Low detectable prostate specific antigen after radical prostatectomy--treat or watch?

PURPOSE: We determined whether the pattern of low detectable prostate specific antigen during the first 3 years of followup after radical prostatectomy would predict subsequent biochemical recurrence. MATERIALS AND METHODS: An institutional database was queried to identify 1,136 patients who underwent open retropubic or robot-assisted radical prostatectomy between January 5, 1993 and December 29, 2008. After applying exclusion criteria we used serum prostate specific antigen and the prostate specific antigen pattern during the first 3 years of followup to divide 566 men into 3 groups, including 1) undetectable prostate specific antigen (0.03 ng/ml or less), 2) low detectable-stable prostate specific antigen (greater than 0.03 and less than 0.2 ng/ml, no 2 subsequent increases and/or prostate specific antigen velocity less than 0.05 ng per year) and 3) low detectable-unstable prostate specific antigen (greater than 0.03 and less than 0.2 ng/ml, 2 subsequent increases according to NCCN criteria and/or prostate specific antigen velocity 0.05 ng per year or greater). The primary end point was biochemical recurrence, defined as prostate specific antigen 0.2 ng/ml or greater, or receipt of radiation therapy beyond 3 years of followup. RESULTS: Seven-year biochemical recurrence-free survival was 95%, 94% and 37% in the undetectable, low detectable-stable and low detectable-unstable groups, respectively (log rank test p <0.0001). On multivariate analysis the prostate specific antigen pattern during 3 years postoperatively (undetectable vs low detectable-unstable HR 15.9 and vs low detectable-stable HR 1.6), pathological T stage (pT2 vs greater than pT2 HR 1.8), pathological Gleason score (less than 7 vs 7 HR 2.3 and less than 7 vs 8-10 HR 3.3) and surgical margins (negative vs positive HR 1.8) significantly predicted biochemical recurrence. CONCLUSIONS: The combination of prostate specific antigen velocity and NCCN criteria for biochemical recurrence separated well men with low detectable prostate specific antigen after radical prostatectomy into those who required treatment and those who could be safely watched.

At the crossroad between obesity and gastric cancer.

Obesity has reached epidemic proportions worldwide with disproportionate prevalence in different communities and ethnic groups. Recently, the American Medical Association recognized obesity as a disease, which is a significant milestone that opens the possibilities of treating obesity under standardized health plans. Obesity is an inflammatory disease characterized by elevated levels of biomarkers associated with abnormal lipid profiles, glucose levels, and blood pressure that lead to the onset of metabolic syndrome. Interestingly, inflammatory biomarkers, in particular, have been implicated in the risk of developing several types of cancer. Likewise, obesity has been linked to esophageal, breast, gallbladder, kidney, pancreatic, and colorectal cancers. Thus, there exists a link between obesity status and tumor appearance, which may be associated to the differential levels and the circulating profiles of several inflammatory molecules. For example, mediators of the inflammatory responses in both obesity and gastric cancer risk are the same: pro-inflammatory molecules produced by the activated cells infiltrating the inflamed tissues. These molecules trigger pathways of activation shared by obesity and cancer. Therefore, understanding how these different pathways are modulated would help reduce the impact that both diseases, and their concomitant existence, have on society.