bluuebunny/crossref_metadata_2025_split huggingface dataset:
Overexpression of cyclooxygenase‐2 correlates with cytoplasmic HuR expression in salivary mucoepidermoid carcinoma but not in pleomorphic adenoma
Authors: Cho Nam‐Pyo , Han Hye‐Suk , Soh Yunjo , Son Hyun‐Jin 
Published: August 2010

Background:  The overexpression of cyclooxygenase (COX)‐2 in several human carcinomas suggests that COX‐2 is related to carcinogenesis. Although COX‐2 expression has been shown to be up‐regulated in carcinomas of the salivary gland, its mechanisms are not completely understood. HuR is an mRNA‐binding protein that controls the stability of certain transcripts including COX‐2.Methods:  The expression of COX‐2 and HuR was determined by immunohistochemistry in 28 cases of salivary pleomorphic adenoma and 18 cases of salivary mucoepidermoid carcinoma.Results:  28.6% and 72.2% of the pleomorphic adenomas and mucoepidermoid carcinomas showed high COX‐2 expression respectively. 35.7% of pleomorphic adenomas and 72.2% of mucoepidermoid carcinomas were tested positive for HuR in the cytoplasm of tumor cells. There was a correlation between a high COX‐2 immunoreactivity and cytoplasmic HuR expression in mucoepidermoid carcinomas but not in pleomorphic adenomas.Conclusion:  This study suggests that cytoplasmic HuR is correlated with COX‐2 expression in salivary mucoepidermoid carcinomas. In addition, the immunoreactivity of COX‐2 and cytoplasmic HuR might be used to evaluate the nature of a borderline malignancy in the salivary glands.
A possible CD1a Langerhans cell–mast cell interaction in chronic hyperplastic candidosis
Authors: Ali Ahmed , Rautemaa Riina , Hietanen Jarkko , Beklen Arzu , Konttinen Yrjö 
Published: August 2010

Aims:  T lymphocyte–antigen‐presenting cell (APC) interaction plays a central role in T lymphocyte activation and APC maturation. We therefore studied the CD1a‐positive Langerhans cells with respect to receptor activator of nuclear factor kappa B ligand (RANKL)‐positive cells in chronic hyperplastic candidosis (CHC).Materials and methods:  Tissue sections of CHC were compared with leukoplakia and healthy oral mucosa using RANKL and CD1a monoclonal antibodies in an avidin–biotin peroxidase complex protocol. Two different antigen‐retrieval protocols, pepsin preincubation and Tris–EDTA heat treatment, were used.Results:  CD1a‐positive Langerhans cells were in healthy and leukoplakia epithelium found in the middle layer, but in CHC in all layers of the epithelium, at the basement membrane and as mononuclear round cells in the lamina propria. Use of pepsin digestion enabled studies of mast cells and their activation in the form of degranulation of RANKL.Conclusions:  The numerical, morphological and topographical versatility of the CD1a‐positive Langerhans cells in CHC can be clarified by dendritic cell (DC) recruitment into the epithelium. RANK‐positive and RANKL‐sensitive DCs have ample opportunity to interact with local T lymphocytes. Use of an optimized antigen‐retrieval protocol enabled demonstration of an active engagement (degranulation) of mast cells, which represent a rapidly available source of soluble RANKL.
Frequent high telomerase reverse transcriptase expression in primary oral squamous cell carcinoma
Authors: Freier Kolja , Pungs Susanne , Flechtenmacher Christa , Bosch Franz X. , Lichter Peter , Joos Stefan , Hofele Christof 
Published: August 2010

