E-cadherin expression were evaluated in 276 gastric cancer patients by immunohistochemistry, and the results were compared with the clinicopathological findings of the subjects. RESULTS: Dysadherin was not expressed in normal gastric epithelium. Both dysadherin and E-cadherin were localized to the cell membrane. Dysadherin expression was sometimes largely localized to infiltrating tumor cells or cells dissociating. Ninety gastric cancer patients (32.6%) were positive for dysadherin, and 151 patients (54.7%) showed preservation of E-cadherin expression. Expression of dysadherin was associated with moderately differentiated carcinoma and hematogenous metastasis, whereas reduced expression of E-cadherin showed an association with poorly differentiated carcinoma and peritoneal dissemination. As a result, dysadherin positivity and reduced E-cadherin expression were associated with a poor prognosis. In addition, patients with both dysadherin positivity and reduced E-cadherin had the worst prognosis. Multivariate analysis revealed that reduced E-cadherin expression was an independent prognostic factor, but dysadherin expression was not. CONCLUSION: Combined analysis of dysadherin and E-cadherin expression may help to predict the prognosis and the mode of metastasis in gastric cancer patients. Patients with dysadherin positivity have a higher risk of hematogenous metastasis, whereas patients with reduced E-cadherin expression have an increased risk of peritoneal dissemination.

Aged↗
PubMed2004

Metastin and its variant forms suppress migration of pancreatic cancer cells.

Metastin, a post-translationally modified variant of KiSS1, was recently identified as an endogenous peptide agonist for a novel G-protein coupled receptor, hOT7T175 (AXOR12, GPR54). In this study, we analyzed the role of KiSS1 and hOT7T175 in both pancreatic cancer tissues and pancreatic cancer cell lines. Furthermore, we synthesized novel short variant forms of metastin and tested the inhibitory effect of those variants on in vitro cell functions that are relevant to metastasis. Pancreatic cancer tissues showed significantly lower expression of KiSS1 mRNA than normal tissues (p=0.018), while cancer tissues showed significantly higher expression of hOT7T175 mRNA than normal pancreatic tissues (p=0.027). In human pancreatic cancer cell lines, KiSS1 mRNA was highly expressed in 2 out of 6 pancreatic cancer cell lines, while hOT7T175 mRNA was expressed in all cell lines at various degrees. PANC-1 cells showed the highest expression of hOT7T175. Exogenous metastin did not suppress cell proliferation but significantly reduced the in vitro migration of PANC-1 cells (p<0.01). Metastin induced activation of ERK1 in PANC-1 and AsPC-1 cells. Finally, we synthesized 3 novel short variant forms of metastin, FM053a2TFA, FM059a2TFA, and FM052a4TFA. These metastin variants significantly suppressed the migration of PANC-1 cells and activated ERK1. These data suggest that the metastin receptor, hOT7T175, is one of the promising targets for suppression of metastasis, and that small metastin variants could be an anti-metastatic agent to pancreatic cancer.

Cell Line, Tumor↗
PubMed2004

Repeated resection for extrahepatic recurrences after hepatectomy for ruptured hepatocellular carcinoma.

In March 1999, a 54-year-old man with chronic hepatitis C was referred to our hospital because of ruptured hepatocellular carcinoma (HCC) located in Couinaud's segments 4 and 8. He underwent central bisegmentectomy of the liver with partial resection of the diaphragm. After the first surgery, extrahepatic metastases were found on different occasions in the abdominal wall, thoracic cavity, and greater omentum and were all surgically resected. In February 2001, the serum protein induced by vitamin K absence or antagonist-II (PIVKA-II) level increased markedly to 19,000 mAU/l. Magnetic resonance imaging showed a massive right subphrenic tumor with invasion to the right diaphragm and posterior segment of the liver. The patient underwent en bloc resection of the tumor, diaphragm, posterior segment of the liver, and right lower pulmonary lobe. After the surgery, the PIVKA-II level rapidly decreased, and it has remained within the normal range to date. Two years after the last surgery, the patient is doing well without any extrahepatic recurrence, although small intrahepatic recurrences have been completely treated by radiofrequency ablation and transcatheter arterial chemoembolization. Ruptured HCC often exacerbates the risk of peritoneal dissemination and is usually difficult to completely resect. This is an extremely rare case of a patient who successfully underwent five repeated resections for extrahepatic recurrences after hepatectomy for ruptured HCC.

