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Yoshikazu Kuroda

Publications and source records attributed to Yoshikazu Kuroda.

At least 19 recordsLinked to original sources
PubMed2006

Superior anti-tumor protection and therapeutic efficacy of vaccination with allogeneic and semiallogeneic dendritic cell/tumor cell fusion hybrids for murine colon adenocarcinoma.

Cancer immunotherapy by dendritic cell (DC)/tumor cell fusion hybrids (DC/TC hybrids) has been shown to elicit potent anti-tumor effects via the induction of immune responses against multiple tumor-associated antigens. In the present study, we compared the anti-tumor effects of vaccinating Balb/c mice (H-2(d)) with CT26CL25 colon carcinoma cells that had been fused with either syngeneic DCs from Balb/c mice, allogeneic DCs from C57BL/6 mice (H-2(b)) or semiallogeneic DCs from B6D2F1 mice (H-2(b/d)). Preimmunization with either semiallogeneic or allogeneic DC/TC hybrids induced complete protection from tumor challenge, whereas mice preimmunized with syngeneic DC/TC hybrids were only partially protected (75% tumor rejection). The average number of pulmonary metastases after intravenous tumor injection decreased significantly following immunization with semiallogeneic or allogeneic DC/TC hybrids (8.3 +/- 7.9 or 16.3 +/- 3.5, mean +/- SD) relative to syngeneic DC/TC hybrids (67.8 +/- 6.3). These data demonstrate that vaccination with semiallogeneic DC/TC hybrids resulted in the greatest anti-tumor efficacy. Anti-tumor effects showed by in vivo studies were virtually accomplished by the frequency of induced CTLs specific to both gp70 and beta-galactosidase assessed by using pentameric assay. Among the fusion vaccines tested, semiallogeneic DC/TC hybrids induced the highest ratio of Th1 cytokine IFN-gamma to Th2 cytokine IL-10. In addition, allogeneic or semiallogeneic DC/TC hybrids elicited a significantly stronger NK activity than syngeneic DC/TC hybrids. These findings suggest that in clinical settings, DCs derived from a healthy donor (which are generally characterized as more semiallogeneic than allogeneic) may be more capable than autologous DCs of inducing promising anti-tumor effects in vaccinations with DC/TC hybrids.

Adenocarcinoma↗
PubMed2006

Adenocarcinoma arising in gastric inverted hyperplastic polyp: a case report and review of the literature.

A 54-year-old man, found to have a submucosal tumor in the stomach by double contrast roentgenography, endoscopy, and endoscopic ultrasonography, underwent a laparoscopic partial gastrectomy. The pathological examination revealed that the lesion, measuring 45 mm x 35 mm, was an inverted hyperplastic polyp (IHP) located in the submucosal layer and consisting mostly of columnar cells resembling foveolar epithelium and pyloric gland cells. Notably, adenocarcinoma with adjacent dysplasia was observed in the submucosal glands. Transition from hyperplasia to dysplasia and from dysplasia to adenocarcinoma was noted. The adenocarcinoma component was intensely and diffusely positive for p53 overexpression, while the dysplasia component showed only weak and focal positivity, suggesting a role of p53 mutation in the dysplasia-carcinoma sequence. Gastric IHP is very rare, and only 31 cases (in 29 patients) have been reported. Five of these IHPs coexisted with gastric adenocarcinomas, which had all developed separately from the IHP lesions. Therefore, this is the first case of adenocarcinoma arising within gastric IHP itself.

Adenocarcinoma↗
PubMed2006

Double cancer of gall bladder and bile duct not associated with anomalous junction of the pancreaticobiliary duct system.

BACKGROUND: Simultaneous double cancers of the biliary tract are rare. Most of them are thought to be associated with pancreaticobiliary maljunction (PBM); however, the characteristics of tumours without PBM are still unclear. METHODS: Histology, immunoreactivity with carcinoembryonic antigen, carbohydrate antigen 19-9 and p53 and mutations in the K-ras gene were examined in tumours resected from cases of simultaneous double cancers of the biliary tract. RESULTS: Four cases of simultaneous double cancers of the biliary tract were identified among 108 patients with biliary tract cancer (3.7%). None of the four cases associated with PBM, and the results of histological, immunohistochemical and genetic examinations differed between the bile duct and gall bladder cancers in each case. CONCLUSION: Even when they do not associate with PBM, double cancers in the biliary tract are more likely to be the result of multicentric development.