Background:  Gene copy number gain of chromosomal arm 5p is frequently found in oral squamous cell carcinoma (OSCC) suggesting the activation of proto‐oncogenes. TERT is a candidate gene encoding for human telomerase reverse transcriptase (hTERT). The aim of the present study was to elucidate the relevance of TERT copy number gain and high hTERT expression in OSCC.Methods:  Fluorescence in situ hybridization (FISH) for TERT and immunohistochemistry (IHC) for hTERT were performed to analyze TERT copy numbers and hTERT expression, respectively, on tissue microarray (TMA) sections including n = 247 OSCC and n = 105 pharyngeal and laryngeal squamous cell carcinomas (PSCC/LSCC).Results:  Increased hTERT protein expression was more frequently found in OSCC (71.1%, 155/218) than in PSCC/LSCC (36.0%, 35/89) (P < 0.001). By contrast, specific TERT amplifications were less common in OSCC (2.1%, 4/191) compared with PSCC/LSCC (9.9%, 8/81) (P = 0.047).Conclusions:  High hTERT expression is a frequent finding in OSCC. It might be a promising target for the development of specific anti‐neoplastic therapy approaches.
Up‐regulation of vascular endothelial growth factor in synovial fibroblasts from human temporomandibular joint by hypoxia
Authors: Ke Jin , Liu Yu , Long Xing , Li Jian , Fang Wei , Meng Qinggong , Zhang Yufeng 
Published: August 2010

Introduction:  Enhanced expression of vascular endothelial growth factor (VEGF) has been described in patients with internal derangement (ID). Herein, we examined the expression of VEGF in synovial fibroblasts from temporomandibular joint (TMJ) under hypoxia and investigated the regulation of hypoxia‐inducible factor‐1α (HIF‐1α) involved in the expression of VEGF.Methods:  Synovial fibroblasts were prepared from human TMJ. These cells were incubated under hypoxia or normoxia for the indicated time periods. VEGF levels in cultured supernatant were measured by an ELISA. VEGF mRNA isoforms and stability were assessed using RT‐PCR and Northern blot analysis respectively. HIF‐1α accumulation was evaluated by Western blotting and immunofluorescence.Results:  VEGF were significantly induced by hypoxia in synovial fibroblasts. In response to hypoxia, VEGF121 and VEGF165 mRNA were both remarkably increased, while there was no change in VEGF mRNA stability. The accumulation and nuclear translocation of HIF‐1α occurred under hypoxia.Conclusions:  Hypoxia may mainly induce the expression of VEGF121 and VEGF165 in synovial fibroblasts to promote inflamed angiogenesis of TMJ. HIF‐1α, which is clearly activated in response to hypoxia, may control the expression of VEGF in synovial fibroblasts from TMJ.
Immunohistochemical characterization of capsular cells in neuromuscular spindles of the neck
Authors: Triantafyllou Asterios 
Published: August 2010

Background:  To identify capsular components of neuromuscular spindles in man by means of immunohistochemistry.Methods:  Investigation of histologically observed neuromuscular spindles in surgical specimens with the use of markers for sheath cells and basement membranes.Results:  Epithelial membrane antigen and CD34 immunoreactivities were found in the outer and inner capsular layers, respectively. S‐100 protein was not expressed in the capsules and there was more collagen type IV than laminin.Conclusions:  Cells resembling perineurial cells and endoneurial fibroblasts, and basement membrane rich in collagen type IV comprise the capsules of neuromuscular spindles.
Sentinel lymph nodes in cancer of the oral cavity: is central step‐sectioning enough?
Authors: Thomsen Jørn Bo , Christensen Rikke Kølby , Sørensen Jens Ahm , Krogdahl Annelise 
Published: August 2010

