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The Journal focuses on the morphological study of the disease process and\u002For mechanisms. For human pathology, morphological investigation receives priority but manuscripts describing the result of any ancillary methods (cellular, chemical, immunological and molecular biological) that complement the morphology are accepted. Manuscript on experimental pathology that approach pathologenesis or mechanisms of disease processes are expected to report on the data obtained from models using cellular, biochemical, molecular biological, animal, immunological or other methods in conjunction with morphology. 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The role of E‐ and N‐cadherin, however, in hepatocellular carcinoma (HCC) has not yet been elucidated. The aim of the present study was to investigate the expression pattern of E‐ and N‐cadherin in surgically resected HCC specimens according to their relationship with clinicopathological features. The expression patterns of E‐ and N‐cadherin were evaluated on immunohistochemistry in 68 specimens of HCC and adjacent non‐tumor tissue. The most different expression pattern between HCC and non‐tumor tissue was the decreased staining intensity of E‐cadherin (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 37, 54%) and the dot‐like discontinuous staining of N‐cadherin (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 35, 55%). Decreased intensity of E‐cadherin and discontinuous staining of N‐cadherin in HCC was correlated with advanced stage. The risk factors for expression patterns related to recurrence were loss of E‐cadherin expression (odds ratio (OR) = 3.6; 95% confidence interval (CI): 1.1–12.4) and discontinuous staining of N‐cadherin (OR = 1.6; 95% CI: 0.8–3.2). In conclusion, discontinuous staining of N‐cadherin and loss of E‐cadherin expression in HCC predicts a high risk of recurrence after surgical treatment.\u003C\u002Fjats:p>",{"EN":163},"Expression of E‐ and N‐cadherin and clinicopathology in hepatocellular carcinoma",{"VOID":165},"18801083",{"VOID":167},"10.1111\u002Fj.1440-1827.2008.02282.x","PUBLICATION","2024-09-11T23:58:02.603+00:00","Author affiliation is blank",[172],"EN","https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1111\u002Fj.1440-1827.2008.02282.x",[175,186,195,217,229,241,253,264,275],{"id":176,"sortIndex":64,"researcher":24,"roles":177,"affiliations":178,"properties":179},"ae79e56b-39e0-4d79-83a2-c0aaef2d356d",[],[],{"openalex":180,"orcid":182,"title":184},{"VOID":181},"A5100438953",{"VOID":183},"https:\u002F\u002Forcid.org\u002F0000-0002-2356-7822",{"EN":185},"Hyun Soo 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JW, 2005, Epidemiology of hepatocellular carcinoma in Korea, Korean J Hepatol, 11, 303",{},{"id":24,"text":332,"url":24,"identifiers":333},"10.1002\u002Fhep.1840120411",{"doi":332},{"id":24,"text":335,"url":24,"identifiers":336},"10.1002\u002Fhep.1840160122",{"doi":335},{"id":24,"text":338,"url":24,"identifiers":339},"10.1097\u002F01.sla.0000201480.65519.b8",{"doi":338},{"id":24,"text":341,"url":24,"identifiers":342},"10.1002\u002Fjso.20389",{"doi":341},{"id":24,"text":344,"url":24,"identifiers":345},"10.1016\u002Fj.ceb.2005.08.014",{"doi":344},{"id":24,"text":347,"url":24,"identifiers":348},"10.3748\u002Fwjg.v11.i20.3139",{"doi":347},{"id":24,"text":350,"url":24,"identifiers":351},"Ross JS, 1994, E‐cadherin expression in prostatic carcinoma biopsies: Correlation with tumor grade, DNA content, pathologic stage and clinical outcome, Mod Pathol, 7, 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Primary liver cancer in Japan, 1990, Clinicopathologic features and results of surgical treatment, Ann Surg, 211, 277",{},{"id":24,"text":368,"url":24,"identifiers":369},"Matsumura T, 2001, Frequent down‐regulation of E‐cadherin by genetic and epigenetic changes in the malignant progression of hepatocellular carcinomas, Clin Cancer Res, 7, 594",{},{"id":24,"text":371,"url":24,"identifiers":372},"10.1038\u002Fsj.bjc.6690431",{"doi":371},{"id":24,"text":374,"url":24,"identifiers":375},"10.1002\u002Fhep.1840180402",{"doi":374},{"id":24,"text":377,"url":24,"identifiers":378},"10.1053\u002Fjhep.2002.35342",{"doi":377},{"id":24,"text":380,"url":24,"identifiers":381},"10.1002\u002Fhep.510230621",{"doi":380},{"id":24,"text":383,"url":24,"identifiers":384},"Huang