Aged↗
PubMed2006

Microarray analysis of PDGFR alpha+ populations in ES cell differentiation culture identifies genes involved in differentiation of mesoderm and mesenchyme including ARID3b that is essential for development of embryonic mesenchymal cells.

An inherent difficulty in using DNA microarray technology on the early mouse embryo is its relatively small size. In this study, we investigated whether use of ES cell differentiation culture, which has no theoretical limit in the number of cells that can be generated, can improve this situation. Seven distinct ES-cell-derived populations were analyzed by DNA microarray and examined for genes whose distribution patterns are similar to those of PDGFRalpha, a gene implicated in differentiation of mesoderm/mesenchymal lineages. Using software developed in our laboratory, we formed a group of 30 genes which showed the highest similarity to PDGFRalpha, 18 of these genes were shown to be involved in development of either mesodermal, mesenchymal or neural crest cells. This list also contains several genes whose role in embryogenesis has not yet been fully identified. One such molecule is mARID3b. The mARID3b expression is found in the paraxial mesoderm and cranial mesenchyme. mARID3b-null mouse showed early embryonic lethality, and most phenotypes of this mutant appear to develop from a failure to generate a sufficient number of cranial mesenchymal cells. These results demonstrate the potential use of ES cell differentiation culture in identifying novel genes playing an indispensable role in embryogenesis.

Animals↗
PubMed2006

Vascular endothelial growth factor increases in serum and protects against the organ injuries in severe acute pancreatitis.

BACKGROUND: We have demonstrated that apoptosis was detected in liver and kidney cells in severe acute pancreatitis and that cellular injury because of apoptosis may be involved in the mechanism of multiple organ dysfunction syndrome. Vascular endothelial growth factor (VEGF) is a glycoprotein with potent angiogenic, mitogenic, and vascular permeability-enhancing activities specific for endothelial cells. It has been reported that VEGF is implicated in many diseases such as cancer and inflammation. METHODS: Serum VEGF concentrations were determined in patients with acute pancreatitis at the time of admission, and the relationships with severity, blood biochemical parameters on admission, organ dysfunction during the clinical course, and prognosis were analyzed. Moreover, to clarify the role of VEGF in acute pancreatitis, effects of VEGF were investigated in experimental severe acute pancreatitis. RESULTS: Serum VEGF levels were significantly elevated in patients with acute pancreatitis. Serum VEGF levels were not related to severity or prognosis. In male patients, among the various blood biochemical parameters, serum lactate dehydrogenase, and blood urea nitrogen levels were positively correlated with serum VEGF levels. Serum VEGF levels with organ dysfunction (liver and kidney) were higher than those without organ dysfunction. In rat experimental severe acute pancreatitis, serum VEGF levels were significantly elevated. Recombinant VEGF did not affect the lung water content, volume of ascitic fluid, hematocrit, or serum amylase, but improved the hepatic and renal dysfunctions. Apoptosis of liver and kidney was significantly inhibited by the administration of VEGF. CONCLUSIONS: These results suggest that VEGF is closely related to organ dysfunction in severe acute pancreatitis, and that VEGF may function as not a vascular permeability factor, but a protective factor via the anti-apoptotic effect against the organ injuries in this disease.

Acute Disease↗
PubMed2006

Outcomes of surgery for intraductal papillary mucinous neoplasms of the pancreas.

BACKGROUND: Our objective was to evaluate outcomes of surgery for intraductal papillary mucinous neoplasms of the pancreas (IPMN) in terms of the clinicopathological features. METHODS: Fifty-seven patients with IPMN were examined using clinicopathological analyses to evaluate appropriate surgical treatment, including total pancreatectomy (TP). IPMN was classified into two types: main-duct type (MD, n = 33) and branch-duct type (BD, n = 24). RESULTS: Ultrasound (US) and computed tomography (CT) examinations easily revealed the main site of the lesions. Intraoperative US was the most useful device for diagnosis of lateral spreading, and accuracy rates were 74% for MD and 96% for BD. TP was performed on 16 patients and was appropriate for removing neoplastic lesions with malignancy or malignant potential in 12. Three patients who underwent partial pancreatectomy with involved cancer died of progressive disease. MD is a strong predictive factor in malignancy and indicative of TP. Concerning long-term outcomes, 5 of 16 patients suffered from severe hypoglycemia, and 2 of 16 died from this condition. CONCLUSION: Partial resection with cancer clearance was applied for BD-type IPMN. TP should be performed on selected patients with MD-type IPMN.