Background:  Extended histopathologic work‐up has increased the detection of micrometastasis in sentinel lymph nodes in malignant melanoma and breast cancer. The aim of this study was to examine if (A) step‐sectioning of the central 1000 μM at 250 μM levels with immunostaining were accurate when compared with (B) step‐sectioning and immunostaining of the entire sentinel lymph node at 250 μM levels.Methods:  Forty patients with T1/T2 cN0 oral cancer were enrolled. Three patients were excluded. In one patient no sentinel lymph node was identified. The remaining two had unidentified sentinel lymph nodes due to lymphoscintigraphic and surgical sampling error. The central 1000 μM of 147 sentinel lymph nodes were step‐sectioned in 250‐μm intervals and stained with hematoxylin and eosin and CK‐KL1. All lymph nodes were recorded as negative or positive for macrometastases or micrometastases. After inclusion of the last patient the residual tissue of the lymph nodes was totally step‐sectioned at 250‐μm intervals and re‐classified. The tumor deposits were divided into macrometastases and micrometastases and ITC.Results:  Method (A) upstaged 17 lymph nodes and 11 patients compared with method (B), which upstaged 22 lymph nodes and 11 patients. Seven of the patients with positive lymph nodes did not change stage. However, four lymph nodes changed from micrometastases to macrometastases. One patient changed from a micrometastasis to four micrometastases. One pN2c patient with bilateral micrometastases did not change stage, but an additional ipsilateral lymph node with a micrometastasis was identified.Conclusion:  Larger tumor deposits and more metastases are identified by more extensive sectioning of the sentinel lymph nodes. None of the patients was false‐negative due to histopathologic sampling error, but the results indicate that central step‐sectioning of the central 1000 μM cannot completely be relied upon for accurate staging of the patients.
Stromal myofibroblasts in central giant cell granuloma of the jaws cannot distinguish between non‐aggressive and aggressive lesions
Authors: Vered Marilena , Nasrallah Warda , Buchner Amos , Dayan Dan 
Published: August 2010

Objective:  To investigate correlations between myofibroblast density (MFD) and biological behavior of a large series of non‐aggressive and aggressive central giant cell granuloma lesions (CGCGs).Methods:  Twenty‐four non‐aggressive and 17 aggressive lesions were immunohistochemically stained with alpha smooth muscle actin. MFD was assessed using the point counting method in the lesions’ core tissue and in control areas that consisted of non‐involved, connective tissue surrounding the lesion.Results:  All CGCGs contained myofibroblasts among the stromal cells. No significant differences were found in the mean percentage of MFD (%MFD) of non‐aggressive (20.8 ± 15.7%) and aggressive (23.7 ± 22.9%) lesions (P > 0.05) or in the mean %MFD of the respective control areas (1.4 ± 2.2% and 1.7 ± 4.1%; P > 0.05). The mean core tissue %MFD of both lesion types was significantly higher than that of the control areas (P < 0.001).Conclusion:  Myofibroblasts were an integral component of CGCG stromal cells, but their density could not distinguish between non‐aggressive and aggressive lesions.
Diagnostic delay of oral squamous cell carcinoma in two diagnosis centers in Córdoba Argentina
Authors: Morelatto R. A. , Herrera M. C. , Fernández E. N. , Corball A. G. , López de Blanc S. A. 
Published: August 2010

Abstract:  The aim of the present study was to investigate diagnostic delay in oral cancer (OC) in two diagnosis centers in Córdoba, Argentina. Special attention was paid to the role of the patient and the professional in the diagnostic delay.Methods:  Seventy clinical records of patients with newly diagnosed oral squamous cell carcinoma were included.Results:  Both patients and professionals were responsible for the delay in diagnosis. This delay was longer for tumors in early stages. Multiple logistic regression analysis indicated that the professional delay was the most associated variable to the stage of tumor (P = 0.03).Conclusions:  Continuing education in OC and pre‐cancerous lesions is important to reduce the professional delay. The findings of the present study also indicate that 58% of the patients are partially responsible for delay in the diagnosis of OC. Intensive public promotion and educational campaigns against OC are also needed to increase patient awareness.
Presence of ghost cells and the Wnt signaling pathway in odontomas
Authors: Tanaka Akio , Okamoto Motoyoshi , Yoshizawa Dai , Ito Shigeru , Alva Patricia González , Ide Fumio , Kusama Kaoru 
Published: August 2010

