[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 26 of about 26
3. Hobisch A, Ramoner R, Fuchs D, Godoy-Tundidor S, Bartsch G, Klocker H, Culig Z: Prostate cancer cells (LNCaP) generated after long-term interleukin 6 (IL-6) treatment express IL-6 and acquire an IL-6 partially resistant phenotype. Clin Cancer Res; 2001 Sep;7(9):2941-8
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate cancer cells (LNCaP) generated after long-term interleukin 6 (IL-6) treatment express IL-6 and acquire an IL-6 partially resistant phenotype.
  • PURPOSE: The levels of interleukin-6 (IL-6) are frequently elevated in sera from patients with advanced prostate carcinoma.
  • Our main objective was to investigate changes in responsiveness to IL-6 and/or androgen that occur in LNCaP cells after long-term treatment with IL-6.
  • This in vitro model could be of clinical relevance because of its similarity with late-stage prostate carcinoma.
  • EXPERIMENTAL DESIGN: LNCaP human prostate cancer cells were treated with IL-6 at a concentration of 5 ng/ml.
  • LNCaP cells passaged at the same time in the absence of IL-6 were used as controls (LNCaP-IL-6-).
  • Cells were counted after treatment with either IL-6 or the synthetic androgen methyltrienolone (R1881), and cell cycle analysis was performed.
  • Prostate-specific antigen in LNCaP-IL-6+ supernatants was measured by an enzyme immunoassay.
  • RESULTS: The basal proliferation rate in HP LNCaP-IL-6+ cells was higher than that in LNCaP-IL-6- cells.
  • This inability to elicit a growth-inhibitory response was associated with lack of effect on cell cycle distribution in the LNCaP-IL-6+ subline.
  • In parallel, IL-6 binding decreased gradually during long-term IL-6 treatment and, in HP, reached only 33% of the levels measured in controls.
  • However, androgen- and IL-6-induced prostate-specific antigen secretion decreased in long-term IL-6-treated cells.
  • CONCLUSIONS: Long-term treatment of LNCaP human prostate cancer cells with IL-6 leads to abolishment of inhibitory growth response.
  • [MeSH-major] Interleukin-6 / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgens / metabolism. Androgens / pharmacology. Binding, Competitive. Cell Count. Cell Cycle / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Gene Expression Regulation, Neoplastic. Humans. Male. Metribolone / metabolism. Metribolone / pharmacology. Prostate-Specific Antigen / drug effects. Prostate-Specific Antigen / secretion. RNA, Messenger / genetics. RNA, Messenger / metabolism. Signal Transduction. Tritium. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. TRITIUM, RADIOACTIVE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11555613.001).
  • [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; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Interleukin-6; 0 / RNA, Messenger; 10028-17-8 / Tritium; 2C323EGI97 / Metribolone; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


