• Given that family history can be easily assessed in routine clinical practice, it should be regarded as an important parameter to consider alongside PSA level for prostate cancer risk assessment.
With the more sensitive nanoparticle-based lectin-immunoassay we detected a statistically significant increase in the PSA fucosylation in PCa tissue compared to benign tissue (p=0.001) and in urine from PCa patients compared to BPH patients (p=0.030), and an even greater discrimination (p=0.010) when comparing BPH patients to PCa patients with Gleason score≥7.
With the availability of ultra-sensitive PSA assays, early biochemical relapse (eBCR) of prostate cancer is increasingly being detected at values much lower than the conventional threshold of 0.2 ng/ml.
With NSE, BCL2 and PSA (prostate-specific antigen) as identifying markers, the model specifies a putative progression sequence of the prostate cancer cell types.
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).
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.
We, therefore, performed a prospective study to determine whether TPTPB is still superior to TRUS biopsy in the detection of prostate cancer in men with persistently elevated PSA after one previous negative set of TRUS biopsies.
We want to investigate whether MR-US fusion can improve the detection rates of clinically significant prostate cancer in patients with prior negative prostate biopsy with PSA level <10 ng/mL.
We updated the RC3 using multinomial logistic regression analysis, including data on age, PSA, digital rectal examination, and prostate volume, for predicting LR and HR PCa.
We therefore studied VDR gene polymorphisms, as detected by Apal and Taql restriction fragments, in multiethnic Brazilian men (165 patients and 200 controls) for association with prostate cancer risk and parameters of disease severity (serum PSA, Gleason score and tumor stage).No statistical correlations were found.
We report the case of an 82-year-old male patient with a > 8-year history of prostate cancer (PrCa), who developed breast adenocarcinoma (BrCa) (Ki-67+ and negative for ER, PR, PSA and HER2/neu) after prolonged (approximately 7-year) anti-androgen (flutamide) monotherapy for locally advanced PrCa.
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.
We present, for the first time, results on gene expression profiling of CTCs isolated in vivo from high-risk prostate cancer (PCa) patients compared with CTC detected by 3 protein-based assays-CellSearch<sup>®</sup>, PSA-EPISPOT, and immunofluorescence of CellCollector<sup>®</sup> in vivo-captured CTCs-using the same blood draw.
We present a prospective study of men with an elevated PSA and compare the neutrophil/lymphocyte ratio, free percent PSA, PSA density and the presence of circulating prostate cells to detect clinically significant prostate cancer at first biopsy.
We performed a retrospective cohort study using Medicare data evaluating the rates of PSA testing and prostate biopsy among men without prostate cancer between 2011 and 2014.
We investigated the possibility of determining organ confinement of prostate cancer using multiple nuclear texture features determined by fully automated high resolution image analysis combined with preoperative serum PSA levels.
We investigated the effect of factorial randomisation to a 6-month lycopene and green tea dietary advice or supplementation intervention on 159 serum metabolite measures in 128 men with raised PSA levels (but prostate cancer-free), analysed by intention-to-treat.
We identified the best cutoff values for prostate biopsy (0.25 for all prostate cancers and 0.20 for clinically significant prostate cancers) to determine whether to require prostate biopsy when the PSA level is in the diagnostic gray zone.
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.
We identified 52,797 men in the NCDB from 2010 to 2015 diagnosed with very low risk prostate cancer as defined (cT1cM0, PSA <10, Gleason ≤6, <3 biopsy cores positive).
We hypothesized that the assessment of well-defined AR transcriptional targets (e.g., PSA/HK3 mRNA) in CaP tissues will provide in vivo readout of AR dysfunctions.
We have shown that the phenotypically undifferentiated (PSA(-/lo)) prostate cancer cell population harbors long-term self-renewing cancer stem cells (CSC) that resist castration, and a subset of the cells within the PSA(-/lo) population bearing the ALDH(hi)CD44(+)α2β1(+) phenotype (Triple Marker(+)/TM(+)) is capable of robustly initiating xenograft tumors in castrated mice.