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ABSTRACT: PC cell-derived growth factor (PCDGF) is an autocrine growth factor originally purified from the highly tumorigenic teratoma PC cell line. It participates in tumorigenesis and tumour progression through upregulation of cyclin D1. To date, there has been no report on the role of PCDGF in skin cancer, to our knowledge.
To investigate the expression of PCDGF and cyclin D1 in basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and seborrhoeic keratosis (SK), and their relationship with the clinicopathological parameters of SCC.
Immunohistochemical expression of PCDGF and cyclin D1 was examined in 42 SCC, 30 BCC and 20 SK tissues.
PCDGF and cyclin D1 were overexpressed in SCC or BCC tissues compared with normal skin or SK, and their expressions were significantly higher in SCC than in BCC. Moreover, positive expression of PCDGF and cyclin D1 was significantly correlated with depth of invasion and metastasis of SCC. There was significant correlation between PCDGF and cyclin D1 expression in SCC.
Expression of PCDGF and cyclin D1 plays an important role in the tumorigenesis of BCC and SCC. Abnormal expression of PCDGF and Cyclin D1 may be related to invasion and metastasis of SCC.
Clinical and Experimental Dermatology 03/2012; 37(4):411-7. · 1.20 Impact Factor
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ABSTRACT: This pilot study investigated the antibiofilm effects of glass-ionomer cements (GICs) and resin-modified glass-ionomer cements (RMGICs) incorporated with chlorhexidine (CHX) in vivo.
Experimental GICs and RMGICs containing 2% CHX were obtained by mixing CHX with the powder of GICs (CHXGIC) and RMGICs (CHXRMGIC). Four groups of specimens were prepared in a standardized size. After polishing and sterilization, they were bonded to the buccal surface of the molars in the first and second quadrant of volunteers and left untouched for 4 hours and 24 hours, respectively. The bacterial vitality of plaque was then analysed by confocal laser scanning microscopy (CLSM). The bacterial morphology and biofilm accumulation were determined by scanning electron microscopy (SEM). The pH value of biofilm was assessed by Plaque Indicator Kits.
CLSM analysis revealed that bacterial vitality of the biofilm on CHXGIC and CHXRMGIC was significantly lower than that on GIC and RMGIC. SEM analysis indicated that the morphology of bacteria on CHXGIC and CHXRMGIC was irregular. The pH value of biofilm on the experimental materials presented no statistically significant difference.
Twenty-four hour bacterial vitality on GICs and RMGICs with CHX are lower in micro-organisms than on conventional GICs and RMGICs.
Australian Dental Journal 03/2012; 57(1):58-64. · 1.19 Impact Factor
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ABSTRACT: Signal transducers and activators of transcription 3 (STAT3) is a central cytoplasmic transcription factor and regulates a number of pathways important in tumorigenesis including cell cycle progression, apoptosis, tumor angiogenesis, invasion and metastasis.This study aims to investigate the expression of pSTAT3, VEGF and VEGF-C in pancreatic adenocarcinoma and their relations to the clinicopathological features, tumor angiogenesis and prognosis. In the present study, the expression of pSTAT3, VEGF and VEGF-C and microvascular density (MVD) were examined via immunohistochemistry. The clinicopathological information was collected and patients were regularly followed up. The relationship between the parameters and the clinicopathological features were analyzed, and the univariate and multivariate prognostic factors were also analyzed. The expression of pSTAT3 in tumor tissues was significantly higher in contrast to that in normal tissues, and pSTAT3 was related to VEGF and VEGF-C expression, MVD, tumor size, lymphogenous status and TNM staging (P<0.05). Survival analysis suggested that tumor size, TNM staging, pSTAT3 and VEGF expression were risk factors of prognosis, but no independent factors were found. We concluded that pSTAT3, which was a risk factor of prognosis, was abnormally expressed in pancreatic adenocarcinoma and related to tumor size, TNM staging and lymphatic metastasis. pSTAT3 may promote tumor angiogenesis via up-regulating VEGF on protein and even gene levels, and enhance the early lymphatic metastasis through VEGF-C. Better understanding of STAT3 signaling pathways in angiogenesis may contribute to the development of novel therapeutic strategies in angiogenesis and metastasis of pancreatic cancer.
Neoplasma 11/2011; 59(1):52-61. · 1.44 Impact Factor
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ABSTRACT: Raf kinase inhibitor protein (RKIP) may be a suppressor of metastasis: RKIP levels are high in normal tissues, low in primary cancers and lowest or absent in metastatic cancers. This immunohisto chemistry study investigated RKIP protein levels in 250 clinical specimens of human cervical tissue and lymph node metastases (LNM) from 210 patients with normal cervical tissue, cervical intra-epithelial neoplasia (CIN), or cervical cancer with/without LNM. Thirty-nine (86.7%) of the 45 normal-tissue samples were RKIP-positive, six (13.3%) were RKIP-negative; 48/60 (80.0%) CIN samples were positive, 12 (20.0%) were negative; 47/105 (44.8%) cervical cancer tissue samples were positive, 58 (55.2%) were negative; only 7/40 (17.5%) LNM tissue samples were positive, 33 (82.5%) were negative. There was no significant correlation between RKIP positivity and clinical stage, microscopic subtype or pathological differentiation grade. RKIP positivity correlated inversely with LNM. RKIP may play a role in cervical-cancer genesis and metastasis; RKIP down-regulation was associated with metastatic disease in human cervical cancer.
The Journal of international medical research 01/2011; 39(1):229-37. · 0.90 Impact Factor
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Electrochimica Acta. 54(21):4783-4788.
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ABSTRACT: We previously reported that transgenic (Tg) mice expressing human angiotensin-converting enzyme 2 (hACE2), the receptor for severe acute respiratory syndrome coronavirus (SARS-CoV), were highly susceptible to SARS-CoV infection, which resulted in the development of disease of various severity and even death in some lineages. In this study, we further characterized and compared the pathogeneses of SARS-CoV infection in two of the most stable Tg lineages, AC70 and AC22, representing those susceptible and resistant to the lethal SARS-CoV infection, respectively. The kinetics of virus replication and the inflammatory responses within the lungs and brains, as well as the clinical and pathological outcomes, were assessed in each lineage. In addition, we generated information on lymphocyte subsets and mitogen-mediated proliferation of splenocytes. We found that while both lineages were permissive to SARS-CoV infection, causing elevated secretion of many inflammatory mediators within the lungs and brains, viral infection appeared to be more intense in AC70 than in AC22 mice, especially in the brain. Moreover, such infection was accompanied by a more profound immune suppression in the former, as evidenced by the extensive loss of T cells, compromised responses to concanavalin A stimulation, and absence of inflammatory infiltrates within the brain. We also found that CD8(+) T cells were partially effective in attenuating the pathogenesis of SARS-CoV infection in lethality-resistant AC22 mice. Collectively, our data revealed a more intense viral infection and immunosuppression in AC70 mice than in AC22 mice, thereby providing us with an immunopathogenic basis for the fatal outcome of SARS-CoV infection in the AC70 mice.
J Virol. 83(11):5451-65.