Advertisement
4. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


7. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Urology. 1994 Mar;43(3):408-10 [7510915.001]
  • [Cites] J Clin Oncol. 1993 Aug;11(8):1566-72 [7687666.001]
  • [Cites] Mol Endocrinol. 1993 Dec;7(12):1541-50 [8145761.001]
  • [Cites] J Pathol. 1994 Nov;174(3):223-8 [7529834.001]
  • [Cites] J Urol. 1995 Mar;153(3 Pt 2):1070-2; discussion 1072-3 [7531785.001]
  • [Cites] N Engl J Med. 1995 May 25;332(21):1393-8 [7723794.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5451-5 [7777529.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):401-6 [7795646.001]
  • [Cites] J Biol Chem. 1995 Aug 25;270(34):19998-20003 [7650017.001]
  • [Cites] Int J Cancer. 1995 Nov 15;63(4):544-50 [7591265.001]
  • [Cites] Urology. 1996 Jan;47(1A Suppl):44-7; discussion 48-53 [8560678.001]
  • [Cites] Oncogene. 1996 Apr 4;12(7):1565-9 [8622873.001]
  • [Cites] Urology. 1996 Jul;48(1):157-63 [8693644.001]
  • [Cites] Mol Endocrinol. 1997 Apr;11(4):450-9 [9092797.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2122-7 [9482849.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7379-84 [9636157.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4640-5 [9788616.001]
  • [Cites] J Biol Chem. 1998 Nov 27;273(48):31853-9 [9822653.001]
  • [Cites] J Biol Chem. 1998 Dec 4;273(49):32400-7 [9829969.001]
  • [Cites] Clin Cancer Res. 1997 Aug;3(8):1383-8 [9815822.001]
  • [Cites] Nat Med. 1999 Mar;5(3):280-5 [10086382.001]
  • [Cites] Endocrinology. 1999 Apr;140(4):1665-71 [10098501.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5458-63 [10318905.001]
  • [Cites] Curr Opin Genet Dev. 1999 Apr;9(2):140-7 [10322133.001]
  • [Cites] Cancer Res. 1999 Jun 1;59(11):2511-5 [10363963.001]
  • [Cites] J Urol. 1999 Dec;162(6):2192-9 [10569618.001]
  • [Cites] Br J Cancer. 2000 Jan;82(1):39-45 [10638964.001]
  • [Cites] EMBO J. 2000 Feb 1;19(3):359-69 [10654935.001]
  • [Cites] Cancer Res. 2000 Feb 15;60(4):944-9 [10706109.001]
  • [Cites] Urology. 1999 Oct;54(4):745 [10754148.001]
  • [Cites] J Biol Chem. 2000 Jul 7;275(27):20853-60 [10779504.001]
  • [Cites] Br J Cancer. 1999 Sep;81(2):242-51 [10496349.001]
  • [Cites] N Engl J Med. 1998 Oct 8;339(15):1036-42 [9761805.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4709-13 [10987273.001]
  • [Cites] Prostate. 2000 Oct 1;45(2):124-31 [11027411.001]
  • [Cites] Prostate. 2001 Mar 1;46(4):319-26 [11241555.001]
  • [Cites] Cancer Res. 2001 Apr 1;61(7):2892-8 [11306464.001]
  • [Cites] Mol Endocrinol. 2001 May;15(5):797-811 [11328859.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4315-9 [11389051.001]
  • [Cites] J Cell Sci. 2001 Jul;114(Pt 13):2363-73 [11559745.001]
  • [Cites] Mol Cell Endocrinol. 2001 Nov 26;184(1-2):13-24 [11694337.001]
  • [Cites] Br J Cancer. 2001 Dec 14;85(12):1928-36 [11747336.001]
  • [Cites] Lab Invest. 2001 Dec;81(12):1647-51 [11742035.001]
  • [Cites] J Urol. 2002 Jul;168(1):9-12 [12050481.001]
  • [Cites] Am J Pharmacogenomics. 2001;1(4):241-9 [12083956.001]
  • [Cites] Int J Cancer. 1978 Mar 15;21(3):274-81 [631930.001]
  • [Cites] Invest Urol. 1979 Jul;17(1):16-23 [447482.001]
  • [Cites] Cancer Res. 1983 Apr;43(4):1809-18 [6831420.001]
  • [Cites] Horm Res. 1983;18(1-3):18-27 [6411578.001]
  • [Cites] Biochem Biophys Res Commun. 1990 Dec 14;173(2):534-40 [2260966.001]
  • [Cites] Hum Pathol. 1992 Mar;23(3):273-9 [1555838.001]
  • [Cites] Proc Natl Acad Sci U S A. 1992 Jul 15;89(14):6319-23 [1631125.001]
  • [Cites] Cancer Res. 1994 Mar 15;54(6):1566-73 [7511045.001]
  • (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
  •  go-up   go-down


