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1. Comuzzi B, Lambrinidis L, Rogatsch H, Godoy-Tundidor S, Knezevic N, Krhen I, Marekovic Z, Bartsch G, Klocker H, Hobisch A, Culig Z: The transcriptional co-activator cAMP response element-binding protein-binding protein is expressed in prostate cancer and enhances androgen- and anti-androgen-induced androgen receptor function. Am J Pathol; 2003 Jan;162(1):233-41
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  • [Title] The transcriptional co-activator cAMP response element-binding protein-binding protein is expressed in prostate cancer and enhances androgen- and anti-androgen-induced androgen receptor function.
  • Progression of human prostate cancer toward therapy resistance occurs in the presence of wild-type or mutated androgen receptors (ARs) that, in some cases, exhibit aberrant activation by various steroid hormones and anti-androgens.
  • In prostate cancer DU-145 cells, which were transiently transfected with CBP cDNA, hydroxyflutamide enhanced AR activity to a greater extent than bicalutamide in the presence of either wild-type or the mutated AR 730 val-->met.
  • In two sublines of LNCaP cells that contain the mutated AR 877 thr-->ala and overexpressed CBP, increase in AR activity was observed after treatment with hydroxyflutamide but not with bicalutamide.
  • Endogenous CBP protein was detected by Western blot in nuclear extracts from the three prostate cancer cell lines, LNCaP, PC-3, and DU-145, all derived from therapy-resistant prostate cancer.
  • In addition, CBP was expressed in both basal and secretory cells of benign prostate epithelium, high-grade prostate intraepithelial neoplasia, and prostate cancer clinical specimens, as evidenced by immunohistochemical staining.
  • Taken together, our findings demonstrate the selective enhancement of agonistic action of the anti-androgen hydroxyflutamide by the transcriptional co-activator CBP, which is a new, potentially relevant mechanism contributing to the acquisition of therapy resistance in prostate cancer.
  • [MeSH-major] Androgen Antagonists / pharmacology. Androgens / pharmacology. Carcinoma / metabolism. Nuclear Proteins / biosynthesis. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism. Trans-Activators / biosynthesis
  • [MeSH-minor] CREB-Binding Protein. Humans. Lymphatic Metastasis. Male. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Transcriptional Activation / drug effects. Tumor Cells, Cultured / drug effects

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  • (PMID = 12507906.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / CREBBP protein, human; 0 / Nuclear Proteins; 0 / Receptors, Androgen; 0 / Trans-Activators; EC 2.3.1.48 / CREB-Binding Protein
  • [Other-IDs] NLM/ PMC1851122
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2. Nagpal S, Na S, Rathnachalam R: Noncalcemic actions of vitamin D receptor ligands. Endocr Rev; 2005 Aug;26(5):662-87
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  • Physiological and pharmacological actions of 1,25-(OH)(2)D(3) in various systems, along with the detection of VDR in target cells, have indicated potential therapeutic applications of VDR ligands in inflammation (rheumatoid arthritis, psoriatic arthritis), dermatological indications (psoriasis, actinic keratosis, seborrheic dermatitis, photoaging), osteoporosis (postmenopausal and steroid-induced osteoporosis), cancers (prostate, colon, breast, myelodysplasia, leukemia, head and neck squamous cell carcinoma, and basal cell carcinoma), secondary hyperparathyroidism, and autoimmune diseases (systemic lupus erythematosus, type I diabetes, multiple sclerosis, and organ transplantation).
  • As a result, VDR ligands have been developed for the treatment of psoriasis, osteoporosis, and secondary hyperparathyroidism.
  • Furthermore, encouraging results have been obtained with VDR ligands in clinical trials of prostate cancer and hepatocellular carcinoma.
  • [MeSH-minor] Animals. Autoimmune Diseases / drug therapy. Autoimmune Diseases / metabolism. Humans. Ligands. Mice. Models, Molecular. Neoplasms / drug therapy. Neoplasms / metabolism. Osteoporosis / drug therapy. Osteoporosis / metabolism. Psoriasis / drug therapy. Psoriasis / metabolism

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  • (PMID = 15798098.001).
  • [ISSN] 0163-769X
  • [Journal-full-title] Endocrine reviews
  • [ISO-abbreviation] Endocr. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ligands; 0 / Receptors, Calcitriol; 1406-16-2 / Vitamin D
  • [Number-of-references] 284
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3. Segawa N, Nakamura M, Nakamura Y, Mori I, Katsuoka Y, Kakudo K: Phosphorylation of mitogen-activated protein kinase is inhibited by calcitonin in DU145 prostate cancer cells. Cancer Res; 2001 Aug 15;61(16):6060-3
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  • [Title] Phosphorylation of mitogen-activated protein kinase is inhibited by calcitonin in DU145 prostate cancer cells.
  • One of the causes of insensitivity to androgen ablation therapy in prostate cancer is thought to be attributable to elevated neuropeptides secreted by neuroendocrine cells in the tumor mass.
  • Calcitonin (CT), one of these neuropeptides, is reported to be associated with the growth of prostate cancer.
  • There is an increase in mitogen-activated protein (MAP) kinase activation as prostate cancer progresses to a more advanced and androgen-independent disease.
  • We examined the effect of CT on signal transduction and the relation between CT and early-response genes in the human androgen-insensitive prostate cancer cell line, DU145.
  • The basal phosphorylation level of extracellular signal-regulated kinase 1/2, which is a key kinase in the mediation of growth factor-induced mitogenesis in prostate cancer cells, was constitutively up-regulated.
  • The transient increase of c-fos expression was detected after CT treatment, whereas expression of c-jun RNA was down-regulated after CT treatment.
  • In conclusion, these findings suggest that DU145 might be a useful model as a therapeutic approach of neuropeptides in androgen-independent prostatic carcinoma.
  • [MeSH-major] Calcitonin / pharmacology. MAP Kinase Signaling System / drug effects. Mitogen-Activated Protein Kinases / metabolism. Prostatic Neoplasms / enzymology. Sulfonamides
  • [MeSH-minor] Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors. Cyclic AMP-Dependent Protein Kinases / metabolism. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Genes, Immediate-Early / drug effects. Humans. Isoquinolines / pharmacology. MAP Kinase Kinase 1. Male. Mitogen-Activated Protein Kinase 1 / metabolism. Mitogen-Activated Protein Kinase 3. Mitogen-Activated Protein Kinase Kinases / metabolism. Phosphorylation / drug effects. Protein-Serine-Threonine Kinases / metabolism. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Receptors, Calcitonin / biosynthesis. Receptors, Calcitonin / genetics. Tumor Cells, Cultured

