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author:("mérida, Paul")
1.  Prostatic Stones: Evidence of a Specific Chemistry Related to Infection and Presence of Bacterial Imprints 
PLoS ONE  2012;7(12):e51691.
Prostatic stones are a common condition in older men in industrialized countries. However, aging appears not to be the unique pathogenesis of these calcifications. Our morpho-constitutional investigation of 23 stone samples suggested that infection has a significant role in the lithogenic process of prostate calcifications, even without detection of infection by clinical investigation. Most stones (83%) showed bacterial imprints and/or chemical composition, suggestive of a long-term infection process. Chronic infection may induce persistent inflammation of the tissue and secondarily, a cancerization process within a few years. Thus, the discovery of prostate calcifications by computerized tomodensitometry, for example, might warrant further investigation and management to search for chronic infection of the prostate gland.
PMCID: PMC3521648  PMID: 23272143
2.  The prognostic value of FGFR3 mutational status for disease recurrence and progression depends on allelic losses at 9p22 
Developing molecular markers that define high-risk lesions is clinically critical for improving the prognosis determination of the tumors and their treatment. We decided to focus on the two pathways involving FGFR3 and allelic losses at 9p22 to identify a potential combined role in predicting tumor recurrence, progression and/or muscle. Microsatellite and mutational FGFR3 status analyses was performed in tumor tissue of 58 patients in a prospective unicentre study. The results of microsatellite and FGFR3 analyses were dichotomized as follows: loss of heterozygos-ity (LOH) versus retention of heterozygosity (ROH) on the one hand; mutant FGFR3 (mtFGFR3) versus wild-type FGFR3 (wtFGFR3) on the other hand. The combined 9p22/FGFR3 status was strongly correlated with stage (p=0.001) and grade (p<0.001) whereas the single FGFR3 mutational status was not able to predict recurrence, progression or muscle invasion. The survival curves corresponding to each combined status (mtFGFR3/ROH, wtFGFR3/ROH, mtFGFR3/LOH, wtFGFR3/LOH) were significantly different for recurrence (p=0.008), progression (p=0.046) and progression to muscle invasive disease (p=0.004). In case of 9p22 LOH, the FGFR3 mutational status was strongly associated with different clinical outcomes. In a multivariate model, the combined wtFGFR3/9p22 LOH status remained significant in predicting oncologic outcomes. FGFR3 mutations strongly characterize tumors with low malignant potential and favourable clinical outcome in case of allelic losses at 9p22, whereas its prognostic value becomes null or slightly inverts in case of allelic stability. Thus, our findings may also lead to further experiments in order to study interactions between FGFR3 and genes located at 9p22, as CDKN2A.
PMCID: PMC3186048  PMID: 21984968
Bladder cancer; FGFR3; loss of heterozygosity; prognosis; mutations

Results 1-2 (2)