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Diez B.,University of Oviedo | Hidalgo A.,University of Oviedo | Hidalgo A.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa
Gaceta Sanitaria | Year: 2012

Objectives: To determine advertising pressure in three Spanish gynecology journals, to describe the characteristics of the drugs advertised and to analyze compliance with current regulatory standards in drug advertisements. Methods: We identified the number of advertisements, the characteristics of the drugs advertised, the minimum information required by legislation and the advertising message in the selected journals. Results: A total of 139 advertisements were identified, corresponding to 33 distinct products (28 prescription medicines and five over-the-counter drugs). Advertising pressures were 18.13% in Progresos de Obstetricia y Ginecología, 16.18% in Acta Ginecológica and 5.21% in Clínica e Investigación en Ginecología y Obstetricia. Legislative failure occurred in 82.14% of the advertisements and in 22.22% of slogans, while 41.46% of advertising messages were misleading. Conclusion: A critical attitude to advertising among health professionals is advisable. Information contained in advertisements should be contrasted with official and other independent sources. © 2011 SESPAS.


Delgado-Calle J.,University of Cantabria | Sanudo C.,University of Cantabria | Fernandez A.F.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Garcia-Renedo R.,Hospital U.M. Valdecilla | And 2 more authors.
Epigenetics | Year: 2012

Osteoblasts are specialized cells that form new bone and also indirectly influence bone resorption by producing factors that modulate osteoclast differentiation. Although the methylation of CpG islands plays an important role in the regulation of gene expression, there is still scanty information about its role in human bone. The aim of this study was to investigate the influence of CpG methylation on the transcriptional levels of two osteoblast-derived critical factors in the regulation of osteoclastogenesis: the receptor activator of nuclear factor NFκB ligand (RANKL) and its soluble decoy receptor osteoprotegerin (OPG). Quantitative methylation specific PCR (qMSP) and pyrosequencing analysis in various cell types showed that the methylation of regulatory regions of these genes, in the vicinity of the transcription start sites, repressed gene transcription, whereas an active transcription was associated with low levels of methylation. In addition, treatment with the DNA demethylating agent 5-azadeoxycitidine promoted a 170-fold induction of RANKL and a 20-fold induction of OPG mRNA expression in HEK-293 cells, which showed hypermethylation of the CpG islands and barely expressed RANKL and OPG transcripts at baseline. Transcriptional levels of both genes were also explored in bone tissue samples from patients with hip fractures and hip osteoarthritis. Although RANKL transcript abundance and the RANKL:OPG transcript ratio were significantly higher in patients with fractures than in those with osteoarthritis (RANKL: 0.76 ± 0.23 vs. 0.24 ± 0.08, p = 0.012; RANKL:OPG: 7.66 ± 2.49 vs. 0.92 ± 0.21, p = 0.002), there was no evidence for differential methylation across patient groups. In conclusion, the association between DNA methylation and the repression of RANKL and OPG expression strongly suggests that methylation-dependent mechanisms influence the transcription of these genes, which play a critical role in osteoclastogenesis. However, other mechanisms appear to be involved in the increased RANKL/OPG ratio of patients with osteoporotic fractures. © 2012 Landes Bioscience.


Lopez F.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Garcia Inclan C.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Perez-Escuredo J.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Alvarez Marcos C.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | And 4 more authors.
Oral Oncology | Year: 2012

Objetives: Despite improvements in the field of surgery and radiotherapy, the overall prognosis of sinonasal carcinomas is poor, mainly due to the difficulty to resect the tumour completely in this anatomically complex region. Therefore, there is great need for alternative treatments. Knowledge of the KRAS and BRAF mutational status would become clinically important with regard to the possible use of anti-EGFR therapies. Material and methods: DNA was extracted from paraffin embedded tumour samples from 57 cases of sinonasal squamous cell carcinoma (SNSCC) and from fresh frozen tumour samples from 58 cases of intestinal-type sinonasal adenocarcinoma (ITAC). Point mutations were analysed for KRAS exon 2 (codons 12 and 13) and BRAF (exon 15, V600E) by direct sequencing. Results: Neither KRAS nor BRAF showed any mutations in the SNSCC, whereas 7/58 (12%) ITAC harboured KRAS mutations and no BRAF mutations. All seven cases with KRAS mutation concerned well-differentiated and less aggressive (papillary and colonic type) ITAC, all patients being woodworkers and 4/7 tobacco smokers. Conclusion: Neither of SNSCCs carried mutations in KRAS and BRAF and a low frequency of KRAS mutation was found in ITAC. This suggests that KRAS and BRAF mutations play a limited role in the development of sinonasal cancer and that mutation analysis is not useful as a screening test for sensitivity to anti-EGFR therapy in sinonasal cancer. © 2012 Elsevier Ltd. All rights reserved.


Martinez J.G.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Perez-Escuredo J.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Castro-Santos P.,University of Oviedo | Marcos C.A.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | And 4 more authors.
Cellular Oncology | Year: 2012

Background Head and neck squamous cell carcinoma (HNSCC) is a tumour type that generally carries very complex chromosomal aberrations. An interesting feature is the elevated occurrence (58 %) of whole arm translocations and isochromosomes, resulting from breakage and illegitimate recombination in centromeric or pericentromeric regions. We hypothesized that alterations in DNA methylation may play a role in the breakage of centromeric repeat sequences in these tumours. Methods We studied the DNA methylation status of global repeats (LINE-1), subtelomeric repeats (D4Z4) and centromeric repeats (SAT-a) in relation to centromeric instability in a series of HNSCC cancer cell lines and primary tumours. We analysed the methylation status by pyrosequencing and the chromosomal aberrations by microarray CGH. Results We found a significant association between centromeric instability and hypomethylation of LINE-1, but not D4Z4 and SAT-a. Conclusion These data suggest that centromeric instability is associated with genomic DNA hypomethylation only when occurring at specific DNA repeat sequences. © International Society for Cellular Oncology 2012.


Torano E.G.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Petrus S.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Fernandez A.F.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Fraga M.F.,Instituto Universitario Of Oncologia Del Principado Of Asturias Iuopa | Fraga M.F.,CSIC - National Center for Biotechnology
Clinical Chemistry and Laboratory Medicine | Year: 2012

DNA methylation is one of the best-known epigenetic modifications in mammals. The alteration of DNA methylation patterns has been found to be related to many diseases, including cancer. It is well-known that during carcinogenesis, a sitespecific DNA hypermethylation and a global DNA hypomethylation take place. This overall loss of DNA methylation has been proposed as a valid biomarker for cancer. Given its medical utility, in recent years it has become apparent that there is a need to develop methods for the analysis of DNA methylation using different approaches: global, locus-specific, or genome-wide. Here we review some of these techniques and discuss their potential clinical utility. © 2012 by Walter de Gruyter. Berlin. Boston.

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