Estudi de les característiques dels tumors vesicals primaris en funció de la simptomatologia i de la demora en el tractament

L'alta incidència dels tumors vesicals primaris no infiltrants de la muscular pròpia (TNIMP) en el nostre medi fa que moltes vegades es dilati el temps entre el moment de la consulta i el de la intervenció. Volem analitzar si el motiu de consulta i la demora en el tractament influeixen en les característiques d'aquests tumor

Estudi de la recidiva a la primera cistoscòpia dels tumors vesicals superficials primaris en funció del grup de risc

Els tumors vesicals superficials presenten un alt índex de recidiva, essent la recidiva als 3 mesos un factor demostrat de progressió a tumor infiltrant. Per tal d'evitar aquesta recurrència precoç es porten a terme diferents pautes de tractament adjuvan

Valor de l'index de masa corporal (IMC)com a factor pronòstic en el CCR

Sobreprès i obesitat es consideren factors de risc acceptats en el desenvolupament del CCR. L'IGF-1 sembla ser un dels factors responsables donat el seu conegut efecte mitògenic i antiapoptòtic així com la seva capacitat d'interacció amb els sistemes de peroxidació lipídica cel·lular. A diferència d'altres neoplàsies com el CaP, on un IMC elevat és correlaciona amb un pitjor pronòstic, són pocs els estudis publicats fins al moment en CCR, però sembla que en aquest tumors l'IMC elevat podria tenir un efecte protector

Pieloplàstia oberta vs. laparoscòpia: revisió de la nostra sèrie

Si bé la pieloplàstia ha estat des de sempre el tractament d'elecció al nostre centre per l'estenosi pieloureteral, des de fa 4 anys hem optat per l'abordatge laparoscòpic a l'hora de portar a terme aquesta tècnica. Volem comparar el resultat tant clínic com funcional de les pieloplàsties obertes (PO) i laparoscòpiques (PL) portades a terme al nostre centre durant els darrers 8 any

Anàlisi de la concentració sèrica de vitamina D com a factor de risc de càncer de pròstata i agressivitat tumoral

Alguns estudis observacionals han suggerit que el dèficit de vitamina D podria relacionar-se amb un major risc de càncer de pròstata i amb una major incidència en àrees geogràfiques de menor insolació. L'objectiu d'aquest estudi ha sigut relacionar els nivells sèrics de vitamina D i parathormona amb el risc de càncer de pròstata i amb la agressivitat tumora

Prostate cancer genetic propensity risk score may modify the association between this tumour and type 2 diabetes mellitus (MCC-Spain study)

Background: Some studies have reported an inverse association between type 2 diabetes mellitus (T2DM) and prostate cancer (PCa), but results on this issue are still inconsistent. In this study, we evaluate whether this heterogeneity might be related to differences in this relationship by tumour or by individual genetic susceptibility to PCa. Methods: We studied 1047 incident PCa cases and 1379 randomly selected controls, recruited in 7 Spanish provinces for the population-based MCC-Spain case-control. Tumour were classified by aggressiveness according to the International Society of Urological Pathology (ISUP), and we constructed a PCa polygenic risk score (PRS) as proxy for genetic susceptibility. The epidemiological questionnaire collected detailed self-reported data on T2DM diagnosis and treatment. The association between T2DM status and PCa was studied by fitting mixed logistic regression models, and, for its association by aggressiveness of PCa, with multinomial logistic regression models. To evaluate the possible modulator role of PRS in this relationship, we included the corresponding interaction term in the model, and repeated the analysis stratified by PRS tertiles. Results: Globally, our results showed an inverse association between T2DM and overall PCa limited to grade 1 tumours (ORISUP = 1: 0.72; 95% CI: 0.53-0.98), which could be compatible with a detection bias. However, PCa risk also varied with duration of diabetes treatment -inversely to metformin and positively with insulin-, without differences by aggressiveness. When we considered genetic susceptibility, T2DM was more strongly associated with lower PCa risk in those with lower PRS (ORtertile 1: 0.31; 95% CI: 0.11-0.87), independently of ISUP grade. Conclusions: Our findings reinforce the need to include aggressiveness and susceptibility of PCa, and T2DM treatments in the study of the relationship between both diseases

Anàlisi epidemiològica i patològica dels tumors germinals testiculars durant el període 1996-2004

Els tumors germinals testiculars són neoplàssies poc freqüents, representant un 1-2% dels tumors que afecten al varó jove. No obstant sembla que en els últims anys estem assistint a un augment de la seva incidència tal i com ho reflexen algunes dades de la literatura mèdica. La cirurgia juntament amb els protocols de quimioteràpia actuals permeten assolir alts nivells de curaci

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10−15), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe