Serum PSA concentrations are frequently increased in patients with prostatic cancer, but this is also the case in patients with benign prostatic hyperplasia.
Tumor doubling times were overestimated in patients with large volume benign prostatic hyperplasia since hyperplasia increases serum PSA, albeit 12 times less than cancer.
Thus, the mean F/T ratio in prostate cancer is lower than that in BPH and may be helpful to distinguish cancer from BPH especially in the gray zone of total PSA (4-10 ng/ml).
In the majority of reports the RT-PCR assay was highly specific for detection of extraprostatic PSA expression in prostate cancer patients, and negative for detection in men with benign prostatic hyperplasia and in women.
We have used a reverse transcription-PCR assay for prostate-specific antigen mRNA and an immunocytochemical staining method for cytokeratins to test this hypothesis in paired peripheral blood (PB) and bone marrow (BM) specimens from 71 patients with clinically localized disease before radical prostatectomy, 14 patients with advanced-stage carcinoma of the prostate, and 30 controls (young healthy volunteers, patients without prostate disease, and patients with benign prostatic hyperplasia).Controls were negative in BM and PB.
When test samples are controlled for extraneous clinical origin of inflammation or infection, the combination of the IL-8 and f/t PSA assay results may offer an improved approach for distinguishing BPH from CaP.
Prostate biopsies were obtained from transrectal biopsies from 153 patients with an abnormal DRE or a PSA more than 4 ng./ml. or symptoms of BPH and a PSA more than 4 ng./ml.
Altogether, several known genes, such as prostate-specific antigen (PSA), human glandular kallikrein 2 (hK2), phosphatidic acid phosphatase type 2a (PAP2a), alpha-tropomyosin, and insulin-like growth factor binding protein 7 (IGFBP-7), as well as an anonymous transcript (EST), were found to be expressed less in PC-3 than in BPH.
The proportion of free prostate-specific antigen (PSA) is higher in the sera of patients with benign prostatic hyperplasia compared with patients with prostate cancer (PCa).
Molecular forms of prostate-specific antigen (PSA) improve the differentiation between benign prostatic hyperplasia (BPH) and prostate cancer (PCa) in men with total PSA concentrations between 4 and 10 microg/l.
The mean age, IPSS, quality of life score, total PSA, maximum urinary flow rate and the weight of the surgical prostate specimen were found as 65.13 +/- 5.51 years, 23.13 +/- 4.82, 4.78 +/- 0.95, 6.0 +/- 4.1 ng/ml, 6.9 +/- 2.7 ml/s and 62.96 +/- 38.76 g, respectively, in the familial BPH group whereas the same parameters were measured as 68.13 +/- 7.68 years, 24.74 +/- 3.73, 4.52 +/- 0.85, 5.93 +/- 4.75 ng/ml, 4.6 +/- 1.71 ml/s and 70.87 +/- 53.21 g, respectively.
The current approach to prostate cancer diagnosis has major limitations including the inability of prostate-specific antigen (PSA) assays to accurately differentiate between prostate cancer and benign prostate hyperplasia (BPH) and the imprecision of transrectal ultrasound (TRUS) biopsy sampling.
To examine the role of the polymorphisms in the AR and PSA genes in prostate cancer susceptibility, we conducted a case-control study of Austrian Caucasians with 190 newly diagnosed prostate cancer patients and 190 age-matched control men with benign prostatic hyperplasia (BPH).
The mRNA PSA expression in needle biopsy material did not seem to be related to PSA circulating levels in prostate cancer patients (r = 0.281), whereas in BPH patients the two parameters correlated significantly (r = 0.667, p < 0.01).
PSA mRNA was detected by the LightCycler in 28 patients (39%) with pT2 tumors, in 22 patients (38%) with >pT2 tumors, but in only 3 patients (16%) with BPH.
In conclusion, the PSA polymorphisms may not be associated with the risk of prostate cancer development and its disease progression and the risk of BPH in Japanese men, and may also be not related to the serum PSA level in Japanese men with prostate cancer.
The replication alteration accompanied by aneuploidy, detected in peripheral blood cells, distinguishes between CAP patients and individuals with benign prostate hyperplasia (BPH; a common disorder in elderly men) better than the routinely used blood marker, the prostate-specific antigen (PSA).
We found a significantly higher PSA/GG distribution in PC (30%) than either benign prostatic hyperplasia (BPH) (18%) or population controls (16%) (P = 0.025).