Carcinoma, Hepatocellular↗
PubMed2004

Islet film cures diabetes.

Intraportal transplantation of islets is usually performed by a percutaneous, transhepatic catheterization technique for type 1 diabetic patients. We show here an easier method of islet implantation into the liver. An islet film was made using rat islet and was simply placed on the liver of a diabetic recipient rat. Histologic examinations revealed that the islets passed through the liver capsule within a week after the implantation, entered the liver parenchyma within 3 weeks, and were encircled with hepatocytes by day 222. Recipient rats were cured of diabetes; however nonimplanted control rats had high levels of blood glucose. The film-transplanted islets could provide adequate insulin to maintain stable blood glucose levels. This novel method requires little skill and no special instruments. This islet film approach may prove suitable for simple islet transplantation in clinical cases.

Animals↗
PubMed2004

Surgical resection deteriorates gemcitabine-induced leukopenia in pancreatic cancer.

BACKGROUND: Gemcitabine hydrochloride (GEM) is one of the most effective chemotherapeutic agents for pancreatic cancer; however, factors affecting GEM-induced leukopenia have not been clarified yet. In the present study, we analyzed the relationship between patients backgrounds and GEM-induced leukopenia. METHODS: Thirty-eight patients with pancreatic cancer were analyzed for correlation between the dose of GEM and the blood leukocyte number. Moreover, we compared leukopenia in resected and non-resected patients. RESULTS: The incidence of grade 3 or 4 leukopenia was 25% in the non-resected patients, whereas equivalent leukopenia was observed in 57% of the resected patients ( P = 0.048 by the chi(2) test). The relative decrease in blood leukocytes induced by GEM administration was more severe in resected patients (41.3 +/- 9.9%), as compared to non-resected patients (52.6 +/- 16.0%; P = 0.023 by t-test). CONCLUSION: In the present study, we found that the administration of GEM to patients after surgical resection caused more severe leukopenia, as compared to findings in non-resected patients. These data suggested that more frequent monitoring of the leukocyte count and prolonged intervals between GEM administrations are necessary for resected patients with pancreatic cancer.Gemcitabine hydrochloride (GEM) is one of the most effective chemotherapeutic agents for pancreatic cancer; however, factors affecting GEM-induced leukopenia have not been clarified yet. In the present study, we analyzed the relationship between patients' backgrounds and GEM-induced leukopenia.

Aged↗
PubMed2004

A randomized multicenter trial comparing resection and radiochemotherapy for resectable locally invasive pancreatic cancer.

BACKGROUND: Though the outcome of resection for locally invasive pancreatic cancer is still poor, it has gradually improved in Japan, and the 5-year survival is now about 10%. However, the advantage of resection over radiochemotherapy has not yet been confirmed by a randomized trial. We conducted this study to compare surgical resection alone versus radiochemotherapy without resection for locally invasive pancreatic cancer using a multicenter randomized design. METHODS: Patients with pancreatic cancer who met our preoperative criteria for inclusion (pancreatic cancer invading the pancreatic capsule without involvement of the superior mesenteric artery or the common hepatic artery, or without distant metastasis) underwent laparotomy. Patients with operative findings consistent with our criteria were randomized into a radical resection group and a radiochemotherapy group (200 mg/m(2)/day of intravenous 5-fluorouracil and 5040 cGy of radiotherapy) without resection. The 2 groups were compared for mean survival, hazard ratio, 1-year survival, quality of life scores, and hematologic and blood chemical data. RESULTS: Twenty patients were assigned to the resection group and 22 to the radiochemotherapy group. There was 1 operative death. The surgical resection group had better results than the radiochemotherapy group as measured by 1-year survival (62% vs 32 %, P=.05), mean survival time (>17 vs 11 months, P < .03), and hazard ratio (0.46, P=.04). There were no differences in the quality of life score or laboratory data apart from increased diarrhea after surgical resection. CONCLUSIONS: Locally invasive pancreatic cancer without distant metastases and major arterial invasion appears to be best treated by surgical resection.