Adult↗
PubMed2006

Significant elevation of serum interleukin-18 levels in patients with acute pancreatitis.

BACKGROUND: We have reported that peripheral lymphocyte reduction due to apoptosis is linked to the development of subsequent infectious complications in patients with severe acute pancreatitis and that Th1 (helper T cell type 1)/Th2 (helper T cell type 2) balance tends to cause Th1 suppression in experimental severe acute pancreatitis. It has been reported that interleukin (IL)-18 is a cytokine produced from Kupffer cells and activated macrophages, and that IL-18 acts on Th1 cells and in combination with IL-12 strongly induces production of interferon-gamma. However, the role of IL-18 in acute pancreatitis has not yet been fully understood. METHODS: Serum IL-18 concentrations were determined by an enzyme-linked immunosorbent assay in 43 patients with acute pancreatitis at the time of admission. The relationships with etiology, pancreatic necrosis, severity, blood biochemical parameters on admission, infection, and organ dysfunction during the clinical course and prognosis were analyzed. RESULTS: Serum IL-18 levels in patients with acute pancreatitis (656+/- 11pg/ml) were significantly higher than those in healthy volunteers (126+/- pg/ml). Serum IL-18 levels were significantly positively correlated with the Ranson score and Japanese severity score. Among the blood biochemical parameters on admission, base excess and total protein were significantly negatively correlated with serum IL-18 levels. Moreover, the CD4/CD8 rate of lymphocytes, serum IL-6 levels, and serum IL-8 levels were significantly positively correlated with serum IL-18 levels. On day 7 after admission, the CD4/CD8 rate of lymphocytes and the rate of CD4-positive lymphocytes were significantly positively correlated with serum IL-18 levels. Furthermore, serum IL-18 levels in patients with hepatic dysfunction (980+/- 25pg/ml) were significantly higher than those without hepatic dysfunction (464+/- 8pg/ml). Serum IL-18 levels were not related to infection or prognosis. Elevation of serum IL-18 levels continued during 4 weeks after admission. CONCLUSIONS: These results suggest that serum IL-18 levels are significantly elevated and are correlated with severity in patients with acute pancreatitis and that IL-18 may be closely related to helper T cell response and hepatic dysfunction in this disease.

Acute Disease↗
PubMed2006

Elevation of plasma tissue factor levels in patients with severe acute pancreatitis.

BACKGROUND: Coagulative disorders are known to occur in severe acute pancreatitis (SAP), and they are related to its severity and organ dysfunctions. Tissue factor (TF) is a transmembrane glycoprotein that activates the extrinsic pathway of the blood coagulation cascade. Plasma TF levels increase in patients with sepsis and acute coronary syndrome. However, plasma TF levels in SAP have not yet been reported. METHODS: We measured plasma TF antigen levels by enzyme-linked immunosorbent assay in 36 patients with acute pancreatitis at the time of admission. The relationships between their plasma TF levels and various factors (severity, etiology, pancreatic necrosis, organ dysfunction, and prognosis) were analyzed. The utility of plasma TF as a clinical marker was evaluated. RESULTS: Plasma TF levels significantly increased in patients with SAP compared with healthy volunteers and drinkers, respectively. Plasma TF level in alcoholic SAP with pancreatic necrosis was significantly higher than that in alcoholic SAP without pancreatic necrosis or that in nonalcoholic SAP with pancreatic necrosis. The incidence of an abnormally high level of plasma TF was 63.6% in alcoholic SAP with pancreatic necrosis. The area under the ROC curve of plasma TF for detection of pancreatic necrosis in alcoholic SAP was 0.773 and was superior to those of Japanese severity score and lactate dehydrogenase. CONCLUSIONS: Plasma TF levels were elevated in patients with SAP, particularly in those with alcoholic SAP with pancreatic necrosis, suggesting that TF may be closely related to the development of pancreatic necrosis in alcoholic SAP and that the plasma TF level may be a useful marker for it.

Acute Disease↗
PubMed2006

Immunosuppression in patients with severe acute pancreatitis.

