[Serous cystadenoma of the pancreas with hypoplasia of the dorsal pancreas: report of a case].
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Cystadenocarcinoma, Serous↗
Biomedical subjects
T Morisaki
Publications and source records attributed to T Morisaki.
Preoperative exocrine pancreatic function predicts risk of leakage of pancreaticojejunostomy.
BACKGROUND: The objective of this study was to clarify the relationship between preoperative exocrine pancreatic function and pancreatic anastomotic leakage after pancreatectomy. METHODS: Fifty-five patients who underwent proximal pancreatectomy with pancreaticojejunostomy were reviewed with regard to preoperative exocrine pancreatic function, size of the main pancreatic duct, postoperative pancreatic juice output, and pancreaticojejunostomy leakage. RESULTS: There were 32 patients with a normal value at the preoperative N-benzoyl-L-tyrosyl-p-aminobenzoic acid (BT-PABA) excretion test (> 70%) and 23 with a low BT-PABA value (< or = 70%). The greatest diameter of the main pancreatic duct in the group with normal BT-PABA results was significantly smaller than that in the group with low BT-PABA results (4.6 +/- 2.7 mm vs 7.1 +/- 4.2 mm; P < .05). The output of pancreatic juice during a 10-day period (from postoperative days 5 through 14) in the group with normal BT-PABA results was significantly higher than that in the group with low BT-PABA results (1738 +/- 898 mL vs 1072 +/- 1174 mL; P < .05). Pancreatic leakage occurred in 8 (25%) of the 32 patients in the group with normal BT-PABA results and in none of the 23 patients in the group with low BT-PABA results (P < .01). CONCLUSIONS: Patients with normal exocrine pancreatic function produce a larger amount of pancreatic juice than those with low exocrine pancreatic function and have a potential risk of anastomotic leakage after pancreatectomy.
4-Aminobenzoic Acid↗
Cloning and characterization of NE-dlg: a novel human homolog of the Drosophila discs large (dlg) tumor suppressor protein interacts with the APC protein.
We have cloned a cDNA for a novel human homolog of the Drosophila discs large (dig) tumor suppressor protein, termed NE-dlg (neuronal and endocrine dig). Northern blot analysis revealed that the gene is highly expressed in neuronal and endocrine tissues. Fluorescence in situ hybridization (FISH) and radiation hybrid mapping studies localized the NE-dlg gene to chromosome Xq13. We also found that the NE-dlg gene encoded a 100 kDa protein. Immunolocalization studies using an NE-dlg antibody showed that the protein tended to be expressed in non-proliferating cells, such as neurons, cells in Langerhans islets of the pancreas, myocytes of the heart muscles, and the prickle and functional layer cells of the esophageal epithelium. Proliferative cells, including various cultured cancer cell lines and basal cells in the esophageal epithelium, showed little expression of the NE-dlg protein. In addition, yeast two-hybrid screening and in vitro binding assays revealed that the NE-dlg interacted with the carboxyl-terminal region of the APC tumor suppressor protein. These data suggest that NE-dlg negatively regulates cell proliferation through its interaction with the APC protein.
Adaptor Proteins, Signal Transducing↗
Cloning and expression of cDNA encoding heart-type isoform of AMP deaminase.
Mouse cDNA for the heart-type (H) isoform of AMP deaminase (EC 3.5.4.6., AMPD) has been isolated and characterized. The cDNA for the Ampd gene expressed in heart is predicted to encode a peptide of 766 amino acids with a molecular mass of 88 kDa. The coding region of this cDNA was quite homologous to the human AMPD3 gene which encodes the erythrocyte-type (E) isoform of AMPD, although the H-isoform of rodent AMPD was reported to be immunologically distinct from the E-isoform of human AMPD. The non-coding region of the isolated cDNA is not homologous to human AMPD3, while rodent Ampd1 has similarity to human AMPD1 in the non-coding region as well as in the coding region. The transcripts for the cloned cDNA were expressed in heart, slow-twitch skeletal muscle and non-muscle tissues. Prokaryotic expression showed that this cDNA encodes a catalytically active enzyme which reacts to the specific antibody raised to the H-isoform of AMPD.
AMP Deaminase↗
Melanoma antigen-encoding gene-1 expression in invasive gastric carcinoma: correlation with stage of disease.