Adult↗
PubMed2004

Chronic exposure of transforming growth factor beta 1 confers a more aggressive tumor phenotype through downregulation of p21(WAF1/CIP1) in conditionally immortalized pancreatic epithelial cells.

BACKGROUND: Recent studies have demonstrated that transforming growth factor beta 1 (TGF-beta1) expression is markedly enhanced in invasive ductal pancreatic adenocarcinomas, although the precise role of TGF-beta1 in pancreatic carcinogenesis remains unclear. We analyzed TGF-beta1 expression in pancreatic intraepithelial neoplasias (PanINs) and the effects of chronic TGF-beta1 exposure on conditionally immortalized pancreatic epithelial (IMPE) cells. METHODS: Sixty-one PanIN lesions were immunohistochemically stained with a polyclonal rabbit antibody against human TGF-beta1. Growth-inhibitory effects of short-term exposure to TGF-beta1 were examined in IMPE cells. IMPE cells resistant to TGF-beta1 (IMPE-Tr cells) were generated by continuous exposure to 1 ng/mL of TGF-beta1 for more than 50 days. Phenotypic alterations of IMPE-Tr cells were examined by soft agar and Matrigel assay and Western blot analysis. IMPE and IMPE-Tr cells were injected subcutaneously into nude mice for an in vivo tumorigenicity assay. RESULTS: Forty-six percent of PanINs (28/61) were positive for TGF-beta1 expression, whereas all the epithelia of normal pancreatic ducts were negative. TGF-beta1 treatment showed the marked growth-inhibitory effects (>75%) in IMPE cells, whereas its effects were not observed in IMPE-Tr cells. IMPE-Tr cells were more spindle shaped compared with IMPE cells. In soft agar and Matrigel, formations of many colonies were observed in IMPE-Tr cells, but not in IMPE cells. Interestingly, the expression of p21(WAF1/CIP1) was induced by short-term exposure to TGF-beta1 in IMPE cells, whereas the induction was decreased in IMPE-Tr cells. All of the IMPE-Tr cell-injected mice (5/5) had subcutaneous tumors, although no tumor was found in the IMPE cell-injected mice. CONCLUSIONS: TGF-beta1 expression in PanINs and neoplastic transformation of IMPE cells by long-term exposure to TGF-beta1 suggest that TGF-beta1 may act as a tumor promoter in the early stage of pancreatic carcinogenesis.

Animals↗
PubMed2004

Survivin expression is a prognostic marker in pancreatic cancer patients.

BACKGROUND: In this study, we assessed survivin expression in pancreatic cancer specimens from patients who underwent either pancreatic resection alone or pancreatic resection plus postoperative radiation therapy (PORT) to evaluate whether survivin expression is predictive of sensitivity to PORT and outcome in pancreatic cancer patients. METHODS: Fifty-two patients who underwent pancreatic resection for ductal adenocarcinomas were included in this study. Forty-seven pancreatic ductal adenocarcinoma and 5 normal pancreatic tissues were evaluated for survivin expression by immunohistochemistry. Then the relationship between survivin expression and clinicopathologic data were analyzed. RESULTS: Sixty-eight percent (32/47) of pancreatic cancer tissues were positive for survivin expression; 32% (15/47) were negative. Normal pancreatic exocrine tissues were negative for survivin expression (0/5). Survival of the patients with positive survivin was significantly shorter than those with negative survivin (P = .02). Survivin was an independent variable that correlated with overall survival (P = .01). There was no difference in survival time between patients with and without PORT. Likely, PORT showed no impact on survival time in survivin-positive patients (P = .12) as well as in survivin-negative patients (P = .95). CONCLUSIONS: The results suggest that survivin expression in pancreatic cancer tissues could be a useful prognostic marker in pancreatic cancer patients.