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  • (PMID = 11507054.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Isoquinolines; 0 / RNA, Messenger; 0 / Receptors, Calcitonin; 0 / Sulfonamides; 127243-85-0 / N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide; 9007-12-9 / Calcitonin; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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4. Hudson E, Rashid M, Carter AC, Lester JF: Basaloid carcinoma of the prostate: a case report and review of the literature. Eur J Cancer Care (Engl); 2008 Sep;17(5):509-11
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  • [Title] Basaloid carcinoma of the prostate: a case report and review of the literature.
  • Malignant tumours arising from the basal cells of the prostate gland are extremely rare, and the majority of reports in the literature suggest a relatively indolent clinical course.
  • We report a case of infiltrative basaloid carcinoma of the prostate in a 68-year old man that did not respond to systemic chemotherapy.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 18616505.001).
  • [ISSN] 1365-2354
  • [Journal-full-title] European journal of cancer care
  • [ISO-abbreviation] Eur J Cancer Care (Engl)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 7
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5. Angelucci A, Muzi P, Cristiano L, Millimaggi D, Cimini A, Dolo V, Miano R, Vicentini C, Cerù MP, Bologna M: Neuroendocrine transdifferentiation induced by VPA is mediated by PPARgamma activation and confers resistance to antiblastic therapy in prostate carcinoma. Prostate; 2008 May 1;68(6):588-98
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  • [Title] Neuroendocrine transdifferentiation induced by VPA is mediated by PPARgamma activation and confers resistance to antiblastic therapy in prostate carcinoma.
  • BACKGROUND: Prostate cancer (PCa) is the most commonly diagnosed cancer in men in the Western Countries.
  • When prostatectomy fails to eradicate the primary tumor, PCa is generally refractory to all therapeutic approaches.
  • NET was an early event detectable through the expression of neuro-endocrine (NE) markers within 72 hr after VPA treatment and it was associated to a reduction in the overall cell proliferation.
  • When we interrupted VPA treatment we observed the recovery in residual cells of the basal proliferation rate both in vitro and in a xenograft model.
  • In order to counteract the VPA-induced NET, the inhibition of PPARgamma may represent a suitable adjuvant treatment strategy and awaits further experimental validation.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Transdifferentiation / drug effects. Enzyme Inhibitors / pharmacology. Neurosecretory Systems / drug effects. PPAR gamma / metabolism. Prostatic Neoplasms / drug therapy. Valproic Acid / pharmacology
  • [MeSH-minor] Anilides / pharmacology. Animals. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Drug Combinations. Histone Deacetylase Inhibitors. Humans. Male. Mice. Mice, Nude. Proto-Oncogene Proteins c-bcl-2 / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 18288684.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-chloro-5-nitrobenzanilide; 0 / Anilides; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / PPAR gamma; 0 / Proto-Oncogene Proteins c-bcl-2; 614OI1Z5WI / Valproic Acid
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6. Fournès B, Sadekova S, Turbide C, Létourneau S, Beauchemin N: The CEACAM1-L Ser503 residue is crucial for inhibition of colon cancer cell tumorigenicity. Oncogene; 2001 Jan 11;20(2):219-30
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  • [Title] The CEACAM1-L Ser503 residue is crucial for inhibition of colon cancer cell tumorigenicity.
  • CEACAM1 (also known as biliary glycoprotein, C-CAM or CD66a) is a cell adhesion molecule of the immunoglobulin family behaving as a tumor inhibitory protein in colon, prostate, liver, endometrial and breast cancers.
  • We have recently defined a number of cis-acting motifs within the long cytoplasmic domain participating in tumor cell growth inhibition.
  • In this study, we provide evidence that treatment with phorbol esters leads to increased phosphorylation of in vivo (32)P-labeled CEACAM1-L in mouse CT51 carcinoma cells, in the mouse 1MEA 7R.1 liver carcinoma cells and in 293 human embryonic kidney cells transfected with the Ceacam1-L cDNA.
  • Basal level Ser phosphorylation was abrogated by treatment with the staurosporine inhibitor, but not by the protein kinase C-specific inhibitor calphostin C or other inhibitors such as H7 or sphingosine.
  • Specific inhibitors of protein kinase A or calmodulin kinase had only minimal effects on the levels of basal or PMA-induced Ser phosphorylation.
  • Furthermore, PMA treatment of the CT51 cells induced cell spreading and cellular relocalization of the CEACAM1-L protein.
  • Since Ser503 has been described as a PMA-induced phosphorylation site in other cell systems, we investigated whether Ser503 was involved in these responses in mouse intestinal cells.
  • No differences were noticed in the basal or the PMA-induced phosphorylation levels, kinase inhibitor sensitivity or the PMA-induced relocalization of the protein between the wild-type and the Ser503Ala mutant CEACAM1-L.
  • However, we provide evidence that Ser503 participates in CEACAM1-L-mediated tumor inhibition as its mutation to an Ala led to in vivo tumor development, contrary to the tumor inhibitory phenotype observed with the wild-type CEACAM1-L protein.
  • [MeSH-minor] Amino Acid Sequence. Animals. Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors. Carcinoembryonic Antigen. Carcinogenicity Tests. Carcinoma / drug therapy. Carcinoma / metabolism. Carcinoma / pathology. Cell Adhesion Molecules. Enzyme Inhibitors / pharmacology. Epithelial Cells / metabolism. Female. Humans. Mice. Mice, Inbred BALB C. Molecular Sequence Data. Naphthalenes / pharmacology. Point Mutation. Protein Kinase C / antagonists & inhibitors. Protein Kinase C / metabolism. Serine / metabolism. Staurosporine / pharmacology. Tetradecanoylphorbol Acetate / pharmacology. Thionucleotides / pharmacology. Tumor Cells, Cultured