BACKGROUND: A human melanoma antigen-encoding gene-1, MAGE-1 gene, may be linked to the neoplastic transformation. In the present study, we extended this association with human gastric carcinomas. Specifically, we focused on the relationship between MAGE-1 gene expression and the histologic stage of gastric carcinoma. METHODS: We used a reverse transcription-polymerase chain reaction assay (RT-PCR) to analyze the expression of the MAGE-1 gene in 38 endoscopic biopsy specimens from gastric carcinomas. We also studied the relationship between the expression of MAGE-1 gene and the genetic expression of several tumor invasion-related factors, including 72 kD type IV collagenase (MMP2), urokinase-type plasminogen activator (uPA), platelet-derived growth factor A (PDGF-A), and vascular endothelial growth factor (VEGF). RESULTS: Eleven of the 38 tumor samples (28.9%) expressed the MAGE-1 gene. MAGE-1 gene expression was present only in two of the 38 adjacent nontumor samples (5.3%). MAGE-1 gene expression in the 38 tumor samples was significantly correlated with the histological stage of disease (P = 0.0008), especially with the depth of histologically confirmed tumor invasion (t1 vs. t2 or greater, P = 0.00048). The expression of MAGE-1 gene correlated with the expression of MMP2 (P = 0.0064), uPA (P = 0.0390), and PDGF-A (P = 0.00018). CONCLUSIONS: These data suggest that the MAGE-1 gene may be activated in gastric carcinomas during periods of their development or invasion. In addition, a relationship between MAGE-1 gene expression and expression of invasion-related factors has been demonstrated.
Antigens, Neoplasm↗
Preoperative assessment of tumor angiogenesis by vascular endothelial growth factor mRNA expression in homogenate samples of breast carcinoma: fine-needle aspirates vs. resection samples.
BACKGROUND AND OBJECTIVES: Tumor angiogenesis is receiving increased attention as a prognostic factor and also as a possible target for new anticancer agents. We investigated whether extent of vascular endothelial growth factor (VEGF) mRNA expression correlated with degree of neovascularization, and whether this expression in fine-needle aspirates could be a marker for assessing angiogenic potential of breast tumors. METHODS: VEGF mRNA expression was semiquantitated by reverse transcriptase-polymerase chain reaction (RT-PCR) followed by Southern blotting. Tumor neovascularization was assessed by immunohistochemical staining with anti-CD31 (PECAM) antibody. RESULTS: There was a positive correlation between degree of neovascularization and semiquantitated VEGF mRNA expression in invasive ductal carcinomas (r2 = 0.346, n = 48, P < 0.05). Extent of VEGF mRNA expression in fine-needle aspirates was closely correlated with that in resected invasive ductal carcinomas equal to or less than 3 cm in size (r2 = 0.874, n = 14, P < 0.05). CONCLUSION: These data suggest that semiquantitation of VEGF mRNA expression in fine-needle aspirates is useful for assessing angiogenic potential of invasive ductal carcinomas.
Biopsy, Needle↗
Genomic organization of Ampd3, heart-type AMPD gene, located in mouse chromosome 7.
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AMP Deaminase↗
Mouse Mef2b gene: unique member of MEF2 gene family.
The myocyte enhancer factor 2 (MEF2) gene family, which belongs to the MADS [MCM1, agamous, deficiens, serum response factor (SRF)] superfamily, is thought to play an important role in differentiation of myocytes, including cardiomyocytes. To better understand the mouse Mef2 gene family, the mouse Mef2b gene, which was found to be expressed in undifferentiated embryonal cells, was characterized. The Mef2b gene was found to be more than 30 kb in length, consisting of 11 exons. Eight exons correspond to coding regions and the remaining 3 exons for the 5' part are alternatively used. Two internal exons are subject to alternative splicing, resulting in production of four subtypes of mouse MEF2B peptides. Fluorescence in situ hybridization (FISH) and inter-specific backcross analysis identified the Mef2b gene locus. Mef2b gene was expressed in heart or skeletal muscle of early mouse embryo, but not in those of adult mouse. Functionally, mouse MEF2B did not exhibit DNA binding with the MEF2 consensus element in vitro, but did cause transcriptional activation of the MEF2 element, although it was less effective than human MEF2B. Based on these results, mouse MEF2B seems to have a unique character, distinct from other MEF2 family members.
Amino Acid Sequence↗
A new prognostic strategy for gastric carcinoma: mRNA expression of tumor growth-related factors in endoscopic biopsy specimens.