Background:  Although it has been reported that ghost cells are present in odontomas, the generation mechanism of these cells is unclear. To evaluate the presence of ghost cells and involvement of the Wnt signaling pathway, we examined the expression of hard keratins, β‐catenin and Lef‐1 in odontomas.Methods:  Sixty‐nine cases of odontoma were examined immunohistochemically with the use of antibodies against human hair proteins, β‐catenin and Lef‐1.Results:  Expression of hard keratins was found only in the cytoplasm of ghost cells in 46 (66.7%) of the 69 odontomas. Compound odontomas (78.8%) showed a higher incidence of ghost cells than complex odontomas (29.4%). Histopathologically, ghost cells were found within odontogenic epithelium adjacent to immature enamel and in the centre of Liesegang‐ring‐like calcified materials. Expression of β‐catenin and Lef‐1 was observed in the cytoplasm and nucleus of odontogenic epithelial cells adjacent to the ghost cells in immature odontomas.Conclusion:  These findings suggest that odontoma is a hard keratin‐expressing tumor‐like lesion, and that the Wnt signaling pathway may be involved in the formation of ghost cells in odontomas.
Functional −1562 C‐to‐T polymorphism in matrix metalloproteinase‐9 (MMP‐9) promoter is associated with the risk for oral squamous cell carcinoma in younger male areca users
Authors: Tu Hsi‐Feng , Wu Cheng‐Hsien , Kao Shou‐Yen , Liu Chung‐Ji , Liu Tsung‐Yun , Lui Man‐Tin 
Published: August 2010

Background:  Circulating matrix metalloproteinase‐9 (MMP‐9) is a prognostic factor for gastric cancer and vascular diseases, and has been associated with head and neck cancers. The −1562 C‐to‐T polymorphism in MMP‐9 promoter (abbreviated MMP‐9−1562 C>T polymorphism) leads to differential transcription, and is associated with increased susceptibility to neoplastic and vascular diseases. Thus, our aim was to determine whether a functional MMP‐9 polymorphism might also influence the risk or affect the progression of areca‐associated oral cancers.Methods:  Genomic DNAs were obtained from peripheral blood cells of male subjects with areca‐associated oral squamous cell carcinoma (OSCC) (n = 192), oral submucosal fibrosis (OSF) (n = 73), and non‐diseased areca users (n = 191). The PCR‐based restriction fragment length polymorphism analysis was performed for MMP‐9 genotyping.Results:  MMP‐9
−1562 C>T polymorphism was not associated with the risk of OSCC or OSF. However, when subjects were stratified by the median age, an association with the risk of OSCC was found in younger patients (P = 0.029). The T allele frequency was significantly higher in the subset of older patients with buccal mucosa OSCC than older patients with OSCC in counterpart locations. The joint MMP‐9−1562 C>T and MMP‐3−1171 5A>6A functional polymorphisms were not associated with OSCC risk or patient survival.Conclusion:  Aberrant MMP‐9 expression is closely related to tumor invasiveness and the prognosis of head and neck cancers. However, functional MMP‐9−1562 C>T polymorphism is associated with OSCC risk only in younger areca chewers. The impact of aging or areca‐related effect on this functional polymorphism should be elucidated.
Immunohistochemical detection of uPA, uPAR, PAI‐1, and maspin in ameloblastic tumors
Authors: Kumamoto H. , Ooya K. 
Published: August 2010