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  • (PMID = 11313949.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Antigens, Differentiation; 0 / CD66 antigens; 0 / Carcinoembryonic Antigen; 0 / Ceacam1 protein, mouse; 0 / Cell Adhesion Molecules; 0 / Enzyme Inhibitors; 0 / Naphthalenes; 0 / Thionucleotides; 121263-19-2 / calphostin C; 127191-97-3 / KN 62; 23645-17-2 / adenosine-3',5'-cyclic phosphorothioate; 452VLY9402 / Serine; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; E0399OZS9N / Cyclic AMP; EC 2.7.11.13 / Protein Kinase C; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; H88EPA0A3N / Staurosporine; NI40JAQ945 / Tetradecanoylphorbol Acetate
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7. Palayoor ST, Burgos MA, Shoaibi A, Tofilon PJ, Coleman CN: Effect of radiation and ibuprofen on normoxic renal carcinoma cells overexpressing hypoxia-inducible factors by loss of von Hippel-Lindau tumor suppressor gene function. Clin Cancer Res; 2004 Jun 15;10(12 Pt 1):4158-64
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  • [Title] Effect of radiation and ibuprofen on normoxic renal carcinoma cells overexpressing hypoxia-inducible factors by loss of von Hippel-Lindau tumor suppressor gene function.
  • PURPOSE: Tumor hypoxia is a major limiting factor for radiation therapy.
  • Hypoxia-inducible factors (HIFs) are overexpressed in several human cancers and are considered prognostic markers and potential targets for cancer therapy.
  • EXPERIMENTAL DESIGN: Renal clear cell carcinoma (RCC) cell lines overexpressing HIFs under normoxic conditions because of inactivation of von Hippel-Lindau tumor suppressor gene function (VHL-ve) and their matched pairs in which overexpression of HIFs was abolished by expression of functional VHL (VHL+ve) were irradiated.
  • RCC cells were also treated with ibuprofen, a radiosensitizer and HIF inhibitor in prostate cancer cells.
  • The effect of ibuprofen on radiosensitization and HIF and VHL proteins was compared in RCC matched-pair cell lines.
  • RESULTS: The data showed only small differences in the radiosensitivity between the cells overexpressing HIFs and cells with basal HIF levels.
  • Ibuprofen inhibited HIFs in VHL+ve cells expressing basal levels of HIFs.
  • [MeSH-major] Carcinoma / drug therapy. Carcinoma / radiotherapy. Ibuprofen / pharmacology. Kidney Neoplasms / drug therapy. Kidney Neoplasms / radiotherapy. Trans-Activators / physiology. Transcription Factors / physiology. Tumor Suppressor Proteins / physiology. Ubiquitin-Protein Ligases / physiology
  • [MeSH-minor] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Basic Helix-Loop-Helix Transcription Factors. Blotting, Western. Cell Line. Cell Survival. Dose-Response Relationship, Drug. Dose-Response Relationship, Radiation. Enzyme-Linked Immunosorbent Assay. Humans. Hypoxia-Inducible Factor 1, alpha Subunit. Immunoblotting. Mutation. Oxygen / metabolism. Prognosis. Radiation Tolerance. Time Factors. Transfection. Up-Regulation. Vascular Endothelial Growth Factor A / metabolism. Von Hippel-Lindau Tumor Suppressor Protein

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  • (PMID = 15217953.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Basic Helix-Loop-Helix Transcription Factors; 0 / HIF1A protein, human; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / Vascular Endothelial Growth Factor A; 0 / endothelial PAS domain-containing protein 1; EC 6.3.2.19 / Ubiquitin-Protein Ligases; EC 6.3.2.19 / VHL protein, human; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein; S88TT14065 / Oxygen; WK2XYI10QM / Ibuprofen
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8. Stratton MS, Greenstein B, Udayakumar TS, Nagle RB, Bowden GT: Androgens block interleukin-1 beta-induced promatrilysin expression in prostate carcinoma cells. Prostate; 2002 Sep 15;53(1):1-8
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  • [Title] Androgens block interleukin-1 beta-induced promatrilysin expression in prostate carcinoma cells.
  • We now demonstrate that IL-1 beta-induced but not IL-6-induced promatrilysin expression can be blocked by androgens in the prostate carcinoma cell line LNCaP (lymph node-derived carcinoma cells of the prostate).
  • Testosterone also had no effect on basal promatrilysin expression or basal NF kappa B transactivation activity.
  • These data suggest a mechanism in vivo by which invasive and metastatic prostatic carcinoma cell clones refractory to hormone ablation therapy may develop after chemical or surgical castration.
  • Furthermore, these data suggest that, perhaps, upstream targets such as the cytokines IL-1 beta and IL-6 may provide alternative drug targets for inhibiting prostate cancer progression.
  • [MeSH-major] Carcinoma / pathology. Enzyme Precursors / biosynthesis. Interleukin-1 / pharmacology. Interleukin-6 / pharmacology. Metalloendopeptidases / biosynthesis. Prostatic Neoplasms / pathology. Testosterone / pharmacology
  • [MeSH-minor] Blotting, Northern. Drug Resistance, Neoplasm. Enzyme-Linked Immunosorbent Assay. Humans. Male. Neoplasm Invasiveness. Neoplasm Metastasis. Signal Transduction. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 Wiley-Liss, Inc.
  • (PMID = 12210475.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Precursors; 0 / Interleukin-1; 0 / Interleukin-6; 3XMK78S47O / Testosterone; EC 3.4.24.- / Metalloendopeptidases; EC 3.4.24.- / promatrilysin
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9. Jarry H, Stromeier S, Wuttke W, Nahrstedt A: Petasiphenone, a phenol isolated from Cimicifuga racemosa, in vitro inhibits proliferation of the human prostate cancer cell line LNCaP. Planta Med; 2007 Feb;73(2):184-7
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  • [Title] Petasiphenone, a phenol isolated from Cimicifuga racemosa, in vitro inhibits proliferation of the human prostate cancer cell line LNCaP.
  • ) (CR) inhibit the proliferation of the human prostate cancer cell line LNCaP.
  • & Zucc. which inhibits the growth of various human leukemia cell lines.
  • Because of the structural similarity, we examined whether 1 affects the proliferation of LNCaP cells and the secretion of prostate-specific antigen (PSA).
  • Under basal conditions as well as under co-incubation with 10 nM estradiol [E2 or 1 nM dihydrotestosterone (DHT)], 1 dose-dependently inhibited proliferation of LNCaP cells while PSA release per cell was not altered.
  • We report for the first time that a defined compound isolated from CR inhibits the growth of the human prostate cancer cells LNCaP.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Caffeic Acids / pharmacology. Cimicifuga / chemistry. Phenols / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Carcinoma / drug therapy. Carcinoma / pathology. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Male. Plant Extracts / chemistry

