Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0600139 (Prostate Cancer)
 4,540 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tumor cell migration is a fundamental process of metastasis. Pertussis toxine inhibits lysophosphatidic acid related cell migration by ADP-ribosylation of G proteins. We examined the influence of pertussis toxine (PTX) on progression and metastasis of the human hormone-insensitive prostate cancer cell line PC-3 after orthotopic implantation in nude mice. In 30 athymic male nude mice (NMRI) 5x10(5) PC-3 cells were injected into the dorsal prostate. After 7 d 15 mice received a total of six intraperitoneal injections of 5 micro g PTX/100 g body weight at an interval of 4 d. The other 15 mice received phosphate buffered saline and served as control. All mice were killed at 37 d followed by macroscopical and histological evaluation of local tumor growth and metastasis. In the control group tumorigenicity was 100% (15 out of 15). Mean weight of the tumor bearing unit of prostate and seminal vesicles was 541 mg (243-763 mg). The rate of positive lymphnodes was 100% with a mean transversal diameter of 3.9 mm (1.2-5.4 mm). In the PTX group local take rate was 100% with a mean weight of 251 mg (88-478 mg) (P two sided <0.0001). The rate of positive lymphnodes was 60% (9 out of 15) (P=0.017) with a mean transversal diameter of 2.3 mm (1.0-4.5 mm). PTX following orthotopic implantation of the human hormone-insensitive PC-3 cell line significantly reduces local tumor growth as well as metastasis to locoregional lymphnodes.
Prostate Cancer Prostatic Dis 1999 Jan
PMID:Influence of pertussis toxine on local progression and metastasis after orthotopic implantation of the human prostate cancer cell line PC3 in nude mice. 1249 64

We have identified a novel function for a member of the transient receptor potential (TRP) protein super-family, TRPM2, in prostate cancer cell proliferation. TRPM2 encodes a non-selective cation-permeable ion channel. We found that selectively knocking down TRPM2 with the small interfering RNA technique inhibited the growth of prostate cancer cells but not of non-cancerous cells. The subcellular localization of this protein is also remarkably different between cancerous and non-cancerous cells. In BPH-1 (benign), TRPM2 protein is homogenously located near the plasma membrane and in the cytoplasm, whereas in the cancerous cells (PC-3 and DU-145), a significant amount of the TRPM2 protein is located in the nuclei in a clustered pattern. Furthermore, we have found that TRPM2 inhibited nuclear ADP-ribosylation in prostate cancer cells. However, TRPM2 knockdown-induced inhibition of proliferation is independent of the activity of poly(ADP-ribose) polymerases. We conclude that TRPM2 is essential for prostate cancer cell proliferation and may be a potential target for the selective treatment of prostate cancer.
Prostate Cancer Prostatic Dis 2010 Jun
PMID:Novel role for the transient receptor potential channel TRPM2 in prostate cancer cell proliferation. 2002

We recently reported that colored potato extracts and an anthocyanin rich fraction suppressed lymph-node carcinoma of the prostate (LNCaP) and prostate cancer-3 (PC-3) prostate cancer cell proliferation and induced apoptosis via caspase-dependent and caspase-independent pathways. Chlorogenic acid, caffeic acid, gallic acid, catechin, malvidin, and glycoalkaloids (alpha-chaconine and solanine) have now been identified as the major bioactive components of potato, and their effects on LNCaP and PC-3 cell proliferation and apoptosis have been investigated. alpha-chaconine (5 microg/ml) and gallic acid (15 microg/ml) exhibited potent antiproliferative properties and increased cyclin-dependent kinase inhibitor p27 levels in both cell lines. Both alpha-chaconine and gallic acid induced poly [adenosine diphosphate (ADP)] ribose polymerase cleavage and caspase-dependent apoptosis in LNCaP cells; however, caspase-independent apoptosis through nuclear translocation of endonuclease G was observed in both LNCaP and PC-3 cells. alpha-chaconine and gallic acid activated c-Jun N-terminal protein kinase (JNK), and this response played a major role in induction of caspase-dependent apoptosis in LNCaP cells; whereas modulation of JNK and mitogen-activated protein kinase did not affect alpha-chaconine- and gallic acid-induced caspase-independent apoptosis. These results suggest that apoptosis induced by whole potato extracts in prostate cancer cell lines may be in part due to alpha-chaconine and gallic acid.
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PMID:The bioactive compounds alpha-chaconine and gallic acid in potato extracts decrease survival and induce apoptosis in LNCaP and PC3 prostate cancer cells. 2057 21

The combined clinical and molecular heterogeneity of prostate cancer necessitates the use of prognostic, predictive, and diagnostic biomarkers to assist the clinician with treatment selection. The pathologist plays a critical role in guiding molecular biomarker testing in prostate cancer and requires a thorough knowledge of the current testing options. In the setting of clinically localized prostate cancer, prognostic biomarkers such as Ki-67 labeling, PTEN loss or mRNA-based genomic signatures can be useful to help determine whether definitive therapy is required. In the setting of advanced disease, predictive biomarkers, such as the presence of DNA repair deficiency mediated by BRCA2 loss or mismatch repair gene defects, may suggest the utility of poly-ADP ribosylase inhibition or immune checkpoint blockade. Finally, androgen receptor-related biomarkers or diagnostic biomarkers indicating the presence of small cell neuroendocrine prostate cancer may help guide the use of androgen receptor signaling inhibitors and chemotherapy. In this review, we examine the current evidence for several prognostic, predictive and diagnostic tissue-based molecular biomarkers in prostate cancer management. For each assay, we summarize a recent survey of the International Society of Urology Pathology (ISUP) members on current testing practices and include recommendations for testing that emerged from the ISUP Working Group on Molecular Pathology of Prostate Cancer and the 2019 Consultation Conference on Molecular Pathology of Urogenital Cancers.
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PMID:Report From the International Society of Urological Pathology (ISUP) Consultation Conference on Molecular Pathology of Urogenital Cancers. I. Molecular Biomarkers in Prostate Cancer. 3204 6