In this study, we have applied RNA in situ hybridization and immunohistochemistry assays to measure the expressions of SRRM4, NEPC markers (SYP, CD56, and CHGA), and adenocarcinoma (AdPC) markers (AR, PSA) in a series of tissue microarrays constructed from castrate-resistant prostate tumors, treatment-naïve tumors collected from radical prostatectomy, and tumors treated with neoadjuvant hormonal therapy (NHT) for 0-12 months.
With respect to prostate cancer, prostatic acid phosphatase, prostate‑specific antigen, prostate‑specific membrane antigen (PSMA), prostate stem cell antigen, T‑cell receptor γ alternate reading frame protein, transient receptor potential‑p8 and six‑transmembrane epithelial antigen of the prostate 1 are among the identified target antigens for prostate tumors.
Expression of mRNA and protein of AR as well as its target gene prostate-specific antigen (PSA) was much higher in metastatic prostate tumors than in primary prostate tumors.
Further studies revealed osteoblastic spinal metastasis, prostate enhancement on CT and prostate-specific antigen (PSA) level of 90 ng/mL, concerning for concomitant prostate neoplasm.
In our previous studies in the rat JDCaP prostate cancer model, TAK-448 showed more rapid and profound reductions in plasma testosterone (T) and prostate-specific antigen (PSA, a biomarker of prostate tumor growth) levels than the gonadotropin releasing hormone (GnRH) analog leuprolide (TAP-144); however, its effects on tumor volume and subsequent tumor recurrence have not been elucidated fully.
Furthermore, the lower expression levels of CCND2 markedly correlated with prostate tumor progression to high Gleason score and elevated PSA levels, and served as an independent predictor of biochemical relapse and overall survival in a large cohort of prostate cancer patients.
We also demonstrated that immunization of mice with the bivalent vaccine (Ad<sub>5</sub>-PSA+PSCA) inhibited the growth of established prostate tumors.
In addition, immunoreactivity of the DNA repair enzyme, polymerase (PARP-1) and the cytoskeletal-remodeling regulator, cofilin was evaluated in prostate tumor specimens pre- and post-radiotherapy and correlated with pre-treatment prostate-specific antigen levels (PSA).
Preclinical studies demonstrated the ability of an adenovirus/PSA (Ad/PSA) vaccine to induce strong anti-PSA immune responses, and these responses were capable of destroying prostate-specific antigen (PSA)-secreting mouse prostate tumors.
Statistical analysis showed a positive correlation between increased GLCE expression and Gleason score, TNM staging, and prostate-specific antigen (PSA) level in the prostate tumors (Pearson correlation coefficients GLCE/Gleason = 0.56, P < 0.05; GLCE/TNM = 0.62, P < 0.05; and GLCE/PSA = 0.88, P < 0.01), suggesting GLCE as a candidate molecular marker for advanced prostate cancer.
However, the lack of specificity of prostate-specific antigen as a marker for prostate cancer combined with the asymptomatic and slow-growing nature of prostate tumors has resulted in many men being overdiagnosed and subjected to surgery or treatment with adverse side effects.
Here we show that the oncolytic Ad[ZH/3] vector significantly prolonged survival time and reduced serum prostate-specific antigen levels in an orthotopic prostate tumor model in nude mice to the same extent as wild-type Ad5.
The observation that mCMV/PSA(FL) is not effective against TRAMP-PSA is consistent with our previous findings that HLA-DRB1*1501-restricted immune responses to PSA are associated with suppression of effective CD8 T-cell responses to TRAMP-PSA tumors.
Our findings demonstrate the therapeutic benefits of simvastatin for prostate cancer and suggest a link between simvastatin, regulation of Akt activity, and PSA expression in prostate tumors.
The in vivo tumor growth study showed that immunization of mice with Ad5-PSA/PSCA vaccine induced strong antitumor immunity when challenged with mouse prostate tumor cell lines (RM11) expressing human PSA (RM11/PSA).
To compare the prostate antigen 3 (PCA3) test with (1)H-magnetic resonance spectroscopic imaging ((1)H-MRSI) and dynamic contrast-enhanced magnetic resonance imaging (DCEMR) combined examination in the detection of prostate tumor foci in patients with persistently elevated prostate-specific antigen (PSA) levels and prior negative random transrectal ultrasound (TRUS)-guided biopsy.
Suppression of androgen receptor signaling and prostate specific antigen expression by (-)-epigallocatechin-3-gallate in different progression stages of LNCaP prostate cancer cells.
Nevirapine induced extensive reprogramming of gene expression in vitro with up-regulation of genes that might be silenced during prostate tumor progression (i.e., K18, PSA and androgen receptor) and down-regulation of genes involved in the progression toward an androgen-independent phenotype (i.e., K5, EGFR1, EGF and VEGF-A).
Here we characterize a second candidate tissue biomarker, hCAP-D3, expressed in subtype-1 prostate tumors. hCAP-D3 expression, assayed by RNA in situ hybridization on a tissue microarray comprising 225 cases, was associated with decreased tumor recurrence after radical prostatectomy (P=0.004), independent of pathologic tumor stage, Gleason grade, and preoperative prostate-specific antigen levels.