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  • (PMID = 17295185.001).
  • [ISSN] 0032-0943
  • [Journal-full-title] Planta medica
  • [ISO-abbreviation] Planta Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / 3,4-dihydroxyphenacyl caffeate phenylpropanoid ester; 0 / Antineoplastic Agents, Phytogenic; 0 / Caffeic Acids; 0 / Phenols; 0 / Plant Extracts
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10. Hassan HT: Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy. Leuk Res; 2004 Jul;28(7):667-71
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  • [Title] Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy.
  • Several garlic compounds including allicin and its corresponding sulfide inhibit the proliferation and induce apoptosis of several human non-leukaemia malignant cells including breast, bladder, colorectal, hepatic, prostate cancer, lymphoma and skin tumour cell lines.
  • Recently, topic application of ajoene has produced significant clinical response in patients with skin basal cell carcinoma.
  • More significantly, ajoene profoundly enhanced the apoptotic effect of the two chemotherapeutic drugs: cytarabine and fludarabine in human CD34-positive resistant myeloid leukaemia cells through enhancing their bcl-2 inhibitory and caspase-3 activation activities.
  • Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
  • Since acute myeloid leukaemia (AML) is a heterogeneous malignant disease in which disease progression at the level of CD34-positive cells has a major impact on resistance to chemotherapy and relapse and the inability to undergo apoptosis is a crucial mechanism of multi-drug resistance in AML patients.
  • The recent findings of the potent enhancing activity of ajoene on chemotherapy-induced apoptosis in CD34-positive resistant human myeloid leukaemia cells suggest a novel promising role for the treatment of refractory and/or relapsed AML patients as well as elderly AML patients.
  • [MeSH-major] Disulfides / therapeutic use. Garlic. Leukemia, Myeloid / drug therapy. Plant Extracts / therapeutic use
  • [MeSH-minor] Acute Disease. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Drug Resistance, Neoplasm. Drug Synergism. Humans

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  • (PMID = 15158086.001).
  • [ISSN] 0145-2126
  • [Journal-full-title] Leukemia research
  • [ISO-abbreviation] Leuk. Res.
  • [Language] eng
  • [Publication-type] Editorial; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Disulfides; 0 / Plant Extracts; 99A0041VG8 / ajoene
  • [Number-of-references] 66
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11. Lovrić E, Gatalica Z, Eyzaguirre E, Kruslin B: Expression of maspin and glutathionine-S-transferase-pi in normal human prostate and prostatic carcinomas. Appl Immunohistochem Mol Morphol; 2010 Oct;18(5):429-32
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  • [Title] Expression of maspin and glutathionine-S-transferase-pi in normal human prostate and prostatic carcinomas.
  • Maspin expression functions as an inhibitor of tumor progression preventing the local invasion and etastatic spread of prostate cancer cells.
  • GST-pi has an essential role in the inactivation of xenobiotic agents and protection from oxidative stress and in resistance to chemotherapy.
  • DESIGN: Maspin and GST-pi expression were assessed in needle core and transurethral resection prostatic biopsies from 42 patients (34 with carcinoma, and 8 with normal prostate gland) using immunohistochemical methods.
  • RESULTS: Maspin and GST-pi were strongly and consistently coexpressed in the cytoplasm of basal cells of normal prostatic glands, whereas normal luminal cells were inconsistently weakly positive.
  • In contrast, only 1 case of prostatic carcinoma expressed GST-pi.
  • CONCLUSION: Consistent coexpression of maspin and GST-pi was observed in basal cells of the prostatic glands, which could be used as an additional immunohistochemical test in the evaluation of prostatic malignancy.

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  • (PMID = 20453817.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / SERPIN-B5; 0 / Serpins; EC 2.5.1.18 / Glutathione S-Transferase pi
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12. Uphoff J, Woziwodzki J, Schattka SO, Kollias A: [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis]. Aktuelle Urol; 2008 Sep;39(5):373-7
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  • [Title] [Loss of differentiation of a prostate adenocarcinoma after hormone therapy: the example of a metastasis in the spongy body of the penis].
  • [Transliterated title] Differenzierungsverlust eines Adenokarzinoms der Prostata nach Hormontherapie: am Beispiel einer Schwellkörpermetastase des Penis.
  • Prostate cancer as the most frequent malignoma of the male is the main primary lesion.
  • Changes in the morphology of the prostate carcinoma are specially known for the occurrence of small-cell neuroendocrine and undifferentiated carcinomas.
  • Often prior to the transformation an anti-androgen therapy has been undertaken.
  • At this state of the disease, there is only the possibility of a palliative therapy with a poor prognosis.
  • The increasing histological dedifferentiation of the tumour tissue can make it difficult or even impossible to identify the primary lesion.
  • [MeSH-major] Adenocarcinoma / secondary. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / secondary. Carcinoma, Transitional Cell / secondary. Cell Transformation, Neoplastic / pathology. Diphosphonates / therapeutic use. Gonadotropin-Releasing Hormone / antagonists & inhibitors. Neoplasms, Multiple Primary / drug therapy. Penile Neoplasms / secondary. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Biomarkers, Tumor / analysis. Biopsy. Bone Neoplasms / drug therapy. Bone Neoplasms / pathology. Bone Neoplasms / secondary. Bone Neoplasms / surgery. Combined Modality Therapy. Cystectomy. Diagnosis, Differential. Disease Progression. Humans. Lymphatic Metastasis. Male. Neoplasm Staging. Penis / pathology. Penis / surgery. Prostate / pathology. Prostate / surgery. Prostatectomy