Background:  To evaluate the roles of extracellular matrix (ECM)‐degrading serine proteinase in progression of odontogenic tumors, expression of urokinase‐type plasminogen activator (uPA), uPA receptor (uPAR), plasminogen activator inhibitor‐1 (PAI‐1), and maspin was analyzed in ameloblastic tumors as well as in tooth germs.Methods:  Tissue specimens of 10 tooth germs, 45 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the use of antibodies against uPA, uPAR, PAI‐1, and maspin.Results:  Immunohistochemical reactivity for uPA, uPAR, PAI‐1, and maspin was detected in normal and neoplastic odontogenic tissues: uPA was recognized predominantly in mesenchymal cells, uPAR was evident in epithelial cells, PAI‐1 was found in both epithelial and mesenchymal cells, and maspin was expressed only in epithelial cells. The levels of uPA and uPAR immunoreactivity in ameloblastic tumors were slightly higher than the levels in tooth germs, while PAI‐1 reactivity in ameloblastomas tended to be lower than that in tooth germs. The level of maspin immunoreactivity in ameloblastomas was significantly higher than that in tooth germs, and ameloblastic carcinoma showed decreased maspin reactivity.Conclusion:  Expression of uPA, uPAR, PAI‐1, and maspin in tooth germs and ameloblastic tumors suggests that interactions among these molecules contribute to ECM degradation and cell migration during tooth development and tumor progression. Altered expression of the serine proteinase and its associated molecules in ameloblastic tumors may be involved in oncogenesis of odontogenic epithelium.
Immunohistochemical detection of phosphorylated JNK, p38 MAPK, and ERK5 in ameloblastic tumors
Authors: Kumamoto H. , Ooya K. 
Published: August 2010

Background:  To evaluate roles of mitogen‐activated protein kinases (MAPKs) in oncogenesis and cytodifferentiation of odontogenic tumors, expression of phosphorylated JNK (p‐JNK), p38 MAPK (p‐p38 MAPK), and ERK5 (p‐ERK5) was analyzed in ameloblastic tumors as well as in tooth germs.Methods:  Ten tooth germs, 47 ameloblastomas, and 5 malignant ameloblastic tumors were examined immunohistochemically with the antibodies against p‐JNK, p‐p38 MAPK, and p‐ERK5.Results:  Immunoreactivity for p‐JNK was detected in epithelial or neoplastic cells detached from the basement membrane in 7 tooth germs and 7 ameloblastomas, and the expression levels of p‐JNK in ameloblastic tumors were significantly lower than that in tooth germs. Expression of p‐p38 MAPK was found in epithelial or neoplastic cells in tooth germs and ameloblastic tumors except for two ameloblastomas, and increased expression was found in keratinizing cells of acanthomatous ameloblastomas. The expression level of p‐p38 MAPK in ameloblastomas was significantly higher than the levels in tooth germs and malignant ameloblastic tumors. Immunoreactivity for p‐ERK5 was found predominantly in epithelial or neoplastic cells near the basement membrane in tooth germs and ameloblastic tumors. The expression levels of p‐ERK5 in ameloblastic tumors were slightly higher than that in tooth germs, and plexiform ameloblastomas showed significantly higher p‐ERK5 expression than follicular ameloblastomas.Conclusion:  Expression of p‐JNK, p‐p38 MAPK, and p‐ERK5 in tooth germs and ameloblastic tumors suggests that these MAPK signaling pathways contribute to cell proliferation, differentiation, or apoptosis in both normal and neoplastic odontogenic tissues. Altered expression of these phosphorylated MAPKs in ameloblastic tumors may be involved in oncogenesis and tumor cell differentiation.
Investigation of functional gene polymorphisms: IL‐1B, IL‐6 and TNFA in benign migratory glossitis in Brazilian individuals
Authors: Guimarães André Luiz Sena , Correia‐Silva Jeane de Fátima , Diniz Marina Gonçalves , Xavier Guilherme Machado , Horta Martinho Campolina Rebello , Gomez Ricardo Santiago 
Published: August 2010

