The results suggest that some VDR gene polymorphisms in Korean men might not only be associated with prostate cancer risk but also significantly related to prostate cancer-related risk factors such as PSA level, tumor stage, and Gleason score.
Prostate cancer (PCa) patients are risk-stratified on the basis of clinical stage and PSA level at diagnosis and the Gleason Score (GS) in prostate biopsy.
When we evaluated these two tSNPs together based on the risk alleles (that is, rs6434568 C and rs16834898 A), we found that the combined genotypes with four risk alleles were associated with an increased risk of PCa compared with those carrying 0-3 risk alleles (1.53, 1.19-1.97), and this increased risk was more pronounced among subjects of≤70 years (1.80, 1.24-2.62), Gleason score≥7 (1.68, 1.28-2.22) and PSA level≥20 (1.64, 1.24-2.18).
We re-evaluated all 623 men with prostate cancer in our 188 hereditary prostate cancer families and identified a subset of 244 men with more aggressive disease based upon meeting at least one of the following clinical and/or pathologic criteria: tumor grade Gleason score > or = 7, tumor stage T2c or higher, pretreatment PSA > or = 20 ng/ml, rising PSA after treatment, evidence of metastasis, or death from prostate cancer.
Following negative initial findings of biopsy sample analysis, total serum PSA levels and serum PSA kinetics are ineffective indicators of a need for a repeat biopsy; therefore, patients suspected of having prostate cancer might undergo several unnecessary biopsy procedures.
Effects of G/A polymorphism, rs266882, in the androgen response element 1 of the PSA gene on prostate cancer risk, survival and circulating PSA levels.
Our results suggest that rs4962416, previously associated only with prostate cancer, is also associated with PSA levels, with 12% increase for each copy of the minor allele C. The study enabled the replication of the effect for the majority of previously reported genetic variants in a set of clinically relevant prostate cancers.
Group II had a lower risk of PSA progression [hazard ratio (HR) = 0.43, 95% confidence interval (CI) 0.27,0.69, p = 0.001], metastasis development (HR = 0.51, 95% CI 0.27,0.97, p = 0.040) and overall mortality (HR = 0.49, 95% CI 0.26,0.92, p = 0.027), but not of PCa-specific death (HR = 0.45, 95% CI 0.19,1.08, p = 0.074).
When a quality prostate MRI is obtained, current evidence now supports its use in men at risk of harboring prostate cancer prior to their first biopsy, as well as in men with a rising PSA following an initial negative standard prostate biopsy procedure.
In all, 155 patients diagnosed with prostate cancer and 195 controls with negative digital rectal examinations and PSA levels of <4 ng/dL were enrolled in this study.
We examined whether the DNA-PK activity of peripheral blood lymphocytes (PBLs) was related to biochemical (prostate-specific antigen: PSA) relapse and radiation toxicity in prostate cancer patients who have received radiotherapy.
Between 1995 and 2001, 206 men with unfavorable-risk PC were randomized to receive radiation therapy alone or in combination with 6 months of androgen deprivation therapy (ADT); 108 men experienced PSA failure and formed the study cohort.
All men had intermediate- (T1-2, Gleason score 7 and/or prostate-specific antigen [PSA] 10-20 ng/mL) or high-risk (T3 and/or Gleason score 8-10 and/or PSA 20-50 ng/mL) localized PCa diagnosed between 1 January 2006 and 31 December 2014.
PSA-N quantification appears to be an important method for predicting biochemical recurrence and characterizing the recurrence risk of localized prostate cancer patients with pathologically normal pelvic lymph nodes.
We identified 6.509 patients with prostate cancer who had received hormonal therapy with a post-hormonal therapy PSA ≥2ng/mL, 363 of whom had non-metastatic, castrate-resistant prostate cancer.
In tissue samples, SPRY1 expression levels were significantly lower in prostate cancer patients with PSA recurrence after surgical treatment (P = 0.0076) and JAG1 expression levels were significantly higher in Gleason sum (GS) 8-9 disease than in GS 5-6 (P = 0.0121).
Important randomized trials show a clear benefit to androgen deprivation therapy (ADT) in both intermediate-risk prostate cancer and postprostatectomy patients with rising PSA.
In secondary analyses, the model predicted the endpoints of prostate cancer death (in SYS cases) and systemic progression beyond 5 years (in PSA controls) with hazard ratios 2.5 and 4.7, respectively (log-rank p-values of 0.0007 and 0.0005).
Analyses were restricted to 2007 patients who harbored low-risk PCa at ≥10-cores initial biopsy according to D'Amico classification (PSA <10.0 ng/ml, Gleason score <7 and clinical stage ≤T2a).
The Val158Met polymorphism of the catechol-O-methyltransferase gene is associated with the PSA-progression-free survival in prostate cancer patients treated with estramustine phosphate.