Materials and Methods: The study population included 177 men elig

Materials and Methods: The study population included 177 men eligible for active surveillance who fulfilled clinicobiological criteria and biopsy criteria as group 1-less than 3 positive cores and

less than 3 mm total tumor length, group 2-less than 3 positive cores with cancer involvement of less than 50% in any core and group 3-less than 33% of positive cores. Prostate specific antigen density cutoffs were also studied in these groups. Pathological findings on radical prostatectomy specimens and biochemical recurrence-free survival were studied. Median followup after radical prostatectomy was 34 months.

Results: A majority of Gleason score 6 disease was observed in group 1 (51.7%) whereas a majority of Gleason score 7 or greater disease was reported in groups 2 (53.6%) Selleck R788 and 3 (55.4%). Extracapsular extension was noted in 17.5% of radical prostatectomy specimens in group 3 vs 11.2% in group 1 (p = 0.175). The risk of AZD5153 mw overall unfavorable disease (defined as pT3-4 stage and/or Gleason score 8 or greater) was significantly higher in men with cancer involvement of 3 mm or greater on initial biopsy (27.3% vs

13.5%, respectively, p = 0.023). The 3-year biochemical recurrence-free survival rate was 94.0% and was not affected by the 3 active surveillance definitions.

Conclusions: Even with the use of a 21-core biopsy protocol the rate of unfavorable disease in radical prostatectomy specimens remains increased in men eligible for active surveillance. Patients must be informed of this risk of misclassification. which ranges from 20% to 28% in men who fulfill the less stringent biopsy criteria.”
“Elucidation of the cellular and molecular mechanisms of the circadian clock, along with the realization that these mechanisms are operative in both central and peripheral tissues, has revolutionized circadian biology. Tyrosine-protein kinase BLK Further, these

observations have resulted in an explosion of interest in the health implications of circadian organization and disorganization at both molecular and physiological levels. Thus, recent research has implicated mutations and polymorphisms of circadian clock genes in diabetes and obesity, cardiovascular disease, and cancer. At the neuro-behavioral level, circadian clock genes have also been implicated in sleep disorders, drug and alcohol addiction, and other psychiatric conditions. While such findings are frequently described as revealing “”non-circadian”" effects of clock genes, it remains possible that most of these non-circadian effects are in fact secondary to the loss of cellular and systemic rhythmicity. This review summarizes the evidence linking circadian clock genes to biobehavioral dysregulation, and considers criteria for defining a pleiotropic clock gene effect as non-circadian. (C) 2010 Elsevier Ltd. All rights reserved.

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