Prostate cancer is the most common noncutaneous malignancy among men in the USA and is most frequently diagnosed through prostate-specific antigen (PSA)-based screening. Nevertheless, PSA testing has become increasingly controversial. In this review, we will present the evidence supporting the role of PSA in prostate cancer screening.
Numerous studies have shown that the risk of current and future prostate cancer is directly related to the serum PSA level. Moreover, increasing PSA levels predict a greater risk of adverse pathologic features and worse disease-specific survival. Substantial epidemiologic evidence has suggested a reduction in advanced disease and improvements in prostate cancer survival rates since the introduction of PSA-based screening. Recently, evidence from a randomized trial further validated that PSA testing reduces both metastatic disease and prostate cancer-specific mortality.
PSA is a valid marker for prostate cancer and its aggressiveness. Level 1 evidence is now available that PSA-based screening reduces both the rate of metastatic disease and prostate cancer-specific mortality.
"Identifying the subset of patients with aggressive disease at the time of surgery (radical prostatectomy, RP) may allow for the use of more tailored therapeutic strategies. The probability of recurrent disease has been predicted on the basis of preoperative serum prostate-specific antigen (PSA) levels, sex steroids levels and other clinicopathological parameters such as tumor stage, biopsy Gleason score and surgical margins12345678910. Integration of gene expression profiling and clinical variables has increased prediction accuracy for recurrent and aggressive disease1112. "
[Show abstract][Hide abstract] ABSTRACT: Metastasis-associated protein 1 (MTA1), a negative epigenetic modifier, plays a critical role in prostate cancer (PCa) progression. We hypothesized that MTA1 overexpression in primary tumor tissues can predict PCa aggressiveness and metastasis. Immunohistochemical staining of MTA1 was done on archival PCa specimens from University of Mississippi Medical Center and University of Iowa. We found that nuclear MTA1 overexpression was positively correlated with the severity of disease progression reaching its highest levels in metastatic PCa. Nuclear MTA1 overexpression was significantly associated with Gleason > 7 tumors in African Americans but not in Caucasians. It was also a predictor of recurrent disease. We concluded that MTA1 nuclear overexpression may be a prognostic indicator and a future therapeutic target for aggressive PCa in African American men. Our findings may be useful for categorizing African American patients with a higher probability of recurrent disease and metastasis from those who are likely to remain metastasis-free.
[Show abstract][Hide abstract] ABSTRACT: Lysophosphatidylcholine acyltransferase 1 (LPCAT1), the enzyme catalyzing the reaction in remodeling of phosphatidylcholine (PC) has been reported to express in prostate. However, its diagnostic and prognostic values remain unclear.
Immunohistochemistry (IHC) for LPCAT1 was performed on the tissue microarray (TMA) slides containing 251 samples from 148 patients with various prostatic disorders. The association of expression level of LPCAT1 with the progression of prostate cancer was analyzed.
LPCAT1 IHC mean score was the highest in metastatic prostate cancer (8.00±1.28), which was significantly higher than that in primary prostate cancer (4.63±3.00, p=9.73E-07), in high grade prostatic intraepithelial neoplasia (HGPIN, 2.72±2.47, p=1.02E-12), and in benign prostate (2.68, p=6.17E-12). The mean score in primary prostate cancer was significantly higher than that in HGPIN (p=4.09E-04) and in benign prostate (p=2.74E-04). There was no significant difference in the mean score between HGPIN and benign prostate (p=0.951). LPCAT1 IHC score also correlated to the tumor grade and stage of prostate cancer. Patients who underwent prostatectomy for prostate cancer and developed biochemical recurrence or clinical metastasis had higher LPCAT1 IHC score than those who underwent prostatectomy for prostate cancer and did not develop biochemical recurrence and clinical metastasis. The association of LPCAT1 with the progression of prostate cancer was independent of patient race and age, PSA level and positivity of surgical resection margins.
LPCAT1 correlates with the progression of prostate cancer and could be a new biomarker in diagnosis, prognosis and studying the pathogenesis of prostate cancer.
[Show abstract][Hide abstract] ABSTRACT: To clarify the association of kallikrein-related peptidase 3 (KLK3) rs2735839 G/A polymorphism with serum prostate-specific antigen (PSA) levels in Japanese men.
Subjects were participants of the Japan Multi-Institutional Collaborative Cohort (J-MICC) Study who visited the Seirei Preventive Health Care Center in Shizuoka, Japan. Among the 5,040 individuals aged 35-69 years who were enrolled in 2006-2007, serum PSA data were available for 2,323 male subjects without a past history of prostate cancer. The diagnostic criteria for PSA positivity was PSA ≥ 4.0 ng/ml. Genotyping of the KLK3 polymorphism was conducted by the polymerase chain reaction with the confronting two-pair primers (PCR-CTPP) method.
The mean ± SD of PSA levels (mg/dl) were 1.54 ± 1.73 for those with KLK3 rs2735839 G/G genotype, 1.34 ± 1.33 for G/A, and 1.20 ± 1.23 for A/A, which was significantly different (p < 0.0001). The age-adjusted odds ratios of PSA test positivity were 0.62 (95% confidence interval 0.41-0.94) for those with G/A + A/A relative to those with G/G.
The present study revealed that the KLK3 rs2735839 G allele was significantly associated with higher serum PSA levels also in Japanese.
Urologia Internationalis 03/2012; 89(1):39-44. DOI:10.1159/000332197 · 1.43 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.