Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Data are presented demonstrating that adenylate kinase (AK; EC 2.7.4.3) is an oncodevelopmental enzyme in the prostate of Copenhagen rats. We selected the Dunning tumor (dorsal rat prostate) as a model system because it most nearly approximates the human pathology. Four sublines of the tumor (R3327-H, R3327-AT, MAT Lu, and MAT LyLu) were studied. The tumor sublines were maintained as solid tumors in syngeneic rats and as monolayers in tissue culture. AK activity appeared in conjunction with malignant transformation of the dorsal prostate. We also determined the normal developmental enzyme pattern: AK was present in prostates of newborns, but was undetectable in prostates of adults. However, AK increased after castration. Therefore, we propose AK as a potential oncofetal tumor marker in prostatic cancer.
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PMID:Adenylate kinase: an oncodevelopmental marker in an animal model for human prostatic cancer. 299 6

A total of 12 patients with metastatic hormone refractory prostate cancer were treated by combining cryoablation and granulocyte macrophage colony-stimulating factor administration. Besides prostate-specific antigen (PSA) measurements, peripheral blood mononuclear cells were also obtained; the frequency of tumor-specific T cells was tested ex vivo in an interferon-gamma enzyme-linked immunospot assay after stimulating with autologous prostate cancer-derived protein lysates. To assess cytolytic activity, T cells were coincubated with human prostate cancer cells (LNCaP) or renal cancer cells (GRC-1), and release of cytosolic adenylate kinase was measured by a luciferase assay. The median PSA decline percentage was 69.4% (range: 30.5% to 92.5%) and the median time to the nadir PSA was 4 months after therapy (range: 3 to 6). The median time to disease progress was 18 months, and 1 patient obtained a 92.5% PSA decline and a greater than 50% reduction of lung disease and survived 31 months. Four or 8 weeks after treatment, the tumor-specific T-cell responses were increased in peripheral blood mononuclear cell. The cytolytic activity against LNCaP was also increased significantly whereas no response was found against GRC-1. It seemed that there was no direct correlation between the degree of T-cell response and decline in PSA. Combined cryoablation with granulocyte macrophage colony-stimulating factor treatment was suggested to be an alternative approach for metastatic hormone refractory prostate cancer and could induce tumor-specific immunologic response.
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PMID:Combined cryoablation and GM-CSF treatment for metastatic hormone refractory prostate cancer. 1930 97

One of the major challenges in prostate cancer therapy remains the development of effective treatments for castration-resistant prostate cancer (CRPC), as the underlying mechanisms for its progression remain elusive. Previous studies showed that androgen receptor (AR) is crucially involved in regulation of metabolism in prostate cancer (PCa) cells throughout the transition from early stage, androgen-sensitive PCa to androgen-independent CRPC. AR achieves such metabolic rewiring directively either via its transcriptional activity or via interactions with AMP-activated protein kinase (AMPK). However, due to the heterogeneous expression and activity status of AR in PCa cells, it remains a challenge to investigate the links between AR status and metabolic alterations. To this end, we compared the proteomes of three pairs of androgen-sensitive (AS) and androgen-independent (AI) PCa cell lines, namely, PC3-AR(+)/PC3, 22Rv1/Du145, and LNCaP/C42B, using an iTRAQ labeling approach. Our results revealed that most of the differentially expressed proteins between each pair function in metabolism, indicating a metabolic shift between AS and AI cells, as further validated by multiple reaction monitoring (MRM)-based quantification of nucleotides and relative comparison of fatty acids between these cell lines. Furthermore, increased adenylate kinase isoenzyme 1 (AK1) in AS relative to AI cells may result in activation of AMPK, representing a major regulatory factor involved in the observed metabolic shift in PCa cells.
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PMID:Proteomic Comparison and MRM-Based Comparative Analysis of Metabolites Reveal Metabolic Shift in Human Prostate Cancer Cell Lines. 2614 61