OBJECTIVE: The study analyzed the prognostic value of the transcription of several tumor growth-related genes in gastric carcinoma biopsy specimens. SUMMARY BACKGROUND DATA: The nodal status is one of the most significant prognostic factors in gastric carcinoma. There are, however, no satisfactory parameters for the preoperative assessment of nodal status. METHODS: A reverse transcriptase-polymerase chain reaction analysis was used to analyze the transcription of several tumor growth-related genes in endoscopic biopsy specimens from 78 gastric carcinomas. The factors examined were cyclin D1, cyclin E, urokinase-type plasminogen activator, 72-kd type IV collagenase, vascular endothelial growth factor, platelet-derived growth factor-A (PDGF-A), transforming growth factor-beta, and interleukin-10. The relation between the mRNA expression and the clinical pathologic parameters was analyzed statistically. RESULTS: The incidence of PDGF-A (p = 0.010) and transforming growth factor-beta (p = 0.009) mRNA expression increased as the pathologic stage advanced. Nodal metastasis correlated with cyclin D1 (p = 0.045), cyclin E (p = 0.037), urokinase-type plasminogen activator (p = 0.047), and PDGF-A (p = 0.003) mRNA. Interestingly, the expression of PDGF-A mRNA showed a positive correlation (p = 0.004) with the early presence of lymph node metastases. CONCLUSIONS: Tumor growth-related factor mRNA in biopsy specimens may be a new prognostic tool.
Biopsy↗
Immunosuppressive cytokines (IL-10, TGF-beta) genes expression in human gastric carcinoma tissues.
BACKGROUND: Contribution of immunosuppressive cytokines to tumor progression in many types of cancers has been suggested. To characterize the in vivo expression of immunosuppressive cytokines in gastric cancer, we analyzed the messenger RNA (mRNA) expression of transforming growth factor-beta (TGF-beta) and interleukin-10 (IL-10) in human gastric carcinoma tissues. METHODS: Both tumor tissues and nontumor tissues from each resected specimen of 29 primary gastric carcinomas were tested for IL-10 and TGF-beta mRNA expression by the reverse transcriptase-polymerase chain reaction (RT-PCR), and the mRNA expression was correlated with various pathological parameters of the tumors. RESULTS: Among the 29 tumors, mRNAs of TGF-beta and IL-10 were detected in 79% and 62% of tumor samples, respectively. These cytokines were detected only in 31% for TGF-beta and 17% for IL-10 in nontumor samples. Both mRNAs were frequently expressed in the poorly differentiated adenocarcinomas and the tumor tissues with high degree of stage or lymph node metastasis. CONCLUSIONS: Local expression of immunosuppressive cytokines may contribute to the progression of primary gastric carcinomas possibly through immunosuppression.
Actins↗
Induction of inflammatory cytokines in effusion cavity by OK-432 injection therapy for patients with malignant effusion: role of interferon-gamma in enhancement of surface expression of ICAM-1 on tumor cells in vivo.
The intracavitary injection of OK-432, a streptococcal preparation, has been shown to be an effective immunotherapy for patients with malignant effusion. We found that this therapy increases surface expression of intercellular adhesion molecule-1 (ICAM-1) on tumor cells, and that the degree of increased ICAM-1 was correlated with therapeutic effects. In the present study, we investigated the ability of OK-432-induced inflammatory cytokines, such as interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), and interleukin-1 beta (IL-1 beta), to enhance ICAM-1 expression. We treated 17 patients who had a malignant effusion with OK-432. At 24 hr after OK-432 injection, ICAM-1 levels on tumor cells were increased significantly in responders except in one case (n=9), whereas no change was evident in nonresponders except in two cases (n=8). Induced maximum levels of IFN-gamma in responders were significantly higher than those in nonresponders. In contrast, there was no significant difference in the induced TNF-alpha or IL-1 beta levels between the two groups. Two types of cultured tumor cells derived from responder patients were successfully established from the 17 different tumor cells in effusion. We performed an in vitro study using these cultured tumor cells. Treatment of the two cultured tumor cells with recombinant IFN-gamma, but not recombinant TNF-alpha or IL-1 beta, significantly increased their ICAM-1 expression to a clinically detectable level. Direct treatment of the tumor cells with cell-free effusion samples obtained from the same patients 24 hr after the therapy successfully increased ICAM-1 expression and this action was blocked completely only by a pretreatment with anti-IFN-gamma mAb. Our results suggests that in this therapy IFN-gamma plays a crucial role in enhancing ICAM-1 expression by tumor cells and that induced IFN-gamma levels may be a useful marker for evaluation of the therapeutic effect.
Aged↗
Role of nitric oxide derived from alveolar macrophages in the early phase of acute pancreatitis.