BACKGROUND: In severe acute pancreatitis (SAP), immunologic impairment in the early phase may be linked to subsequent infectious complications. In this study, immunologic alterations in patients with SAP were analyzed, and immunologic parameters related to infectious complications were clarified. METHODS: A total of 101 patients with SAP were analyzed retrospectively. Various immunologic parameters on admission were analyzed and compared between the infection group and noninfection group during SAP. Furthermore, chronologic change in the lymphocyte count was investigated, and its utility for predicting infection was compared with conventional scoring systems. RESULTS: Serum immunoglobulin G (IgG), serum IgM, lymphokine-activated killer cell activity, and natural killer cell activity were low, and the incidence of abnormally low values was 50.0%, 65.0%, 45.5%, and 42.4%, respectively. Serum complement factor 3 was significantly negatively correlated with the APACHE II score. The lymphocyte count was decreased below the normal range, and was significantly negatively correlated with the APACHE II score. CD4-, CD8-, and CD20-positive lymphocyte counts were below the normal range, and CD4- and CD8-positive lymphocyte counts were significantly lower in the infection group. The lymphocyte count on day 14 after admission was significantly lower in the infection group and was more useful for predicting infection than conventional scoring systems. CONCLUSIONS: Immunosuppression occurs from the early phase in SAP, and quantitative impairment of lymphocytes, mainly T lymphocytes, may be closely related to infectious complications during SAP. CD4- and CD8-positive lymphocyte counts on admission and the lymphocyte count on day 14 after admission may be useful for predicting infection.

APACHE↗
PubMed2006

Intrahepatic segmental primary sclerosing cholangitis: report of a case.

A 67-year-old woman was referred to our hospital for investigation of epigastric discomfort. Computed tomography (CT) showed dilatation of the intrahepatic bile duct in the left lobe of the liver, endoscopic cholangiography showed complete stenosis of the left main branch of intrahepatic bile duct, and CT during angiography showed decreased portal blood flow to segment 3 of the liver. Based on these findings, we suspected intrahepatic cholangiocarcinoma and performed left lobectomy of the liver. However, pathological examination revealed fibrosis and infiltration of inflammatory lymphoid cells around the stenotic bile duct and periportal area, without any evidence of malignancy. Since these findings were compatible with sclerosing cholangitis and the patient did not have a disorder that would cause secondary sclerosing cholangitis, the final diagnosis was primary sclerosing cholangitis (PSC). It is difficult to distinguish segmental PSC from cholangiocarcinoma; thus we think surgical resection is an appropriate therapeutic and diagnostic procedure for segmental intrahepatic bile duct stenosis.

Aged↗
PubMed2006

Breakdown of intestinal mucosa via accelerated apoptosis increases intestinal permeability in experimental severe acute pancreatitis.

BACKGROUND: Bacterial translocation plays an important role for infectious complications in severe acute pancreatitis (SAP). Breakdown of intestinal mucosal integrity may increase intestinal permeability and may be implicated in bacterial translocation. It is suggested that increase in intestinal permeability is correlated with the changes of tight junction and/or apoptosis in intestinal epithelial cells. The aim of this study was to investigate the changes of intestinal mucosa and its permeability in SAP. METHODS: SAP was induced by injection of 3% sodium deoxycholate into the biliopancreatic ducts in rats. Permeability of intestinal wall was assayed ex vivo by measuring the leaked amount of FITC-dextran from the ileum pouch. Alteration of tight junction proteins such as zonula occludens (ZO)-1 and Occludin was evaluated by Western blotting and immunofluorescence staining. Apoptotic change of intestinal mucosa was detected by TUNEL staining and DNA fragmentation ELISA. In vitro, apoptosis-inducing effect of pancreatitis-associated ascitic fluid (PAAF) was examined using T84 cells. Integrity of monolayer cells was assessed by transepithelial electric resistance (TEER). RESULTS: Permeability of ileum was significantly increased 6 h after induction of SAP. Blood endotoxin level was significantly elevated and bacterial translocation occurred 18 h after induction of SAP. Six hours after induction of SAP, expressions of ZO-1 and Occludin were not altered, but apoptosis of ileum mucosa was significantly accelerated. Addition of PAAF to T84 cells did not affect expressions of ZO-1 or Occludin, but significantly increased the apoptosis and significantly decreased TEER. CONCLUSIONS: These results suggest that breakdown of intestinal mucosa via accelerated apoptosis may increase in intestinal permeability in SAP and that PAAF contains factor(s) that accelerates the apoptosis of intestinal epithelial cells.

Animals↗
PubMed2006

Successful 40-hour preservation of the canine small intestine with the cavitary 2-layer method with glutamine supplementation.