Background:  Benign migratory glossitis (BMG) is a very common immunological oral disease of unknown aetiology.Methods and subjects:  Fifty‐three consecutive subjects affected by BMG and 53 age‐ and sex‐matched control subjects were genotyped for IL‐1B, IL‐6 and TNFA polymorphisms. Binary logistic regression models were fitted and values of P < 0.05 were considered significant.Results:  A significant difference in the distribution of IL‐1B genotypes was observed in the group with BMG in univariate analyses (P = 0.01). The multivariate analyses showed that the CT genotype of the IL1‐B gene was significantly associated with a high risk to develop BMG (P = 0.02, OR 2.76). The combined presence of IL‐1β high and intermediate producers genotypes was also associated with BMG in multivariate analyses (P = 0.01, OR 3.05). IL‐6 and TNFA polymorphisms were not associated with BMG in the univariate and multivariate analyses.Conclusion:  Our findings demonstrate that the polymorphism +3954 IL‐1B is associated with an increased risk of BMG development and suggest a genetic basis for disease development.
In vitro candidacidal activity of a synthetic killer decapeptide (KP) against Candida albicans cells adhered to resin acrylic discs
Authors: Manfredi M. , Merigo E. , Salati A. , Conti S. , Savi A. , Polonelli L. , Bonanini M. , Vescovi P. 
Published: August 2010

Background:  Oral Candida spp., and C. albicans in particular, are considered as important aetiological agents in the pathogenesis of denture‐induced stomatitis. Several studies have reported that C. albicans is able to easily adhere to different medical devices, such as vascular and urinary catheters or acrylic denture surfaces, and that adhesion is a fundamental step in the initial pathogenic process of colonization and further possible infection. Recently, a synthetic decapeptide (KP) derived from the sequence of a single‐chain recombinant anti‐idiotypic antibody, acting as a functional internal image of a microbicidal, broad spectrum yeast killer toxin, has been reported to kill in vitro C. albicans cells and to exert a therapeutic activity against experimental mucosal and systemic candidiasis.Methods:  The aim of this study was to evaluate, through a CFU assay, the candidacidal activity of KP on sanded acrylic resin discs, previously colonized by C. albicans cells.Results and conclusions: At 100 μg/ml KP showed over 90% of killing activity on C. albicans cells adhered to resin discs, when compared with a scramble peptide used as control. The results of this study suggest a potential effect of KP on C. albicans cells adhered on the surface of resin materials, such as prosthetic dentures.
Analysis of the neoplastic nature and biological potential of sporadic and nevoid basal cell carcinoma syndrome‐associated keratocystic odontogenic tumor
Authors: Katase Naoki , Nagatsuka Hitoshi , Tsujigiwa Hidetsugu , Gunduz Mehmet , Tamamura Ryo , Pwint Han Phuu , Rivera Rosario Santos , Nakajima Motowo , Naomoto Yoshio , Nagai Noriyuki 
Published: August 2010

Background:  Keratocystic odontogenic tumor (KCOT), also known as odontogenic keratocyst, is a benign cystic neoplasm, which may be associated with nevoid basal cell carcinoma syndrome (NBCCS) and if it does, will occur as multiple cystic lesions. KCOT is locally destructive despite its bland histological features. However, the neoplastic nature of KCOT is not well established.Heparanase is an endo‐d‐glucuronidase enzyme that specifically cleaves heparan sulfate (HS) and the increase of its level in tumors promotes invasion, angiogenesis, and metastasis.Methods:  To investigate the neoplastic character of KCOT, we studied the localization patterns of heparanase in KCOT, focusing on the differences between sporadic and NBCCS‐associated KCOTs, by immunohistochemistry and in situ hybridization. To compare the expression pattern of these cysts with non‐tumorous odontogenic developmental cyst, dentigerous cyst was included.Results:  All the odontogenic cysts showed positive immunoreaction for heparanase protein in various intensities. The expression pattern of heparanase gene corresponded to that of protein expression. Interestingly, intense gene and protein expressions were observed in KCOT associated with NBCCS compared with sporadic ones and dentigerous cyst.Conclusions:  The results implied that heparanase expression may be correlated with the neoplastic properties of KCOT, particularly in NBCCS‐associated cases.