BACKGROUND: Acute pancreatitis is known to be often complicated by lung injury; however, the pathogenesis of lung injury in the early phase of acute pancreatitis remains unclear. Alveolar macrophages (AMs) have been suggested to contribute to lung injury by releasing various cytotoxic products including nitric oxide (NO). We investigated the role of AM-derived NO in the pathogenesis of lung injury during the early phase of acute pancreatitis. MATERIALS AND METHODS: Pancreatitis was induced in rats by selective pancreatic duct ligation (SPL). The mRNA expression of inducible NO synthase (iNOS) in AMs from rats after SPL (at 1, 2, 4, 6, 8, 12, 18, and 24 hr) was examined by reverse-transcriptase polymerase chain reaction method. The in vitro production of NO and superoxide by AMs 24 hr after SPL was measured and the cytotoxic effect of AMs on human umbilical vein endothelial cells (HUVECs) was examined with or without the NO synthase inhibitor L-NG-monomethyl-L-arginine (L-NMMA). The in vivo effect of L-NMMA on lung injury was also examined. RESULTS: In this model, serum amylase level peaked 24 hr after SPL, whereas PaO2 bottomed 24 hr after SPL. (In vitro) AMs expressed iNOS mRNA 6 hr after SPL and generated large amounts of NO and superoxide and demonstrated strong cytotoxicity against HUVECs significantly. This cytotoxicity was reduced by the administration of L-NMMA. (In vivo) L-NMMA administrated to rats with pancreatitis apparently reduced lung edema histologically and improved the PaO2. CONCLUSION: Our results suggest that, during early phase of acute pancreatitis, AM-derived NO contributes to lung injury. Administration of the NOS inhibitor L-NMMA prevented lung injury in this model.
Acute Disease↗
Vascular endothelial growth factor and platelet-derived growth factor are potential angiogenic and metastatic factors in human breast cancer.
BACKGROUND: Angiogenesis is a prerequisite for tumor growth and metastasis. Tumor angiogenesis may be mediated by several angiogenic factors such as vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF), transforming growth factor-alpha, and basic fibroblast growth factor. METHODS: Differential mRNA expressions of VEGF, PDGF (A chain), transforming growth factor-alpha and basic fibroblast growth factor in 32 primary invasive breast tumors were examined by reverse transcriptase-polymerase chain reaction. We analyzed relationships between mRNA expressions of these angiogenic factors and the degree of angiogenesis, tumor size, and metastasis. Quantification of angiogenesis was achieved by the immunohistochemical staining of endothelial cells with antibody to CD31. RESULTS: VEGF and PDGF-A mRNAs were expressed more frequently in breast tumors than in nontumor breast tissues, whereas no difference was found in expression frequency of either transforming growth factor-alpha or basic fibroblast growth factor mRNA. Vascular counts in tumors correlated with each expression frequency of VEGF and PDGF-A mRNA. PDGF-A mRNA was expressed more frequently in tumors with lymph node metastasis than in those without metastasis. CONCLUSIONS: Expression of VEGF and PDGF mRNAs detected by reverse transcriptase-polymerase chain reaction in breast tumors correlates with tumor-related characteristics of angiogenesis and metastatic potential. Analysis of these mRNAs by reverse transcriptase-polymerase chain reaction may be useful for assessing the biologic behavior of a breast tumor before surgical treatment.
Angiogenesis Inducing Agents↗
Subunit composition of AMPD varies in response to changes in AMPD1 and AMPD3 gene expression in skeletal muscle.
Adenosine monophosphate deaminase (AMPD), a central enzyme in energy metabolism in skeletal muscle, is encoded by a multigene family in higher eukaryotes. Denervation was used as a stimulus to induce a change in fiber type composition of rat gastrocnemius muscle and, consequently, gene expression. Specific antisera and nucleic acid probes were used to assess changes in expression of the AMPD1 and AMPD3 genes. Total AMPD activity in denervated skeletal muscle increased by 34%. The composition of the AMPD tetrameric holoenzyme was altered in two ways: The percentage of AMPD holoenzyme molecules consisting of one or more AMPD3 subunits increased three-fold, and the percentage of AMPD1 mRNA that excludes exon 2-encoded sequences doubled. These results suggest that expression of the AMPD1 and AMPD3 genes may be coordinated in myocytes to effect production of an AMPD holoenzyme of varying subunit composition.
AMP Deaminase↗
The MEF2B homologue differentially expressed in mouse embryonal carcinoma cells.