Aged↗
PubMed2004

Hepatic regeneration and enforced PDX-1 expression accelerate transdifferentiation in liver.

BACKGROUND: Pancreatic duodenal homeobox gene-1 (PDX-1) has a dual task as a key regulator in pancreatic organogenesis and in functional maintenance of beta cells in adults. Recent studies have shown a close lineage relationship between the liver and the pancreas. In this study, we analyzed the plasticity of the liver by enforced expression of PDX-1 in streptozotocin (STZ)-treated mice under the condition of hepatic regeneration. METHODS: Replication-deficient adenoviruses were constructed by the cosmid-adenoviral DNA terminal protein complex method. Mice were treated with STZ (200 mg/kg ip), and a 40% partial hepatectomy was performed at day 0. After 24 hours, Ad-pdx-1 or Ad-lacZ 2.0 x 10(9) PFU/body was injected via the tail vain into nontreated (control), STZ-treated, or STZ plus partial hepatectomy (Hx)-treated ICR mice. After 7 and 14 days, expression of PDX-1 and islet hormones was examined by immunohistologic and reverse transcription-polymerase chain reaction analysis. Blood glucose concentrations were measured every 2 days. Immunoreactive insulin (IRI) of serum and liver extract was measured by ELISA. RESULTS: Most hepatocytes of Ad-pdx-1-infected mice were positive for PDX-1 expression by immunohistochemistry. In nontreated mice, very few cells expressed insulin and other hormones. In contrast, insulin and somatostatin were expressed in STZ-treated mice, and more cells were expressed in STZ plus Hx-treated mice. In addition, other beta-cell markers like GLUT2 and glucokinase were observed. Hyperglycemia was improved in STZ-treated mice and STZ plus Hx-treated mice. IRI of serum and liver extract was increased in STZ-treated mice and STZ plus Hx-treated mice. The insulin positive area of the liver in STZ plus Hx-treated mice was larger than that in nontreated and STZ-treated mice. CONCLUSIONS: Ectopic PDX-1 expression alone may be insufficient to induce insulin-producing cells in the liver. STZ-induced hyperglycemia plus partial hepatectomy that leads to diabetic state and hepatic regeneration may stimulate the transdifferentiation of liver cells into insulin-producing cells.

Adenoviridae↗
PubMed2004

Expression of pancreatic duodenal hoemobox-1 in pancreatic islet neogenesis after surgical wrapping in rats.

BACKGROUND: Surgical wrapping (SW) of the pancreas causes islet neogenesis in rodents. Pancreatic duodenal hoemobox-1 (PDX-1) is one of the transcriptional factors needed by pancreatic stem cells to develop a mature pancreas. The purpose of this study was to determine whether islet neogenesis arises from ductal cells and whether PDX-1 is involved in this process. METHODS: SW consisted of nonocclusive wrapping of the pancreas in rats. The wrapped pancreas was then harvested, insulin content was measured, and immunohistochemical analysis for insulin, cytokeratin, and PDX-1 was performed. RESULTS: The endocrine area of the wrapped pancreas significantly increased after SW. Double immunostaining identified cells positive for both insulin and cytokeratin in or along the epithelial cell lining of the ductal structures and in the centroacinar cells. PDX-1-positive cells were detected in both control islets and islets examined after SW, but these cells were observed in the exocrine area only after SW. Double staining also showed that cells positive for PDX-1 but negative for insulin were present in the exocrine area 1 day after SW and that cells positive for both PDX-1 and insulin had developed 3 days after SW. CONCLUSIONS: In the process of adult islet neogenesis after SW, cells in the acini and ductal structures developed into PDX-1-expressing cells, supposedly progenitor cells, which in turn became insulin-producing cells and thus might be the origin of small islets.

Animals↗
PubMed2004

Hexokinase II and VEGF expression in liver tumors: correlation with hypoxia-inducible factor 1 alpha and its significance.