BACKGROUND: We recently reported that the cavitary 2-layer method (cTLM) allowed stable 24-hour preservation of canine intestine. The aim of this study was to examine the possibility of the 40-hour preservation by cTLM that is supplemented with glutamine. METHODS: Canine jejunal segments (40 cm) were allotransplanted heterotopically without storage (group 1), after 40-hour cold storage with University of Wisconsin solution (group 2), cTLM (group 3), UW with 2% glutamine (group 4), or cTLM with 2% glutamine (group 5). Mucosal glutamine, histidine, tryptophan, glutathione, and adenosine triphosphate concentrations were determined immediately after preservation. At day 7 after the transplantation, maltose absorption test and histopathologic analysis were performed. RESULTS: Mucosal glutamine concentrations increased significantly with glutamine supplementation during preservation in groups 4 and 5 (P < .01). Mucosal adenosine triphosphate levels in cTLM groups (groups 3 and 5) were similar to those in group 1; group 4 showed very low levels after preservation, despite glutamine supplementation. Mucosal glutathione did not differ among groups 2, 3, 4, and 5 and were significantly lower than in group 1. In the absorption test, serum glucose curves showed a peak level by 30 minutes in groups 1 and 5; delayed peaks were seen in groups 2, 3, and 4 compared with group 1. The villous heights were 879, 555, 685, 688, and 773 microm in groups 1, 2, 3, 4, and 5, respectively (group 1 vs group 2, 3, and 4: P < .05). CONCLUSION: cTLM that was supplemented with glutamine extended a safe preservation period up to 40 hours in canine segmental small intestinal transplantation, although this study failed to elucidate a precise mechanism of the glutamine beneficial effect on the graft mucosa.

Adenosine Diphosphate↗
PubMed2006

Significant increase of serum high-mobility group box chromosomal protein 1 levels in patients with severe acute pancreatitis.

OBJECTIVE: Multiple organ failure because of systemic inflammatory response in the early phase and sepsis in the late phase is the main contributor to high mortality in severe acute pancreatitis (SAP). High-mobility group box chromosomal protein 1 (HMGB1) was recently identified as a potent proinflammatory mediator and increases in various pathological conditions such as sepsis. The aim of this study was to investigate contributions of HMGB1 in SAP. METHODS: We measured serum HMGB1 concentrations by an enzyme-linked immunosorbent assay in 45 patients with SAP at the time of admission. Furthermore, relationship between their serum HMGB1 levels and clinical factors was analyzed. RESULTS: The mean value of serum HMGB1 levels was significantly higher in patients with SAP (5.4 +/- 1.3 ng/mL) than that in healthy volunteers (1.7 +/- 0.3 ng/mL). Serum HMGB1 levels were significantly positively correlated with the Japanese severity score and Glasgow score. Serum HMGB1 levels were significantly positively correlated with lactate dehydrogenase, C-reactive protein, and total bilirubin. The HMGB1 levels were higher in patients with organ dysfunction and infection during the clinical course. The HMGB1 levels in nonsurvivors were higher than those in survivors. Serum HMGB1 levels gradually declined after the admission. CONCLUSIONS: Serum HMGB1 levels were significantly increased in patients with SAP and were correlated with disease severity. These results suggest that HMGB1 may act as a key mediator for inflammation and organ failure in SAP.

Bacterial Infections↗
PubMed2006

Immunohistochemical study of the relationship between Ki-67 labeling index of proliferating cells of gynecomastia, histological phase and duration of disease.

Gynecomastia is a benign proliferative lesion caused by various etiological factors and may result from a relative imbalance between serum estrogen and androgen levels. The histological alterations are similar, and gynecomastia can progress from a florid type to a fibrous type. The Ki-67 labeling index (LI) of gynecomastia specimen was investigated and higher Ki-67 LI was observed in florid and intermediate than in fibrous gynecomastia (P = 0.017). A correlation was found between the duration of disease and Ki-67 LI (P = 0.041): the shorter the duration the higher the Ki-67 LI. Thus, Ki-67 LI seems a useful tool to examine proliferation activity of gynecomastia and can assist in determination of appropriate treatment of gynecomastia with hormonal therapy.

Adolescent↗
PubMed2006

Significance of Akt phosphorylation on tumor growth and vascular endothelial growth factor expression in human gastric carcinoma.