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  • (PMID = 18798127.001).
  • [ISSN] 0001-7868
  • [Journal-full-title] Aktuelle Urologie
  • [ISO-abbreviation] Aktuelle Urol
  • [Language] ger
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Diphosphonates; 33515-09-2 / Gonadotropin-Releasing Hormone
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13. Gupta S, Adhami VM, Subbarayan M, MacLennan GT, Lewin JS, Hafeli UO, Fu P, Mukhtar H: Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2004 May 1;64(9):3334-43
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  • [Title] Suppression of prostate carcinogenesis by dietary supplementation of celecoxib in transgenic adenocarcinoma of the mouse prostate model.
  • Epidemiological studies and clinical observations suggest that nonsteroidal anti-inflammatory drugs and certain selective cyclooxygenase (COX)-2 inhibitors may reduce the relative risk of clinically evident prostate cancer.
  • This prompted us to investigate the chemopreventive potential of celecoxib, a selective COX-2 inhibitor, against prostate carcinogenesis in a transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • Similar to prostate cancer in humans, prostate malignancies in TRAMP mice progress from precursor intraepithelial lesions, to invasive carcinoma that metastasizes to lymph nodes, liver, lungs, and occasionally to bone.
  • The basal enzyme activity and protein expression of COX-2 is significantly higher (>4-fold) in the dorsolateral prostate of TRAMP mice up to 24 weeks of age compared with their nontransgenic littermates.
  • Eight-week-old TRAMP mice were randomly divided and fed either control diet (AIN 76A) or a custom prepared AIN 76A diet containing 1500-ppm celecoxib ad libitum for 24 weeks, a dosage that would compare with the normal recommended dose for the treatment of human disease.
  • Studies from two independent experiments, each consisting of 10 mice on test, showed that the cumulative incidence of prostate cancer development at 32 weeks of age in animals fed with AIN 76A diet was 100% (20 of 20) as observed by tumor palpation, whereas 65% (13 of 20), 35% (7 of 20), and 20% (4 of 20) of the animals exhibited distant site metastases to lymph nodes, lungs, and liver.
  • Celecoxib feeding resulted in a significant decrease in prostate (56%; P < 0.0003) and genitourinary weight (48%; P < 0.008).
  • Sequential magnetic resonance imaging analysis of celecoxib-fed mice documented lower prostate volume compared with the AIN 76A-fed group.
  • Histopathological examination of celecoxib-fed animals showed reduced proliferation, and down-modulation of COX-2 and prostaglandin E2 levels in the dorsolateral prostate and plasma, respectively.
  • Celecoxib supplementation also resulted in enhanced in vivo apoptosis in the prostate as monitored by several techniques including a recently perfected technique of 99mTc-labeled annexin V in live animals followed by phosphor imaging.
  • Our findings suggest that celecoxib may be useful in chemoprevention of prostate cancer.
  • [MeSH-minor] Animals. Biomarkers, Tumor / metabolism. Celecoxib. Cell Division / drug effects. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Dietary Supplements. Dinoprostone / blood. Female. Immunohistochemistry. Isoenzymes / biosynthesis. Isoenzymes / genetics. Isoenzymes / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Neoplasm Metastasis. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Proliferating Cell Nuclear Antigen / biosynthesis. Prostaglandin-Endoperoxide Synthases / biosynthesis. Prostaglandin-Endoperoxide Synthases / genetics. Prostaglandin-Endoperoxide Synthases / metabolism. Pyrazoles. RNA, Messenger / biosynthesis. RNA, Messenger / genetics

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  • (PMID = 15126378.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 89739
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Biomarkers, Tumor; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Proliferating Cell Nuclear Antigen; 0 / Pyrazoles; 0 / RNA, Messenger; 0 / Sulfonamides; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; JCX84Q7J1L / Celecoxib; K7Q1JQR04M / Dinoprostone
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14. Gupta S, Takebe N, Lorusso P: Targeting the Hedgehog pathway in cancer. Ther Adv Med Oncol; 2010 Jul;2(4):237-50
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  • The Hedgehog (Hh) pathway is a major regulator of many fundamental processes in vertebrate embryonic development including stem cell maintenance, cell differentiation, tissue polarity and cell proliferation.
  • Constitutive activation of the Hh pathway leading to tumorigenesis is seen in basal cell carcinomas and medulloblastoma.
  • A variety of other human cancers, including brain, gastrointestinal, lung, breast and prostate cancers, also demonstrate inappropriate activation of this pathway.
  • Targeted inhibition of Hh signaling may be effective in the treatment and prevention of many types of human cancers.
  • The discovery and synthesis of specific Hh pathway inhibitors have significant clinical implications in novel cancer therapeutics.
  • Initial clinical trials in basal cell carcinoma and treatment of select patients with medulloblastoma have shown good efficacy and safety.
  • We review the molecular basis of Hh signaling, the current understanding of pathway activation in different types of human cancers and we discuss the clinical development of Hh pathway inhibitors in human cancer therapy.

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  • (PMID = 21789137.001).
  • [ISSN] 1758-8359
  • [Journal-full-title] Therapeutic advances in medical oncology
  • [ISO-abbreviation] Ther Adv Med Oncol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC3126020
  • [Keywords] NOTNLM ; GDC-0449 / Hedgehog / basal cell carcinoma / cancer stem cells / medulloblastoma
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15. Campistol JM, Eris J, Oberbauer R, Friend P, Hutchison B, Morales JM, Claesson K, Stallone G, Russ G, Rostaing L, Kreis H, Burke JT, Brault Y, Scarola JA, Neylan JF: Sirolimus therapy after early cyclosporine withdrawal reduces the risk for cancer in adult renal transplantation. J Am Soc Nephrol; 2006 Feb;17(2):581-9
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  • [Title] Sirolimus therapy after early cyclosporine withdrawal reduces the risk for cancer in adult renal transplantation.
  • Median times to first skin and nonskin malignancies were compared between treatments using a survival analysis.
  • At 5 yr, the median time to a first skin carcinoma was delayed (491 versus 1126 d; log-rank test, P = 0.007), and the risk for an event was significantly lower with SRL-ST therapy (relative risk SRL-ST to SRL-CsA-ST 0.346; 95% confidence interval 0.227 to 0.526; P < 0.001, intention-to-treat analysis).
  • The relative risks for both basal and squamous cell carcinomas were significantly reduced.
  • Nonskin cancers included those of the lung, larynx, oropharynx, kidney, gastrointestinal tract, prostate, breast, thyroid, and cervix as well as glioma, liposarcoma, astrocytoma, leukemia, lymphoma, and Kaposi's sarcoma.
  • Patients who received SRL-based, calcineurin inhibitor-free therapy after CsA withdrawal at month 3 had a reduced incidence of both skin and nonskin malignancies at 5 yr after renal transplantation compared with those who received SRL therapy combined with CsA.
  • [MeSH-minor] Adult. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Drug Therapy, Combination. Follow-Up Studies. Humans. Incidence. Risk Assessment


16. Manin M, Baron S, Goossens K, Beaudoin C, Jean C, Veyssiere G, Verhoeven G, Morel L: Androgen receptor expression is regulated by the phosphoinositide 3-kinase/Akt pathway in normal and tumoral epithelial cells. Biochem J; 2002 Sep 15;366(Pt 3):729-36
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  • The androgen receptor (AR) is a ligand-responsive transcription factor known to play a central role in the pathogenesis of prostate cancer.
  • However, the regulation of AR gene expression in the normal and pathological prostate remains poorly understood.
  • This study focuses on the effect of the phosphoinositide 3-kinase (PI 3-kinase)/Akt axis on AR expression in vas deferens epithelial cells (VDEC), a suitable model to study androgen regulation of gene expression, and LNCaP cells (derived from a metastasis at the left supraclavicular lymph node from a 50-year-old patient with a confirmed diagnosis of metastatic prostate carcinoma).
  • Taken together, our data show for the first time that the PI 3-kinase/Akt pathway is required for basal and dihydrotestosterone-induced AR protein expression in both VDEC and LNCaP.
  • Since PI 3-kinase/Akt axis is active in prostate cancer, cross-talk between PI 3-kinase/Akt and AR signalling pathways may have implications for endocrine therapy.
  • [MeSH-minor] Animals. Blotting, Northern. Cell Differentiation. Cell Division. Cell Line. Dose-Response Relationship, Drug. Enzyme Inhibitors / pharmacology. Gene Expression Regulation, Enzymologic. Humans. MAP Kinase Signaling System. Male. Mice. Phosphorylation. Protein Binding. Proto-Oncogene Proteins c-akt. RNA / metabolism. Signal Transduction. Time Factors. Transfection. Tumor Cells, Cultured

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  • (PMID = 11971763.001).
  • [ISSN] 0264-6021
  • [Journal-full-title] The Biochemical journal
  • [ISO-abbreviation] Biochem. J.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Proto-Oncogene Proteins; 0 / Receptors, Androgen; 63231-63-0 / RNA; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1222812
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17. White SJ, Lu P, Keller GM, Voelkel-Johnson C: Targeting the short form of cFLIP by RNA interference is sufficient to enhance TRAIL sensitivity in PC3 prostate carcinoma cells. Cancer Biol Ther; 2006 Dec;5(12):1618-23
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  • [Title] Targeting the short form of cFLIP by RNA interference is sufficient to enhance TRAIL sensitivity in PC3 prostate carcinoma cells.
  • The pro-apoptotic death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has received significant attention as a novel cancer therapeutic, since it selectively induces apoptosis in malignant and not normal cells.
  • Unfortunately, prostate cancer cells display little if any susceptibility to TRAIL-induced apoptosis.
  • However, sensitivity to TRAIL is enhanced by doxorubicin, which correlated with a decrease in expression of the caspase-8 inhibitor cFLIP (Kelly et al., Cancer Biol Ther 1:520).
  • In this study we show that doxorubicin induces a time- and dose-dependent loss of cFLIP protein, but does not affect steady-state mRNA levels.
  • Although proteasome inhibitors increased basal levels of short cFLIP isoforms, cFLIPS declined at a similar rate in the absence or presence of proteasome inhibition during doxorubicin treatment.
  • We conclude that doxorubicin-mediated downregulation of cFLIPS, which occurs at the post-transcriptional level independent of proteasome-mediated pathways, is sufficient to enhance TRAIL sensitivity in PC3 prostate carcinoma cells.
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. DNA Primers. Daunorubicin / pharmacology. Doxorubicin / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Humans. Male. RNA Interference. Reverse Transcriptase Polymerase Chain Reaction. TNF-Related Apoptosis-Inducing Ligand / physiology. Transfection

