The median survival of patients with a CA 19-9 less than the post-Proteasome inhibitor treatment median was 13.5 months compared with 7.2 months for those with a CA 19-9 level greater than the median (P=0.003). Patients with no decline in CA 19-9 had a significantly lower tumor response rate and a significantly worse overall survival (6 months compared to 13.9 months, P=0.0002). On multivariate analysis, pretreatment CA Inhibitors,research,lifescience,medical 19-9 values greater than and less than the median value of 420 U/mL, post-treatment CA 19-9 values, and a tumor marker decrease during therapy were significantly independent prognostic factors for overall survival. In another concurrent CRT
with conventional fractionation as the primary treatment in sixty-nine patients with LAPC, Koom et al. documented that the powerful cutoff points were pretreatment CA 19-9 level of 1,200 U/mL, post-treatment CA 19-9 level of 100 U/mL, and CA 19-9 decline of 40% (11). Their
data support the theory that post-treatment CA19-9 levels and CA19-9 decline are significant prognostic factors. These results are Inhibitors,research,lifescience,medical very similar to our findings in the present study. On univariate analysis, Inhibitors,research,lifescience,medical we found that post CRT CA 19-9 <50 U/mL, post CRT CA 19-9 <85.5 U/mL, percent change ≥90%, and histologic grade all showed prognostic significance predictor of survival. The median survival of patients with a CA 19-9 less than the post-treatment median was 10.3 months compared with those with a CA 19-9 level greater than the median value of 85.5 U/mL (P=0.0242). Our results were confirmed on multivariate analysis Inhibitors,research,lifescience,medical showing that a post treatment CA 19-9 level less than the median value of 85.5 U/mL was an independent prognostic factor for overall survival. A strength of our study was that the first post-CRT CA 19-9 levels was tested in 50 point increments and percent change in pre and post
treatment CA 19-9 was tested in 10% increments. This allowed us to detect subtle incremental changes that would otherwise not have been detected if a different method Inhibitors,research,lifescience,medical was used. In addition, all patients with a serum bilirubin more than 2 mg/dL at the time of CA 19-9 measurement were excluded to account for altered biliary excretion, for which bilirubin is a reasonable marker. This has been documented to occur at levels 1.5× the upper limit of normal or at a level of approximately 2.0 mg/dL (15). The retrospective nature and sample size are limitations of Rolziracetam our study. Patients with CA 19-9 levels within normal limits were not tested for the Lewis antigen. Lewisa-b- and are unable to increase their serum CA 19-9 levels and were not excluded from our analysis (16). However, only approximately 5% of the population are Lewisa-b- so this was unlikely to have a significant effect on our patient population In this study, we analyzed CA 19-9 as a prognostic factor and determined its utility in developing treatment strategies and designing future clinical trials.