Mangin P

PGE2 and LTB4 tissue levels in benign and cancerous prostates.

PGE2 and LTB4 are involved in inflammation and carcinogenesis in several tissues but have not been studied in prostate cancer and hyperplasia until now. We therefore measured PGE2 and LTB4 productions in a total of 206 prostate tissues from 116 patients including benign hyperplastic (90), pericancerous (106) and cancerous samples (10). We also analysed the influence of inflammation levels, prostate volume and glandular to epithelial ratio. PGE2 and LTB4 concentrations were measured using specific enzyme immunoassay kits. There was a correlation between PGE2 level, prostatic volume, inflammation score, and decreased glandular surface. By contrast, there was no correlation between LTB4 levels and inflammation or PGE2 production. Cancerous samples had higher LTB4 levels than pericancerous samples, but there was no difference in PGE2 levels. PGE2 and inflammation may be associated to stromal benign prostatic hyperplasia whereas LTB4 may play a role in prostate carcinogenesis.

Differential expression of 37 selected genes in hormone‐refractory prostate cancer using quantitative taqman real‐time RT‐PCR

Progression of prostate cancer to androgen independence remains the primary obstacle to improved survival. The development of more effective treatments depends on our understanding of the molecular events associated with the hormone‐refractory stage. We quantified, among 90 screened genes, the expression of 37 target genes, using real‐time quantitative RT‐PCR. Gene expression was studied in 13 samples of HPRC compared to 33 clinically localised cancers and normal prostate tissue. We identify 19 genes with significant differential expression in HRPC compared to localised prostate cancer. Genes with decreased expression included receptors for growth factors, MMR genes and the serine protease hepsin. Analysis of increased gene expression confirmed the importance of AR upregulation and highlighted genes not previously linked to HRPC, including enzymes involved in steroid synthesis and the antiapoptotic factor survivin. Progression of prostate cancer to the hormone‐refractory state is associated with differential gene expression, which may prove useful for both understanding disease progression and the development of new therapeutic approaches.

Impact de l'obésité sur le PSA lors du dépistage du cancer de la prostate

Resume But L’obesite est associee a des modifications seriques des taux d’androgenes et d’oestrogenes qui pourraient moduler le metabolisme prostatique. L’objectif de ce travail etait de rechercher un lien entre le taux de PSA et le degre d’obesite sur une population candidate au depistage du cancer de la prostate afin de determiner si une adaptation du taux de PSA avant biopsie devrait etre exploree. Materiel Lors d’une campagne de depistage dans un arrondissement francais, les resultats d’un PSA serique et de l’index de masse corporelle (IMC) etait disponible chez 541 hommes. Ces hommes etaient repartis dans 4 groupes de corpulence : Normal (IMC Resultats Le PSA moyen pour chaque groupe diminuait de maniere inversement proportionnelle a l’IMC, avec un taux moyen de 3.7, 2.9, 2.6 et 1.5 pour les groupes Normal, Surpoids, Obesite I et Obesite II+III respectivement. Il existait une difference significative entre ces groupes (p = 0.03). Il existait egalement une correlation inverse entre IMC et PSA (r = 0.1, p = 0.01). Conclusion Dans une population soumise au depistage, le PSA est d’autant plus faible que l’IMC est grand. Une adaptation du seuil de depistage du PSA selon l’IMC devrait etre exploree.