GT, 1999, Correlation of E‐cadherin expression and recurrence of hepatocellular carcinoma, Hepatogastroenterology, 46, 1923",{},{"id":24,"text":386,"url":24,"identifiers":387},"10.1046\u002Fj.1440-1746.2003.03021.x",{"doi":386},{"id":24,"text":389,"url":24,"identifiers":390},"10.1016\u002FS0092-8674(01)00365-8",{"doi":389},{"id":24,"text":392,"url":24,"identifiers":393},"Gwak GY, 2006, Anti‐apoptotic N‐cadherin signaling and its prognostic implication in human hepatocellular carcinomas, Oncol Rep, 15, 1117",{},false,{"id":396,"createTime":397,"updateTime":397,"relativeEntities":398,"slug":399,"properties":400,"entityType":168,"verifyStatus":414,"verifyTime":397,"verifyNote":415,"syncStatus":23,"languages":416,"translateLanguages":24,"viewCount":25,"primaryUrl":417,"fullTextUrl":24,"authors":418,"publicationType":284,"publisherRelationship":627,"citationCount":132,"citationInfo":665,"publishDate":667,"publishYear":668,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":669,"isForceReanalyzing":394},"7e2b530a-a57a-4bae-b4b9-f212dcc7ce50","2024-10-12T23:55:50.217+00:00",[],"Altered-expression-of-microRNA-miR-21-miR-155-and-let-7a-and-their-roles-in-pulmonary-neuroendocrine-tumors",{"mag":401,"keywords":403,"openalex":404,"abstract":406,"title":408,"pm":410,"doi":412},{"VOID":402},"2107044147",{},{"VOID":405},"W2107044147",{"EN":407},"\u003Cjats:p>MicroRNA (miRNA) has a critical effect on tumorigenesis through post‐transcriptional modification and is considered to be potential biomarkers for cancer diagnosis and treatment monitoring. We evaluated the expression pattern of three selected miRNAs (miR‐21, miR‐155, and let‐7a) to evaluate their potential roles by quantitative reverse transcription‐polymerase chain reaction using formalin‐fixed and paraffin‐embedded tissues of 63 surgically resected pulmonary neuroendocrine (NE) tumors (19 typical carcinoids (TCs), 6 atypical carcinoids (ACs), 19 large cell NE carcinomas (LCNECs), and 19 small cell lung carcinomas (SCLCs). Control amplification for U6 small nuclear RNA (U6) was performed in all samples. Normalized Ct values were calculated (Ct\u003Cjats:sub>Experimental miRNA\u003C\u002Fjats:sub>‐Ct\u003Cjats:sub>U6\u003C\u002Fjats:sub>) for each case and recorded. The expression levels of miR‐21 and miR‐155 were significantly higher in high‐grade NE carcinomas (LCNECs and SCLCs) than in carcinoid tumors (TCs and ACs) (each \u003Cjats:italic>P\u003C\u002Fjats:italic> &lt; 0.001). The expression level of miR‐21 in carcinoid tumors with lymph node metastasis was significantly higher than in carcinoid tumors without lymph node metastasis (\u003Cjats:italic>P\u003C\u002Fjats:italic>= 0.010). To the best of our knowledge, the present study is the first to examine the expression patterns of miR‐21 and miR‐155 as an adjunctive diagnostic tool or clinically relevant biomarkers for pulmonary NE tumors.\u003C\u002Fjats:p>",{"EN":409},"Altered expression of microRNA miR‐21, miR‐155, and let‐7a and their roles in pulmonary neuroendocrine tumors",{"VOID":411},"22924844",{"VOID":413},"10.1111\u002Fj.1440-1827.2012.02845.x","VERIFIED","Auto 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Particularly, the similarity of genomic alterations between Fe‐NTA‐induced renal cancer and human cancers suggests that excess iron plays a role also in human carcinogenesis. Furthermore, excess iron is a major pathology in asbestos‐induced mesothelioma, including chrysotile. Despite an analogy to asbestos, multi‐wall carbon nanotubes were distinct in that diameter is another responsible factor for mesothelial carcinogenesis. Recently, non‐thermal plasma emerged as a candidate for medical intervention for wounds and cancers via manipulating oxidative stress. 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cross‐section or longitudinal section, it is difficult to investigate longitudinal features of myocardial cells in the whole heart. Here, introducing the use of tangential sections to obtain longitudinal aspect of myocardial cells in any part of myocardium, the authors evaluated myocardium in the left ventricle in 10 normal hearts and four hearts with hypertrophic cardiomyopathy (HCM). Tangential sections were obtained by peeling the superficial layer of myocardium. After peeling the whole surface, secondary deep layer was peeled. These procedures were repeated more than five times through the wall. Intercalated discs (ICD) were observed immunohistochemically with anti‐N‐cadherin and antidesmoplakin. In normal hearts, myocardial cells were cut longitudinally and ran parallel in tangential sections. They linked end‐to‐end with simple and regular ICD with average lengths of 120–130 µm and average sarcomere numbers of 56–65. In HCM hearts, many myocardial cells were cut almost longitudinally running approximately parallel in tangential sections. Myocardial cells frequently showed side‐to‐side linking characterized by skewed ICD, indistinct ICD counterparts, and longitudinally arranged ICD. Two young HCM hearts had circle‐shaped ICD and vacuole‐like structures highlighted by immunostaining for N‐cadherin, which were actually extracellular structures comparable with irregular side‐to‐side linking. It is considered that side‐to‐side linking of myocardial cells is a characteristic microscopic feature in HCM rather than myocardial disarray.\u003C\u002Fjats:p>",{"EN":2086},"Side‐to‐side linking of myocardial cells in hypertrophic cardiomyopathy: Whole heart microscopic observation with tangential 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II. Spatio‐temporal appearance of proteins involved in cell‐cell contact and communication. Formation of two distinct N‐cadherin\u002Fcatenin complexes, J Cell Sci, 109, 11, 10.1242\u002Fjcs.109.1.11",{"doi":2283},"10.1242\u002Fjcs.109.1.11",{"id":24,"text":2285,"url":24,"identifiers":2286},"10.1242\u002Fjcs.00258",{"doi":2285},{"id":24,"text":2288,"url":24,"identifiers":2289},"10.1006\u002Fjmcc.1999.1086",{"doi":2288},{"id":24,"text":2291,"url":24,"identifiers":2292},"Ferreira‐Cornwell MC, 2002, Remodeling the intercalated disc leads to cardiomyopathy in mice misexpressing cadherins in the heart, J Cell Sci, 115, 1623, 10.1242\u002Fjcs.115.8.1623",{"doi":2293},"10.1242\u002Fjcs.115.8.1623",{"id":24,"text":2295,"url":24,"identifiers":2296},"10.1016\u002Fj.cardiores.2003.08.005",{"doi":2295},{"id":24,"text":2298,"url":24,"identifiers":2299},"Hertig CM, 1996, N‐cadherin in adult rat cardiomyocytes in culture. I. 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Stromal characteristics including cellularity, atypia, mitosis, overgrowth, tissue fragmentation, and the tumor margin were assessed. Benign\u002Fborderline\u002Fmalignant phyllodes tumor (PT) were diagnosed in 90 (69.8%)\u002F30 (23.3%)\u002F9 (7.0%) patients. Among the 90 cases of benign PTs, 67 cases (74.4%) were diagnosed concordantly in CNB. For borderline and malignant PTs, three out of eight (26.6%) and four out of nine (44.4%) cases were diagnosed concordantly in CNBs. All 50 cases of discordant diagnosis were underestimated in matched CNBs, especially in their stromal cellularity and mitosis. The size of tumor is larger in discordant cases of PT (\u003Cjats:italic>P\u003C\u002Fjats:italic>= 0.013). The concordant rate of diagnosis between CNB and surgical excision was about 60% and accordingly, grading of PT based on the histological findings in CNBs has limitation. The discordance comes from heterogeneous stromal properties of PTs.\u003C\u002Fjats:p>",{"EN":2378},"Comparative study of histological features between core needle biopsy and surgical excision in phyllodes 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PP, 2001, Rosen's Breast Pathology, 163",{},{"id":24,"text":2476,"url":24,"identifiers":2477},"10.1016\u002Fj.amjsurg.2006.04.007",{"doi":2476},{"id":24,"text":2479,"url":24,"identifiers":2480},"10.1016\u002F0046-8177(92)90268-8",{"doi":2479},{"id":24,"text":2482,"url":24,"identifiers":2483},"Elston CW, 1998, Systemic Pathology, 147",{},{"id":24,"text":2485,"url":24,"identifiers":2486},"10.1309\u002F5N2C4N5XCB8XW8JL",{"doi":2485},{"id":24,"text":2488,"url":24,"identifiers":2489},"10.1111\u002Fj.1365-2559.2010.03607.x",{"doi":2488},{"id":24,"text":2491,"url":24,"identifiers":2492},"10.1001\u002Farchsurg.138.9.987",{"doi":2491},{"id":24,"text":2494,"url":24,"identifiers":2495},"10.1111\u002Fj.1365-2559.2007.02786.x",{"doi":2494},{"id":24,"text":2497,"url":24,"identifiers":2498},"10.1111\u002Fj.1365-2559.2010.03514.x",{"doi":2497},{"id":24,"text":2500,"url":24,"identifiers":2501},"10.1177\u002F1066896907311378",{"doi":2500},{"id":24,"text":2503,"url":24,"identifiers":2504},"Anderson