BACKGROUND/AIMS: We analyzed the expressions of hexokinase II (HK II), a key enzyme in glycolysis, and VEGF in hepatocellular carcinoma (HCC) and metastatic liver cancer in relation to tumor vascularity, and the participation of hypoxia-inducible factor-1 (HIF-1) was studied. METHODS: A real-time quantitative reverse transcription-polymerase chain reaction was performed to examine the HK II and VEGF mRNA expression. Expression of HIF-1 alpha and HK II protein, and microvessel density (MVD) were examined immunohistochemically. RESULTS: MVD was significantly higher in HCCs than in metastatic liver cancers, and VEGF mRNA expression was positively correlated only with MVD of HCCs. HK II mRNA expression was significantly higher in metastatic liver cancers, however, some cases of HCC pretreated with transcatheter arterial embolization (TAE) showed marked HK II mRNA expression. Both HIF-1 alpha and HK II protein expressions were co-localized in the cancer cells near necrosis, and the intensity of HIF-1 alpha protein expression was significantly correlated with HK II mRNA expression in both tumors. CONCLUSIONS: These results suggest that, in metastatic liver cancers, glycolysis induced by HIF-1 is the predominant energy source under the hypoxic environment and, at least in some TAE-pretreated HCC cases, cancer cells obtain energy for growth by switching the metabolic profile to glycolysis through HIF-1.

Aged↗
PubMed2004

Pancreatic endocrine tumor in Japan.

Japanese clinicians and scientists have contributed significantly to reporting, investigating, and managing patients with pancreatic endocrine tumors and other multiple endocrine neoplasias for the past several decades. This article summarizes the latest progress in this field in Japan. Particularly, our contribution to the development of diagnostic and localization methods is reviewed. Further, the present use of somatostatin receptor scintigraphy and the application of the laparoscopic surgery for pancreatic endocrine tumor in Japan are discussed.

Calcium↗
PubMed2004

Treatment of locally advanced pancreatic cancer: should we resect when resectable?

While the outcome of surgery for locally advanced pancreatic cancer is still quite poor, over the past 2 decades, surgical outcomes have gradually improved in Japan. Because the advantages of surgery over radiochemotherapy have not yet been confirmed by randomized, controlled trials, it has long been discussed whether surgical resection could be indicated for locally advanced pancreatic cancer. We recently performed a multicenter, randomized, controlled trial comparing surgical resection and radiochemotherapy for locally advanced pancreatic cancer. Twenty patients were assigned to the surgery group, and 22 to the radiochemotherapy group. Although there was 1 operative death, surgery offered significantly better results than radiochemotherapy, as measured by 1-year survival (62% vs. 32%, P = 0.05), mean survival time (>17 vs. 11 months, P < 0.03), and hazard ratio (0.46, P = 0.04). There was no significant difference in the quality of life score or laboratory data, apart from increased diarrhea after surgery. In this article, the results of our trial are reviewed in brief, and our opinion on surgical treatment of locally advanced pancreatic cancer is discussed.

Adult↗
PubMed2004

Vascular endothelial growth factor reduces mural cell coverage of endothelial cells and induces sprouting rather than luminal division in an HT1080 tumour angiogenesis model.

Vascular endothelial growth factor (VEGF) plays a central role in tumour angiogenesis. In a mouse intramuscular tumour model using VEGF-transfected HT1080 human fibrosarcoma, we investigated the morphological features and patterns of remodelling in size-matched tumours. Compared with the control tumours (C group), the VEGF-transfected tumours (V group) showed vigorous neovascularization with larger vessels. Fenestrations and disruptions of endothelia were specific to the V group. Three types of vascular remodelling, i.e. sprouting, luminal division and intussusceptive microvascular growth, were present in both groups. Morphometric analyses revealed that mural cell coverage of the endothelial cells was significantly smaller in the V group compared with that in the C group (V group, 28.2 +/- 18.6%; C group, 41.6 +/- 21.1%; P < 0.0001). To determine the prevalence of remodelling patterns, the occurrences of abluminal and luminal processes on endothelial cell surfaces were quantified. Abluminal processes are defined as cytoplasmic protrusions of the abluminal membrane of endothelial cells, which can vary from tiny spurs to solid sprouts of the cell. On the other hand, luminal processes are defined as intraluminal protrusions of the endothelial cell membrane, including various membranous changes from filiform processes to rather thick cytoplasmic bulges. An abluminal process is thought to represent an initial morphological change in sprouting type angiogenesis, and a luminal process to be a sign of implementation of luminal division. The frequency of abluminal processes was significantly higher in the V group than in the C group (V group, 0.243 +/- 0.138/microm; C group, 0.114 +/- 0.101/microm; P < 0.0001). In contrast, the number of luminal processes on the endothelial cells per micrometre was statistically comparable between the groups (V group, 0.285 +/- 0.252/microm; C group, 0.309 +/- 0.236/microm, P = 0.381). These results indicate that sprouting is the main mode of VEGF-induced tumour angiogenesis.