8. Roznovanu SL, Rădulescu D, Novac C, Stolnicu S: The morphologic changes induced by hormone and radiation therapy on prostate carcinoma. Rev Med Chir Soc Med Nat Iasi; 2005 Apr-Jun;109(2):337-42
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The morphologic changes induced by hormone and radiation therapy on prostate carcinoma.
  • The morphologic changes induced by hormone and radiation therapy were evaluated in prostate biopsy and prostatectomy specimens from patients with residual prostate carcinoma.
  • The two therapeutic methods induce changes both in the nonmalignant and malignant residual prostatic tissue.
  • Following hormone therapy, the nonmalignant prostatic tissue showed atrophy of prostatic acini associated with fibrosis, basal cell hyperplasia, degenerative changes of the secretory epithelial cells, and a marked decrease of high-grade intraepithelial neoplasia (HGPIN).
  • In the fragments of residual carcinoma, squamous cell metaplasia, necrosis, and necrobiosis in the foci, vacuolization of the cell cytoplasm, smaller, rare nucleoli, intraluminal crystalloids, higher Gleason score associated with a lower capsular penetration, areas of necrosis and mitoses were found.
  • Following radiation therapy, the nontumoral prostatic tissue showed an increased number of atrophic acini, squamous cell metaplasia, and presence of atypical glands.
  • The morphologic changes induced by radiation therapy in the residual prostatic carcinoma were characterized by an abnormal architectural structure of the glands and presence of cell atypias correlated with the biochemical lowering of serum PSA.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Carcinoma / pathology. Neoplasm, Residual / pathology. Prostate / drug effects. Prostate / radiation effects. Prostatic Neoplasms / pathology
  • [MeSH-minor] Biomarkers, Tumor / blood. Biomarkers, Tumor / radiation effects. Biopsy. Chemotherapy, Adjuvant. Humans. Male. Prostate-Specific Antigen / blood. Prostate-Specific Antigen / radiation effects. Prostatectomy. Radiotherapy, Adjuvant

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16607796.001).
  • [ISSN] 0048-7848
  • [Journal-full-title] Revista medico-chirurgicală̆ a Societă̆ţ̜ii de Medici ş̧i Naturaliş̧ti din Iaş̧i
  • [ISO-abbreviation] Rev Med Chir Soc Med Nat Iasi
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen
  • [Number-of-references] 26
  •  go-up   go-down


9. 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
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


10. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


11. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. VALPROIC ACID .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [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

  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


13. 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
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DAUNORUBICIN .
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


14. Huang X, Zhu D, Lou Y: A novel anticancer agent, icaritin, induced cell growth inhibition, G1 arrest and mitochondrial transmembrane potential drop in human prostate carcinoma PC-3 cells. Eur J Pharmacol; 2007 Jun 14;564(1-3):26-36
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel anticancer agent, icaritin, induced cell growth inhibition, G1 arrest and mitochondrial transmembrane potential drop in human prostate carcinoma PC-3 cells.
  • We screened their effects on cell growth in human prostate carcinoma PC-3 cell line (estrogen receptor positive) in vitro.
  • PC-3 cell line was used for the measurement of anti-carcinoma activities of 0-100 micromol/l icaritin and 30 micromol/l icariin.
  • Primary cultured rat prostate basal cells used as cell growth selective control.
  • When treated with icaritin for 24 to 72 h, cell growth was strongly inhibited (at 48 h IC(50) was 10.74+/-1.59 micromol/l, P<0.001) companied with a mitochondrial transmembrane potential (_Psim) drop.
  • These findings suggested a novel anticancer efficacy of icaritin mediated selectively via induction of cell cycle arrest but not associated with estrogen receptors in PC-3 cells.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Carcinoma / drug therapy. Flavonoids / pharmacology. G1 Phase / drug effects. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Blotting, Western. Cell Cycle / drug effects. Cell Cycle Proteins / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Estradiol / pharmacology. Flow Cytometry. G2 Phase / drug effects. Humans. Immunoblotting. Inhibitory Concentration 50. Male. Membrane Potential, Mitochondrial / drug effects

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17382317.001).
  • [ISSN] 0014-2999
  • [Journal-full-title] European journal of pharmacology
  • [ISO-abbreviation] Eur. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Cell Cycle Proteins; 0 / Flavonoids; 0 / icaritin; 489-32-7 / icariin; 4TI98Z838E / Estradiol
  •  go-up   go-down


15. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


16. Medvedev VL: [Hormone-resistant epithelial cancer of the prostate]. Urologiia; 2001 Jul-Aug;(4):29-33
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


