HPV have been identified as high-risk and low-risk, depending on their association with the development of cancer. HPV infections can be facilitated by co-infection with HIV. Here, we investigated HPV prevalence and genotypes and the risk factors affecting HPV/HIV co-infection. Forty HIV-positive patients had 80 cervical swab samples collected in 2 consecutive years. Polymerase chain reaction and DNA direct sequencing were used to perform HPV genotyping. Statistical analyses were performed regarding risk factors for HPV/HIV co-infection and the occurrence of cervical lesions. HPV DNA was detected in 59 samples (73.75%), and high-risk HPVs were predominant (59.3%). The most prevalent type was HPV56 (17%), followed by HPV16 (15.3%). Patient age did not affect the risk of cervical cancer (P = .84) or HPV prevalence in different years (P = .25/P = .63). CD4 count also did not affect the risk for cervical lesions in the tested samples (P = .15/P = .28). Although the HIV viral load was not correlated with an increase in cervical lesion detection in the first group of analyzed samples (P = .12), it did affect cervical cancer risk in the group of samples analyzed in the following year (P = .045). HIV-infected patients presented a high prevalence of HPV co-infection, and HPV16 and HPV56 were the most prevalent genotypes. Considering this, it is possible that immunodeficiency can contribute to increased susceptibility to HPV56 infection in HIV-infected patients. The association between HIV viral load and the lesions also confirmed the importance of monitoring HIV/HPV co-infected patients with high HIV viral loads.

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BackgroundGlypican 3 (GPC3) is a member of the family of glypican heparan sulfate proteoglycans (HSPGs). The GPC3 gene may play a role in controlling cell migration, negatively regulating cell growth and inducing apoptosis. GPC3 is downregulated in several cancers, which can result in uncontrolled cell growth and can also contribute to the malignant phenotype of some tumors. The purpose of this study was to analyze the mechanism of action of the GPC3 gene in clear cell renal cell carcinoma.MethodsFive clear cell renal cell carcinoma cell lines and carcinoma samples were used to analyze GPC3 mRNA expression (qRT-PCR). Then, representative cell lines, one primary renal carcinoma (786-O) and one metastatic renal carcinoma (ACHN), were chosen to carry out functional studies. We constructed a GPC3 expression vector and transfected the renal carcinoma cell lines, 786-O and ACHN. GPC3 overexpression was analyzed using qRT-PCR and immunocytochemistry. We evaluated cell proliferation using MTT and colony formation assays. Flow cytometry was used to evaluate apoptosis and perform cell cycle analyses.ResultsWe observed that GPC3 is downregulated in clear cell renal cell carcinoma samples and cell lines compared with normal renal samples. GPC3 mRNA expression and protein levels in 786-O and ACHN cell lines increased after transfection with the GPC3 expression construct, and the cell proliferation rate decreased in both cell lines following overexpression of GPC3. Further, apoptosis was not induced in the renal cell carcinoma cell lines overexpressing GPC3, and there was an increase in the cell population during the G1 phase in the cell cycle.ConclusionWe suggest that the GPC3 gene reduces the rate of cell proliferation through cell cycle arrest during the G1 phase in renal cell carcinoma.

Background There is renewed interest in the role played by specific counter-regulatory mechanisms to control the inflammatory host response, poorly investigated in human pathology. Here, we monitored the expression of two anti-inflammatory mediators, annexin 1 and galectin-1, and assessed their potential link to glucocorticoids' (GCs) effective control of nasal polyposis (NP). Methods Total patterns of mRNA and protein expression were analysed by quantitative realtime PCR (qPCR) and Western blotting analyses, whereas ultrastructural immunocytochemistry was used for spatial localization and quantification of each mediator, focusing on mast cells, eosinophils and epithelial cells.Results Up-regulation of the annexin 1 gene, and down-regulation of galectin-1 gene, was detected in polypoid tissue compared with nasal mucosa. Patient treatment with betamethasone augmented galectin-1 protein expression in polyps. At the cellular level, control mast cells and eosinophils displayed higher annexin 1 expression, whereas marked galectin-1 immunolabelling was detected in the granule matrix of mast cells. Cells of glandular duct epithelium also displayed expression of both annexin 1 and galectin-1, augmented after treatment. Conclusion Mast cells and epithelial cells appeared to be pivotal cell types involved in the expression of both annexin 1 and galectin-1. It is possible that annexin 1 and galectin-1 could be functionally associated with a specific mechanism in NP and that GC exert at least part of their beneficial effects on the airway mucosa by up-regulating, in a specific cell target fashion, these anti-inflammatory agonists.

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