Animals↗
PubMed2004

Caspase-3 expression in human gastric carcinoma and its clinical significance.

OBJECTIVES: Caspase-3 is one of the most important molecules in the apoptosis cascade, and the relationship between caspase-3 expression and prognosis has been reported in many types of malignancies. However, the involvement of caspase-3 in human gastric carcinoma is not fully understood. We evaluated caspase-3 expression in human gastric carcinoma to clarify the clinicopathological importance and investigated the apoptosis avoidance mechanism by an immunohistological method. METHODS: Specimens from 151 patients who underwent gastrectomy at the Department of Surgery and Surgical Basic Science of Kyoto University Hospital were investigated. Caspase-3 expression in cancer cells was evaluated by comparing its expression in the germinal center of the lymphoid follicle, and was quantified as the caspase-3 expression index (C3EI). C3EI was compared with the expression of Bcl-2 and the TdT-mediated dUTP biotin nick-end labeling (TUNEL) in 80 randomly selected cases. Actual activation of caspase-3 was determined by immunohistochemistry using monoclonal antibody that recognizes only activated caspase-3. RESULTS: C3EI correlated significantly with lymph node metastasis (negative 105.5-78.7, positive 153.8 +/- 66.1 p = 0.001) and the lower C3EI group had a better prognosis than the higher group (log-rank test, p = 0.0001). Cox multivariate analysis showed that age, operation curability, tumor invasion and C3EI were significant independent determinants of overall survival. Bcl-2 and TUNEL staining had no significant correlations with C3EI. Immunohistochemistry of activated caspase-3 revealed that most caspase-3 in gastric cancer cells was not activated, in accordance with TUNEL assay. CONCLUSIONS: Our results show that C3EI is a novel, independent prognostic factor in gastric cancer patients and cancer cells may avoid apoptosis by inhibiting caspase-3 activation.

Aged↗
PubMed2004

Prognostic significance of dysadherin expression in esophageal squamous cell carcinoma.

OBJECTIVE: Dysadherin is a cancer-associated cell membrane glycoprotein that has been reported to downregulate E-cadherin expression and promote metastasis. To evaluate the role of dysadherin in metastasis of esophageal squamous cell carcinoma (ESCC), we examined dysadherin and E-cadherin expression in patients with this cancer. METHODS: Dysadherin and E-cadherin expression was evaluated in 117 ESCC patients (pT1, 31; pT2, 30; pT3, 39; pT4, 17) by immunohistochemistry. The findings were compared with the clinicopathological data of the patients. RESULTS: Both dysadherin and E-cadherin were localized to the cell membrane. Thirty patients (29.1%) had tumors positive for dysadherin and 41 patients (35.0%) had tumors positive for E-cadherin. Tumors showing dysadherin positivity and negative E-cadherin expression had a significantly worse prognosis than other tumors. When the patients with dysadherin- positive tumors were combined with E-cadherin-negative patients, this group had a worse prognosis (p < 0.0001). Cox multivariate analysis revealed that dysadherin expression was an independent prognostic factor for ESCC (p = 0.003), but E-cadherin expression was not. CONCLUSION: Combined analysis of dysadherin and E-cadherin expression may help to predict the prognosis of patients with ESCC. Our results suggested that expression of dysadherin by this cancer may partly explain the poor prognosis of patients with preservation of E-cadherin expression.

Aged↗