17. 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
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


18. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


19. Hobisch A, Hoffmann J, Lambrinidis L, Eder IE, Bartsch G, Klocker H, Culig Z: Antagonist/agonist balance of the nonsteroidal antiandrogen bicalutamide (Casodex) in a new prostate cancer model. Urol Int; 2000;65(2):73-9
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Antagonist/agonist balance of the nonsteroidal antiandrogen bicalutamide (Casodex) in a new prostate cancer model.
  • Androgen ablation is standard therapy for advanced prostate carcinoma.
  • In the present study we have investigated molecular mechanisms which are responsible for the development of resistance to therapy in advanced prostate cancer.
  • In both cell lines an increase of the basal proliferation rate was observed.
  • The basal androgen receptor activity was 30-fold higher in LNCaP-abl cells compared to that in parental LNCaP cells.
  • This basal activity was reduced in LNCaP-RA cells.
  • The present study provides new information that is useful for a better understanding of therapy-refractory prostate cancer.
  • It is also important for the development of new therapy strategies for advanced carcinoma of the prostate.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Androgens / agonists. Anilides / therapeutic use. Prostatic Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 S. Karger AG, Basel
  • (PMID = 11025427.001).
  • [ISSN] 0042-1138
  • [Journal-full-title] Urologia internationalis
  • [ISO-abbreviation] Urol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Androgens; 0 / Anilides; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. GOSERELIN .
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