OBJECTIVE: Hypoxia is known to be a prevalent stress stimulus and increases the transcription of vascular endothelial growth factor (VEGF) mediated by hypoxia inducible factor-1alpha (HIF-1alpha). We investigated the role of phosphatidyl inositol-3 OH kinase (PI3K)-Akt signaling in the regulation of HIF-1alpha and VEGF expression in human gastric adenocarcinoma. METHODS: The growth-inhibitory and apoptosis-inducing effects of the LY294002 PI3K inhibitor were analyzed in four gastric cancer cell lines and in vivo. The regulatory mechanism of VEGF and HIF-1alpha expression under hypoxic conditions was examined in the cell cultures. In 88 gastric cancer tissue samples, phosphorylated Akt and VEGF expression were analyzed immunohistochemically. RESULTS: LY294002 suppressed cell proliferation but induced apoptosis with decreased levels of phosphorylated Akt. HIF-1alpha expression and VEGF secretion were induced under hypoxic conditions and VEGF protein secretion was significantly decreased by treatment with LY294002. In tumor samples, phosphorylated Akt expression was detected in 57% of the tumors, which was correlated with high VEGF expression, angiogenesis, clinicopathological parameters as well as a poor outcome. CONCLUSIONS: These findings suggest that phosphorylated Akt (Ser473) reflects the grade of malignancy in human gastric adenocarcinomas, not only in terms of tumor growth but also with respect to tumor angiogenesis.

Adenocarcinoma↗
PubMed2006

MDR1 T-129C polymorphism can be predictive of differentiation, and thereby prognosis of colorectal adenocarcinomas in Japanese.

The expression level of MDR1 mRNA was evaluated in colorectal adenocarcinomas and adjacent noncancerous colorectal tissues obtained from 21 Japanese patients. It was lower in the former than in the latter (p=0.012), suggesting its down-regulation as a consequence of malignant transformation of colorectal tissues, possibly with the suppression of differentiation. Relatively lower expression was suggested in moderately-differentiated colorectal adenocarcinomas than well-differentiated ones, but there was no statistical difference (p=0.111). MDR1 mRNA up-regulation was found in a colorectal adenocarcinoma cell line, HCT-15, after treatment with two typical differentiating agents, sodium butyrate and all-trans retinoic acid, suggesting its involvement in the cellular events, resulting in differentiation without malignant transformation. MDR1 T-129C, but not G2677A,T and C3435T, was associated with the lower expression of MDR1 mRNA both in colorectal adenocarcinomas (p=0.040) and adjacent noncancerous colorectal tissues (p=0.023), possibly being an useful invasive marker predicting poorly-differentiated colorectal adenocarcinomas and thereby the poor prognosis of the patients, especially when no extra biopsy samples will be obtained. Further investigations with relatively large number of patients should be undertaken to confirm these preliminary results.

Adenocarcinoma↗
PubMed2006

Correlation between expression of major histocompatibility complex class I and that of antigen presenting machineries in carcinoma cell lines of the pancreas, biliary tract and colon.

To elicit a tumor immune response, tumor antigens represented by major histocompatibility (MHC) class I complex on the cell surface is indispensable. Some investigators demonstrated that many cancer cells reduce expression of beta2-microglobulin, a transporter of antigen presenting (TAP) or low molecular protein (LMP), due to the deletion mutant or point mutation. We investigated gene expression levels of antigen presenting machineries in 13 cell lines of the pancreas, biliary tract and colon cancer by using real-time quantitative PCR. We also evaluated the correlation between expression of MHC class I and that of antigen-processing molecules in these gastrointestinal cancer cell lines. Flow cytometric analysis showed that expression of MHC class I for the pancreatic cancer cell lines was generally lower than that for the biliary tract or colon cancer cell lines. It was further found that the colon cancer cell lines HCT-15/DLD-1 showed no MHC class I expression and lack of protein expression for beta2-microglobulin. Transfection of the wild-type beta2-microglobulin gene restored MHC class I antigen expression on the cell surface for DLD-1. Quantitative real-time PCR demonstrated lower expression for TAP1, TAP2, LMP2 and LMP7 gene in five cancer cell lines. Partial correlation analysis demonstrated that LMP2 was the only antigen presenting machinery which was significantly associated with MHC class I expression. Our results suggest that beta2-microglobulin and LMP2 are important for the expression of MHC class I in 13 gastrointestinal cancer cell lines, while the combined but complex expression of antigen presenting mechanisms was related to MHC class I expression level on the surface of cancer cells.

ATP-Binding Cassette Transporters↗