The MEF2 gene family encodes a MADS-box transcription factor which regulates expression of many muscle-specific genes. We examined the expression of the MEF2 genes in mouse embryonal carcinoma P19 cells before and after in vitro muscle differentiation induced by dimethyl sulfoxide (DMSO). At least three different MADS/MEF2 domains (MEF2A, 2B and 2D) were isolated from P19 cells with the MOPAC technique (mixed oligonucleotides primed amplification of cDNA). Although two of the MADS/MEF2 domain sequences were identical to those of human MEF2A and MEF2D, another domain sequence was similar but not identical to that of human MEF2B. While the transcription of MEF2A and MEF2D was up-regulated during differentiation of P19 cells, the MEF2B homologue was abundantly transcribed in undifferentiated P19, F9 and ES cells and down-regulated in adult heart, skeletal muscle or brain, suggesting that the murine MEF2B homologue might have a function distinct from other members of the MEF2 gene family in embryogenesis and development.
Amino Acid Sequence↗
CEA-mediated homotypic aggregation of human colorectal carcinoma cells in a malignant effusion.
This study was performed to clarify the role of carcinoembryonic antigen (CEA) in the aggregation of colorectal carcinoma (CRC) cells in malignant effusions. We analysed freshly purified CRC cells from one patient, which expressed CEA (98% positive cells) on the surface and formed huge cell aggregates in the patient's ascites. The carcinoma cells expressed Sialyl Lewis A (82%), Sialyl Lewis X (92%) and the beta 1 integrin subunit (78%) but did not express the pair-ligands for these molecules. Cell aggregation was completely inhibited by anti-CEA mAb. The decreased CEA expression induced by phosphatidylinositol-specific phospholipase C (PI-PLC) treatment led to decreased cell aggregation. We also examined the correlation between the degree of cell aggregation and CEA expression using smears of ascites fluid from 27 patients with colorectal cancer. There was a significant correlation between the degree of cell aggregation and CEA expression by CRC cells. The present study provided the first evidence that CEA molecules mediate the homotypic aggregation of CRC cells in malignant effusions.
Adenocarcinoma, Mucinous↗
A possible role of TGF-beta in the formation of malignant effusions.
The detailed mechanisms underlying the formation of malignant effusions are incompletely defined. In order to determine whether transforming growth factor-beta (TGF-beta) would contribute to the formation of malignant effusions, we investigated the effect of TGF-beta on the morphology, growth, and permeability of human mesothelial cells, which are thought to serve as a permeability barrier in the pleuroperitoneal cavities. Treatment of the mesothelial cells with a TGF-beta dose ranging from 0.1 to 10 ng/ml for 96 hr induced distinct morphologic changes in the cells. Each cell increased in size as did the volume of the intercellular spaces. TGF-beta also significantly inhibited the growth of mesothelial cells at a concentration ranging from 0.1 to 10 ng/ml. This growth inhibition was blocked completely by the addition of anti-TGF-beta antibody. Treatment of the mesothelial cells with 2.0 ng/ml TGF-beta significantly increased the permeability of a mesothelial cell monolayer as assessed by a FITC-albumin permeability assay. In our clinical analysis using 10 effusion samples obtained from patients with various types of carcinoma cells, considerable level of TGF-beta could be detected by ELISA, ranged from 0.90 to 8.75 ng/ml. Our data suggest that TGF-beta plays an important role in the formation of malignant effusions through structural and functional damage to the mesothelial cells. Malignant effusions may accumulate in the pleuroperitoneal cavity as a result of the mesothelial cell damage caused by this cytokine which is released from disseminated cancer cells.
Adult↗
Identification of functional domains in AMPD1 by mutational analysis.
AMP deaminase (AMPD) is a complex allosteric enzyme encoded by a multigene family in higher eukaryotes. The amino terminus of each AMPD gene is unique, while the mild and carboxy termini have been highly conserved among all the AMPD genes. Mutational analyses of the AMPD1 gene demonstrate that the catalytic site and a regulatory site, likely an ATP binding site, are located in the highly conserved carboxy terminus. Deletion mutants and a normal splice variant of AMPD1 demonstrate that the amino terminus has a profound influence on catalytic activity of AMPD and by inference from prior studies this region also influences binding of AMPD1 to myosin. Results of these studies suggest a regulatory model in which alternative splicing in the amino terminal region of AMPD1 generates isoforms of AMPD that exhibit differential sensitivity to effector molecules such as ATP.
AMP Deaminase↗