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  • (PMID = 17106251.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA102218
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CASP8 and FADD-Like Apoptosis Regulating Protein; 0 / CFLAR protein, human; 0 / DNA Primers; 0 / RNA, Small Interfering; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 80168379AG / Doxorubicin; ZS7284E0ZP / Daunorubicin
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18. Alberti C: Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features. G Chir; 2010 Nov-Dec;31(11-12):568-74
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  • [Title] Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features.
  • Neuroendocrine differentiation in prostate carcinoma: focusing on its pathophysiologic mechanisms and pathological features. C.
  • Alberti Prostate carcinoma, even at advanced stages, responds in most patients to androgen deprivation therapies, that are able to exploit the androgen-sensitivity of prostate cancer cells.
  • However, more than half of such tumors, within one to three years, escape these treatments, thus progressing to the hormone-refractory condition.
  • Intriguing links between the development of hormone-insensitivity and neuroendocrine (NE) differentiation in prostate carcinoma have been hypothesized.
  • While, some time ago, NE cells have been considered as derived from progenitor neural crest cells, currently are thought to arise, as well as both basal and secretory cells of prostate gland, from common pluripotent stem cells.
  • NE cell are nonproliferative, terminally differentiated, PSA/acid phosphatase and androgen receptor (AR)-negative cells, moreover exhibiting an antiapoptotic phenotype due to survivin expression.
  • The propensity of prostate cancer cells to undergo a transdifferentiation pathway towards NE phenotype is due to several microenvironmental conditions such as androgen depletion (induced by LH-RH analogs or antagonists, antiandrogens, 5-α-reductase inhibitors), ionizing-radiation therapy, adrenergic factors, increase in interleukin-6 signaling cascade.
  • NE differentiation in prostate malignancy arises in three different forms: carcinoid, oat cell carcinoma, focally NE-differentiated conventional tumor.
  • Selective expression of stem cell-associated markers, such as CD44/Oct4A gene, in NE cancerous cells explain their therapy escape together with tumor recurrence and metastasis.
  • Serum levels of CgA reflect NE differentiation in prostate carcinoma more suitably than those of NSE.
  • Intriguingly, intermittent androgen deprivation therapy, by preventing NE differentiation, significantly reduces the risk of a rise in serum CgA levels meanwhile delaying the time of cancer progression due to hormone-independence.
  • Although valuable insights into the nature of NE differentiation in prostate carcinoma have been achieved in the last decades, additional understanding is needed about its pathogenetic mechanisms in order to devise novel therapy strategies to target them.
  • [MeSH-major] Carcinoma / pathology. Carcinoma / physiopathology. Cell Transdifferentiation. Prostatic Neoplasms / pathology. Prostatic Neoplasms / physiopathology
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Androgens / metabolism. Antineoplastic Agents, Hormonal / therapeutic use. Apoptosis / drug effects. Biomarkers / metabolism. Cell Transformation, Neoplastic / drug effects. Chromogranins / metabolism. Humans. Male. Neoplasm Invasiveness. Phosphopyruvate Hydratase / metabolism. Pluripotent Stem Cells / metabolism. Prognosis. Prostate-Specific Antigen / metabolism. Receptors, Androgen / metabolism. Treatment Failure


19. Pallai R, Simpkins H, Chen J, Parekh HK: The CCAAT box binding transcription factor, nuclear factor-Y (NF-Y) regulates transcription of human aldo-keto reductase 1C1 (AKR1C1) gene. Gene; 2010 Jul 1;459(1-2):11-23
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  • Deletion analysis of the 5' flanking, approximately 3.0 kb region of the human AKR1C1 gene identified the region between -128 and -88 as the minimal proximal promoter essential for basal transcription of AKR1C1 in human ovarian (2008 and 2008/C13*), lung (H23 and A549) and liver carcinoma (HepG2) cells.
  • Site-directed mutagenesis studies indicated that the transcription factor binding sites for NF-Y/CEBP were involved in controlling the basal transcription of AKR1C1 in all the cancer cells studied.
  • Chromatin immunoprecipitation (ChIP) analysis confirmed the in vivo association between NF-Y and human AKR1C1 gene promoter in human ovarian, lung and liver carcinoma cells.
  • These results indicate that the NF-Y regulates the basal transcription of AKR1C1 in human ovarian, lung and liver carcinoma cells and the cisplatin-induced transcription in human ovarian carcinoma cells.

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  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
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  • (PMID = 20338228.001).
  • [ISSN] 1879-0038
  • [Journal-full-title] Gene
  • [ISO-abbreviation] Gene
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA098804-03; United States / NCI NIH HHS / CA / R01 CA098804; United States / NCI NIH HHS / CA / CA98804; United States / NCI NIH HHS / CA / R01 CA098804-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CCAAT-Binding Factor; 0 / RNA, Small Interfering; 0 / nuclear factor Y; EC 1.1.1.- / 20-Hydroxysteroid Dehydrogenases; EC 1.1.1.- / 3 alpha-beta, 20 beta-hydroxysteroid dehydrogenase; Q20Q21Q62J / Cisplatin
  • [Other-IDs] NLM/ NIHMS191743; NLM/ PMC2874818
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20. Mazzucchelli R, Montironi R, Santinelli A, Lucarini G, Pugnaloni A, Biagini G: Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients. Prostate; 2000 Sep 15;45(1):72-9
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  • [Title] Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients.
  • BACKGROUND: Recent studies have demonstrated that angiogenesis is a potent prognostic indicator for patients with prostate cancer (PCa) and have pointed out that the evaluation of vascular endothelial growth factor (VEGF) is useful in assessing the angiogenic phenotype in PCa.
  • The aim of the study was to investigate immunohistochemically the expression of VEGF and its correlation with the pattern of capillary architecture in prostate cancer and high-grade prostatic intraepithelial neoplasia (PIN), in untreated and androgen-ablated patients.
  • METHODS: Forty-five patients who underwent radical prostatectomy (RP) for localized prostate carcinoma were recruited for this study.
  • The study population included two groups: 35 patients who did not receive chemo-, hormone, or radiation therapy before surgery, and 10 patients who were under complete androgen blockade (CAB) for 3 months at time of surgery.
  • VEGF was examined by immunohistochemistry, and its tissue expression was compared with the pattern of capillary architecture evaluated by immunostaining the endothelial antigen CD34.
  • RESULTS: In normal tissue, the intensity of the VEGF immunoreactivity in the cytoplasm of secretory cells ranged from negative to low.
  • Very few basal cells stained for VEGF.
  • All prostate cancer specimens stained positively, the intensity of the immunoreaction ranging from low to strong and being correlated with the Gleason score.
  • CAB before surgery downregulated the expression of VEGF and decreased the degree of vascularization, except in the cell areas with neuroendocrine (NE) features.
  • CONCLUSIONS: Our immunohistochemical results indicate that significant levels of VEGF are present in prostate cancer and in a population of PIN lesions, expression being highest in association with NE cells.
  • [MeSH-major] Adenocarcinoma / blood supply. Androgen Antagonists / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Endothelial Growth Factors / biosynthesis. Lymphokines / biosynthesis. Neovascularization, Pathologic / physiopathology. Prostatic Intraepithelial Neoplasia / blood supply. Prostatic Neoplasms / blood supply
  • [MeSH-minor] Aged. Anilides / administration & dosage. Capillaries / anatomy & histology. Capillaries / drug effects. Capillaries / physiopathology. Goserelin / administration & dosage. Humans. Immunohistochemistry. Male. Middle Aged. Nitriles. Prostatectomy. Tosyl Compounds. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10960845.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Nitriles; 0 / Tosyl Compounds; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide
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21. Medvedev VL: [Hormone-resistant epithelial cancer of the prostate]. Urologiia; 2001 Jul-Aug;(4):29-33
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  • [Title] [Hormone-resistant epithelial cancer of the prostate].
  • Hormone-resistance is typical for tumors from urothelial, basal and neuroendocrine PC cells, glandular epithelium cells which lost androgen receptors (AR) and tumors consisting of cells which retain AR but simultaneously express Bcl-2 and/or p53 genes.
  • The development of hormone-resistant cancer 2.5-3 years after hormonal therapy is associated with changes in immunophenotype of tumor cells.
  • Thus, immunophenotype of tumor cells may serve a prognostic marker of hormonal resistance of the tumor and dictate the treatment policy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma, Basal Cell / drug therapy. Carcinoma, Transitional Cell / drug therapy. Drug Resistance, Neoplasm. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Apoptosis. Humans. Immunophenotyping. Male. Middle Aged. Mutation. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / immunology. Prognosis. Receptors, Androgen / genetics. Time Factors