21. Gupta S, Takebe N, Lorusso P: Targeting the Hedgehog pathway in cancer. Ther Adv Med Oncol; 2010 Jul;2(4):237-50
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nature. 2003 Mar 20;422(6929):313-7 [12629553.001]
  • [Cites] Cell Cycle. 2003 May-Jun;2(3):196-8 [12734424.001]
  • [Cites] Cell. 1992 Apr 3;69(1):111-7 [1348213.001]
  • [Cites] Oncogene. 2004 Sep 20;23(43):7274-82 [15378087.001]
  • [Cites] Nature. 2005 Oct 13;437(7061):1018-21 [16136078.001]
  • [Cites] Trends Mol Med. 2005 Dec;11(12):537-45 [16290230.001]
  • [Cites] J Pathol. 2006 Jan;208(1):17-25 [16294371.001]
  • [Cites] Carcinogenesis. 2006 Apr;27(4):748-57 [16339184.001]
  • [Cites] Dev Cell. 2006 Feb;10(2):187-97 [16459298.001]
  • [Cites] Cancer Res. 2006 Jun 15;66(12):6063-71 [16778178.001]
  • [Cites] Nat Rev Drug Discov. 2006 Dec;5(12):1026-33 [17139287.001]
  • [Cites] J Cell Sci. 2007 Jan 1;120(Pt 1):3-6 [17182898.001]
  • [Cites] Curr Biol. 2007 Jan 23;17(2):165-72 [17196391.001]
  • [Cites] Cancer Res. 2007 Mar 1;67(5):2187-96 [17332349.001]
  • [Cites] Oncogene. 2007 Aug 16;26(38):5674-9 [17353904.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 May 15;104(20):8455-60 [17494766.001]
  • [Cites] Nat Med. 2007 Aug;13(8):944-51 [17632527.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12):1164-72 [19726763.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):4048-53 [17360475.001]
  • [Cites] Science. 1996 Jun 14;272(5268):1668-71 [8658145.001]
  • [Cites] Cell. 1996 Jun 14;85(6):841-51 [8681379.001]
  • [Cites] Nat Genet. 1996 Sep;14(1):78-81 [8782823.001]
  • [Cites] Science. 1996 Oct 11;274(5285):255-9 [8824192.001]
  • [Cites] Nat Genet. 1996 Nov;14(3):353-6 [8896571.001]
  • [Cites] Nat Genet. 1996 Nov;14(3):357-60 [8896572.001]
  • [Cites] Am J Med Genet. 1997 Mar 31;69(3):299-308 [9096761.001]
  • [Cites] Cell. 1997 Jul 25;90(2):193-6 [9244291.001]
  • [Cites] Nature. 1997 Oct 23;389(6653):876-81 [9349822.001]
  • [Cites] Nature. 1998 Jan 1;391(6662):90-2 [9422511.001]
  • [Cites] Science. 1998 Jun 5;280(5369):1603-7 [9616123.001]
  • [Cites] Neuron. 1998 Dec;21(6):1243-57 [9883719.001]
  • [Cites] J Anat. 1971 Dec;110(Pt 3):507 [5004470.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5428-37 [14500378.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):846-51 [14520411.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]
  • [Cites] Nature. 2003 Nov 6;426(6962):83-7 [14603322.001]
  • [Cites] Nat Genet. 2004 Mar;36(3):277-82 [14770182.001]
  • [Cites] Endocrinology. 2004 Aug;145(8):3961-70 [15132968.001]
  • [Cites] Eur J Dermatol. 2004 Mar-Apr;14(2):96-102 [15196999.001]
  • [Cites] Cancer Res. 2004 Sep 1;64(17):6071-4 [15342389.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] Cancer Cell. 2004 Sep;6(3):229-40 [15380514.001]
  • [Cites] Cancer Res. 2004 Oct 15;64(20):7545-52 [15492281.001]
  • [Cites] Nature. 2004 Nov 18;432(7015):324-31 [15549094.001]
  • [Cites] Development. 2005 Jan;132(2):335-44 [15604099.001]
  • [Cites] Genes Dev. 2005 Jan 15;19(2):214-23 [15625189.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Apr;6(4):306-17 [15803137.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Aug 9;102(32):11325-30 [16061793.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):832-45 [10071274.001]
  • [Cites] Cell Cycle. 2007 Oct 15;6(20):2458-63 [17726373.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2241-9 [18381430.001]
  • [Cites] Nature. 2008 Sep 18;455(7211):406-10 [18754008.001]
  • [Cites] Cancer Cell. 2008 Sep 9;14(3):238-49 [18772113.001]
  • [Cites] Genes Dev. 2008 Sep 15;22(18):2454-72 [18794343.001]
  • [Cites] Nat Rev Cancer. 2008 Oct;8(10):743-54 [18813320.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):5995-6004 [18829478.001]
  • [Cites] Mol Cancer Res. 2008 Dec;6(12):1928-36 [19074837.001]
  • [Cites] Dev Cell. 2008 Dec;15(6):801-12 [19081070.001]
  • [Cites] Genes Dev. 2009 Jan 1;23(1):24-36 [19136624.001]
  • [Cites] Nat Chem Biol. 2009 Mar;5(3):154-6 [19151731.001]
  • [Cites] Nature. 2009 Apr 9;458(7239):776-9 [19169242.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4254-9 [19246386.001]
  • [Cites] Trends Pharmacol Sci. 2009 Jun;30(6):303-12 [19443052.001]
  • [Cites] Science. 2009 Jun 12;324(5933):1457-61 [19460966.001]
  • [Cites] Cancer Res. 2009 Aug 1;69(15):6007-10 [19638582.001]
  • [Cites] N Engl J Med. 2009 Sep 17;361(12):1202-5 [19726764.001]
  • [Cites] Nature. 1980 Oct 30;287(5785):795-801 [6776413.001]
  • [Cites] Curr Biol. 1999 Apr 22;9(8):445-8 [10226030.001]
  • [Cites] Neuron. 1999 Aug;23(4):713-24 [10482238.001]
  • [Cites] Ann N Y Acad Sci. 1999 Sep 14;883:196-202 [10586245.001]
  • [Cites] Cell. 2000 Jan 21;100(2):185-8 [10660040.001]
  • [Cites] Nat Genet. 2000 Mar;24(3):216-7 [10700170.001]
  • [Cites] Nature. 2001 Mar 29;410(6828):599-604 [11279500.001]
  • [Cites] Annu Rev Neurosci. 2001;24:385-428 [11283316.001]
  • [Cites] Nature. 2001 May 17;411(6835):349-54 [11357142.001]
  • [Cites] Nature. 2001 Nov 1;414(6859):105-11 [11689955.001]
  • [Cites] Genes Dev. 2001 Dec 1;15(23):3059-87 [11731473.001]
  • [Cites] Development. 2001 Dec;128(24):5201-12 [11748155.001]
  • [Cites] Development. 2002 Feb;129(4):843-51 [11861468.001]
  • [Cites] Nat Genet. 2002 Jul;31(3):306-10 [12068298.001]
  • [Cites] Nature. 2002 Aug 22;418(6900):892-7 [12192414.001]
  • [Cites] Science. 2002 Aug 30;297(5586):1559-61 [12202832.001]
  • [Cites] Genes Dev. 2002 Nov 1;16(21):2743-8 [12414725.001]
  • (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
  •  go-up   go-down


22. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1998 Jul 1;58(13):2720-3 [9661880.001]
  • [Cites] Clin Chem. 1998 Apr;44(4):705-23 [9554481.001]
  • [Cites] Endocrinology. 1999 Jan;140(1):350-7 [9886845.001]
  • [Cites] Endocrinology. 1999 Mar;140(3):1481-91 [10067877.001]
  • [Cites] J Cell Biol. 1999 Mar 22;144(6):1337-48 [10087274.001]
  • [Cites] Cell. 1999 Mar 19;96(6):857-68 [10102273.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 May 11;96(10):5458-63 [10318905.001]
  • [Cites] Curr Biol. 1999 Jun 3;9(11):601-4 [10359702.001]
  • [Cites] J Biol Chem. 1999 Nov 5;274(45):32274-8 [10542266.001]
  • [Cites] Biochem J. 1999 Dec 1;344 Pt 2:427-31 [10567225.001]
  • [Cites] J Cell Biol. 2000 Apr 17;149(2):431-46 [10769034.001]
  • [Cites] J Androl. 2000 Sep-Oct;21(5):641-50 [10975410.001]
  • [Cites] Biochem Pharmacol. 2000 Oct 15;60(8):1051-9 [11007941.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6841-5 [11156376.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):3690-4 [11274386.001]
  • [Cites] J Steroid Biochem Mol Biol. 1990 Sep;37(1):39-45 [2242351.001]
  • [Cites] Int J Cancer. 1991 May 10;48(2):189-93 [1708363.001]
  • [Cites] J Biol Chem. 1992 Jan 15;267(2):968-74 [1730684.001]
  • [Cites] Biofactors. 1992 Jan;3(3):151-7 [1599609.001]
  • [Cites] Endocrinology. 1992 Nov;131(5):2378-86 [1385102.001]
  • [Cites] J Androl. 1992 Nov-Dec;13(6):465-75 [1293128.001]
  • [Cites] Ann Intern Med. 1993 May 15;118(10):804-18 [7682387.001]
  • [Cites] J Biol Chem. 1994 Feb 18;269(7):5241-8 [8106507.001]
  • [Cites] Cancer Res. 1994 Oct 15;54(20):5474-8 [7522959.001]
  • [Cites] Cancer Res. 1994 Dec 1;54(23):6049-52 [7525052.001]
  • [Cites] Biochem Biophys Res Commun. 1994 Oct 28;204(2):446-52 [7980500.001]
  • [Cites] Vitam Horm. 1994;49:433-502 [7810075.001]
  • [Cites] N Engl J Med. 1995 May 25;332(21):1393-8 [7723794.001]
  • [Cites] Steroids. 1996 Sep;61(9):531-9 [8883219.001]
  • [Cites] Biochem J. 1996 Nov 1;319 ( Pt 3):657-67 [8920964.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11345-50 [9326612.001]
  • [Cites] Cancer Res. 1999 Jun 15;59(12):2891-7 [10383151.001]
  • [Cites] Biochim Biophys Acta. 1997 Dec 9;1333(3):F217-48 [9426205.001]
  • [Cites] Biochim Biophys Acta. 1998 Jan 2;1401(1):113-20 [9459491.001]
  • [Cites] Genes Dev. 1998 Feb 15;12(4):502-13 [9472019.001]
  • [Cites] J Biol Chem. 1998 Feb 27;273(9):5315-22 [9478990.001]
  • [Cites] Prostate. 1998 Apr 1;35(1):63-70 [9537601.001]
  • [Cites] J Biol Chem. 1998 Dec 4;273(49):32377-9 [9829964.001]
  • (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
  •  go-up   go-down


23. Hassan HT: Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy. Leuk Res; 2004 Jul;28(7):667-71
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


24. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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.

