We describe two simple, reproducible scoring systems for assessing acne severity, and we emphasize the technical problems which could invalidate either technique. Constant baseline data is desirable for any clinical trial, and our data clearly show that acne patients should ideally be off all treatment for at least 2 months before the start of a therapeutic trial.

The majority of prostate cancers are indolent, whereas a significant portion of patients will require systemic treatment during the course of their disease. To date, only high Gleason scores are best associated with a poor prognosis in prostate cancer. No validated serum biomarker has been identified with prognostic power. Previous studies showed that secretory phospholipase A2-IIa (sPLA2-IIa) is overexpressed in almost all human prostate cancer specimens and its elevated levels are correlated with high tumor grade. Here, we found that sPLA2-IIa is overexpressed in androgen-independent prostate cancer LNCaP-AI cells relative to their androgen-dependent LNCaP cell counterparts. LNCaP-AI cells also secrete significantly higher levels of sPLA2-IIa. Blocking sPLA2-IIa function compromises androgen-independent cell growth. Inhibition of the ligand-induced signaling output of the HER network, by blocking PI3K-Akt signaling and the nuclear factor-kappaB (NF-κB)-mediated pathway, compromises both sPLA2-IIa protein expression and secretion, as a result of downregulation of sPLA2-IIa promoter activity. More importantly, we demonstrated elevated serum sPLA2-IIa levels in prostate cancer patients. High serum sPLA2-IIa levels are associated significantly with high Gleason score and advanced disease stage. Increased sPLA2-IIa expression was confirmed in prostate cancer cells, but not in normal epithelium and stroma by immunohistochemistry analysis. We showed that elevated signaling of the HER/HER2-PI3K-Akt-NF-κB pathway contributes to sPLA2-IIa overexpression and secretion by prostate cancer cells. Given that sPLA2-IIa overexpression is associated with prostate development and progression, serum sPLA2-IIa may serve as a prognostic biomarker for prostate cancer and a potential surrogate prostate biomarker indicative of tumor burden.

Human exposure to bisphenol A (BPA) is ubiquitous. Animal studies found that BPA contributes to development of prostate cancer, but human data are scarce. Our study examined the association between urinary BPA levels and Prostate cancer and assessed the effects of BPA on induction of centrosome abnormalities as an underlying mechanism promoting prostate carcinogenesis. The study, involving 60 urology patients, found higher levels of urinary BPA (creatinine-adjusted) in Prostate cancer patients (5.74 µg/g [95% CI; 2.63, 12.51]) than in non-Prostate cancer patients (1.43 µg/g [95% CI; 0.70, 2.88]) (p = 0.012). The difference was even more significant in patients <65 years old. A trend toward a negative association between urinary BPA and serum PSA was observed in Prostate cancer patients but not in non-Prostate cancer patients. In vitro studies examined centrosomal abnormalities, microtubule nucleation, and anchorage-independent growth in four Prostate cancer cell lines (LNCaP, C4-2, 22Rv1, PC-3) and two immortalized normal prostate epithelial cell lines (NPrEC and RWPE-1). Exposure to low doses (0.01–100 nM) of BPA increased the percentage of cells with centrosome amplification two- to eight-fold. Dose responses either peaked or reached the plateaus with 0.1 nM BPA exposure. This low dose also promoted microtubule nucleation and regrowth at centrosomes in RWPE-1 and enhanced anchorage-independent growth in C4-2. These findings suggest that urinary BPA level is an independent prognostic marker in Prostate cancer and that BPA exposure may lower serum PSA levels in Prostate cancer patients. Moreover, disruption of the centrosome duplication cycle by low-dose BPA may contribute to neoplastic transformation of the prostate.

Purpose Most men with elevated serum prostate-specific antigen (PSA) levels and negative biopsies require repeat biopsy because of the lack of a sensitive and specific prostate cancer (CaP) detection test. This study evaluated the diagnostic potential of a duplex assay for CaP by quantifying transcript levels of α-methylacyl-CoA racemase (AMACR) and prostate-cancer antigen 3 (PCA3) in urine sediments following prostatic message. Materials and Methods Urine sediments from 92 patients, 43 with 49 without CaP were collected after digital rectal examination. Transcript levels of AMACR, PCA3, and PSA in total RNA isolated from these samples were determined by absolute qRT-PCR. AMACR and PCA3 scores were obtained by normalizing the transcript level to that of PSA for each sample and multiplying by 100. Results AMACR (p=0.006) and PCA3 (p=0.014) scores, but not serum PSA (p=0.306), discriminated specimens from patients with and without CaP, Receiver-operating-characteristic analysis established the diagnostic cutoff scores for the AMACR and PCA3 tests at 10.7 and 19.9, respectively. As determined from these cutoff scores, the AMACR test has 70% (95% CI, 56-83%) sensitivity and 71% (95% CI, 59-84%) specificity, whereas the PCA3 test has 72% (95% CI, 59-85%) sensitivity and 59% (95% CI, 45-73%) specificity for CaP detection. The combined use of AMACR and PCA3 scores in a dual-marker test increased sensitivity to 81% (95% CI, 70-93%) and specificity to 84% (95% CI, 73-94%). Conclusions Urinary AMACR and PCA3 tests were both superior to serum PSA test for detecting CaP. Their combined use in a dual-marker test further improved sensitivity and accuracy and could be used as a surveillance test after repeat negative prostate biopsies.