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  • (PMID = 11569231.001).
  • [ISSN] 1728-2985
  • [Journal-full-title] Urologii︠a︡ (Moscow, Russia : 1999)
  • [ISO-abbreviation] Urologiia
  • [Language] rus
  • [Publication-type] Comparative Study; English Abstract; Journal Article
  • [Publication-country] Russia
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Receptors, Androgen
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22. McKinstry R, Qiao L, Yacoub A, Dai Y, Decker R, Holt S, Hagan MP, Grant S, Dent P: Inhibitors of MEK1/2 interact with UCN-01 to induce apoptosis and reduce colony formation in mammary and prostate carcinoma cells. Cancer Biol Ther; 2002 May-Jun;1(3):243-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitors of MEK1/2 interact with UCN-01 to induce apoptosis and reduce colony formation in mammary and prostate carcinoma cells.
  • Recent studies have suggested that inhibition of the mitogen activated protein kinase (MAPK) pathway as well as abrogation of cell cycle check-point control can potentiate the lethal actions of chemotherapeutic drugs and radiation.
  • We therefore investigated the impact of combined exposure to the check-point abrogator (UCN-01) in conjunction with MEK1/2 inhibitors upon survival of breast and prostate carcinoma cells.
  • Treatment of cells with UCN-01 alone resulted in prolonged activation of the MAPK pathway.
  • Inhibition of MEK1/2 caused modest reductions in basal MAPK activity and transiently suppressed UCN-01-stimulated MAPK activity below that of MEK1/2 inhibitor alone.
  • Radiation exposure of drug treated cells did not further enhance apoptosis.
  • Treatment of cells with both caspase 9 and caspase 8 inhibitors was required to completely inhibit apoptosis in carcinoma cells.
  • Overexpression of Bcl-(xL) blocked cytochrome c release and cell killing induced by the drug combination.
  • Colony forming assays demonstrated that cells exposed to both agents exhibited a substantial reduction in clonogenic survival compared to either drug alone; moreover, radiation further reduced clonogenic survival despite failing to promote additional apoptosis.
  • Collectively, these data demonstrate that combined exposure of carcinoma cells to UCN-01 and MEK1/2 inhibitors induces apoptosis and interacts with radiation to further reduce clonogenic survival.
  • [MeSH-major] Alkaloids / pharmacology. Apoptosis / drug effects. Breast Neoplasms / pathology. Enzyme Inhibitors / pharmacology. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Prostatic Neoplasms / pathology. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Tyrosine Kinases / antagonists & inhibitors
  • [MeSH-minor] Caspases / metabolism. Cell Cycle / drug effects. Cell Cycle / radiation effects. Cell Division / drug effects. Cell Division / radiation effects. Colony-Forming Units Assay. Cytochrome c Group / metabolism. Drug Synergism. Enzyme Activation. Female. Flavonoids / pharmacology. Humans. In Situ Nick-End Labeling. MAP Kinase Kinase 1. MAP Kinase Kinase 2. MAP Kinase Signaling System / drug effects. MAP Kinase Signaling System / radiation effects. Male. Membrane Potentials / drug effects. Membrane Potentials / radiation effects. Mitochondria / drug effects. Mitochondria / physiology. Mitochondria / radiation effects. Staurosporine / analogs & derivatives. Stem Cells / drug effects. Stem Cells / metabolism. Stem Cells / radiation effects. Tumor Cells, Cultured

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  • [CommentIn] Cancer Biol Ther. 2002 May-Jun;1(3):254-5 [12432272.001]
  • (PMID = 12432271.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA35675; United States / NCI NIH HHS / CA / CA63753; United States / NCI NIH HHS / CA / CA72955; United States / NCI NIH HHS / CA / CA83705; United States / NCI NIH HHS / CA / CA88906; United States / NIDDK NIH HHS / DK / DK52875
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Alkaloids; 0 / Cytochrome c Group; 0 / Enzyme Inhibitors; 0 / Flavonoids; 7BU5H4V94A / 7-hydroxystaurosporine; EC 2.7.1.- / MAP2K1 protein, human; EC 2.7.1.- / MAP2K2 protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.12.2 / MAP Kinase Kinase 1; EC 2.7.12.2 / MAP Kinase Kinase 2; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; EC 3.4.22.- / Caspases; H88EPA0A3N / Staurosporine
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