BO, 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22‐year‐old man presented with a growing lump on the fifth metatarsal of the right foot. Radiographically, the lesion was a calcified mass stuck on to the bone. The T\u003Cjats:sub>2\u003C\u002Fjats:sub>‐weighted magnetic resonance images showed heterogeneity in intensity. A tumor was suspected and an excisional biopsy was done. The lesion was composed of a cartilaginous cap and bone tissue. Histological examination revealed characteristic features of bizarre parosteal osteochondromatous proliferation (BPOP), such as hypercellularity, a blue tinctorial quality in the osteocartilaginous interfaces, and a scattering of binucleated or bizarre enlarged chondrocytes. Immunohistochemically, basic fibroblast growth factor was expressed in nearly all chondrocytes within the cartilaginous cap, while vascular endothelial growth factor was expressed only in enlarged chondrocytes near the osteocartilaginous interfaces. Reverse transcription–polymerase chain reaction detected chondromodulin‐I transcripts in the tissue of the cartilaginous cap. These findings indicate that the processes occurring in BPOP are similar to those occurring in endochondral ossification in the growth plate, and they support the concept that BPOP is a reparative process. BPOP is a rare tumorous lesion of the bone and is occasionally confused with other benign or malignant conditions. Thus, it is important to consider the clinical, radiographical and the gross histological features of the lesion when making a diagnosis.\u003C\u002Fjats:p>",{"EN":2525},"Bizarre parosteal osteochondromatous proliferation (Nora’s lesion) of the 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Pathol., 147, 1592",{},{"id":24,"text":2678,"url":24,"identifiers":2679},"10.1111\u002Fj.1365-2559.1993.tb00075.x",{"doi":2678},{"id":24,"text":2681,"url":24,"identifiers":2682},"10.1016\u002FS1079-2104(99)70222-2",{"doi":2681},{"id":24,"text":2684,"url":24,"identifiers":2685},"10.1177\u002F107110070002100509",{"doi":2684},{"id":24,"text":2687,"url":24,"identifiers":2688},"Twiston Davies CW., 1985, Bizarre parosteal osteochondromatous proliferation in the hand. A case report., J. Bone. Joint Surg. 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During the last quarter of this century, glomerular changes such as IgA nephropathy have also been observed in cases associated with other diseases, such as systemic lupus erythematosus, Schoenlein‐Henoch purpura, liver cirrhosis and chronic inflammatory diseases of the lung. This evidence supports the idea of an IgA nephropathy syndrome. On the other hand, IgA is thought to be an important humoral factor at the mucosal immune system and appears to have an antibody function against various etiologic candidates of extrinsic or intrinsic substances at the mucosal and systemic immune system. Glomerular IgA deposition in IgA nephropathy syndrome is thought to result from elevated levels of circulating immune complexes or aggregated IgA due to an overproduction of polymeric IgA as antibodies in the serum and due to the clearance impairment of IgA immune complexes in the hepatic and splenic phagocytic system. The glomerular IgA subclass is not one‐sided, but should be evaluated in comparison with the age of patients at renal biopsy; this indicates the approximate age of onset. Cirrhotic IgA glomerulonephritis is not related to Hepatitis B or C virus infection, but to the pathophysiologic condition of liver cirrhosis. Various etiologic candidates such as viral, microbial, dietary antigens or auto‐antigens have been listed and experimental models of IgA nephropathy syndrome have provided some clues in understanding the etiology of primary IgA nephropathy. However much still remains to be clarified and some specific epitopes common among these etiologic candidates will have to be identified.\u003C\u002Fjats:p>",{"EN":2765},"Etiology of IgA nephropathy 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