  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier B.V. All rights reserved.
  • [Cites] Mol Cell Biol. 1999 Dec;19(12):8591-603 [10567583.001]
  • [Cites] Exp Cell Res. 1999 Dec 15;253(2):365-71 [10585259.001]
  • [Cites] Genes Cells. 2000 Feb;5(2):111-25 [10672042.001]
  • [Cites] Biochem J. 2000 Apr 1;347 Pt 1:155-61 [10727414.001]
  • [Cites] Biochem J. 2000 Oct 1;351(Pt 1):67-77 [10998348.001]
  • [Cites] Biochem J. 2001 Apr 15;355(Pt 2):537-44 [11284743.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2727-31 [11289154.001]
  • [Cites] J Biol Chem. 2002 Apr 26;277(17):15035-43 [11842089.001]
  • [Cites] Anticancer Drugs. 2002 Sep;13(8):859-68 [12394272.001]
  • [Cites] Prostate. 2003 Mar 1;54(4):275-89 [12539226.001]
  • [Cites] Chem Biol Interact. 2003 Feb 1;143-144:621-31 [12604248.001]
  • [Cites] J Biol Chem. 2003 Aug 29;278(35):32763-70 [12805369.001]
  • [Cites] Int J Cancer. 2004 Aug 20;111(2):246-51 [15197778.001]
  • [Cites] Cancer Chemother Pharmacol. 2004 Oct;54(4):301-7 [15138708.001]
  • [Cites] Cell. 1987 Sep 11;50(6):863-72 [3476205.001]
  • [Cites] J Mol Biol. 1990 Apr 20;212(4):563-78 [2329577.001]
  • [Cites] Biochem Biophys Res Commun. 1992 Dec 30;189(3):1709-15 [1482376.001]
  • [Cites] J Biol Chem. 1993 Mar 15;268(8):5856-60 [8095499.001]
  • [Cites] J Biol Chem. 1993 Jul 25;268(21):16052-8 [8340427.001]
  • [Cites] J Biol Chem. 1994 Jun 3;269(22):15558-62 [7515059.001]
  • [Cites] J Biol Chem. 1994 Aug 12;269(32):20340-6 [8051128.001]
  • [Cites] Cancer Res. 1995 Sep 15;55(18):4105-13 [7664287.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Nov 12;228(2):474-9 [8920937.001]
  • [Cites] Biochem Biophys Res Commun. 1996 Nov 12;228(2):524-9 [8920946.001]
  • [Cites] Mol Reprod Dev. 1997 Nov;48(3):301-9 [9322240.001]
  • [Cites] J Biol Chem. 1997 Oct 17;272(42):26562-72 [9334236.001]
  • [Cites] J Biol Chem. 1997 Oct 31;272(44):27778-86 [9346922.001]
  • [Cites] Circ Res. 1998 Feb 9;82(2):251-60 [9468196.001]
  • [Cites] Nucleic Acids Res. 1998 Mar 1;26(5):1135-43 [9469818.001]
  • [Cites] Cancer Res. 1999 Feb 1;59(3):607-14 [9973208.001]
  • [Cites] FEBS Lett. 1999 Jul 16;455(1-2):111-6 [10428483.001]
  • [Cites] Genomics. 1999 Sep 1;60(2):188-98 [10486210.001]
  • [Cites] Mol Endocrinol. 1999 Oct;13(10):1704-17 [10517672.001]
  • [Cites] Mol Cell Biol. 2005 Jan;25(1):512-22 [15601870.001]
  • [Cites] Mol Endocrinol. 2005 Jan;19(1):148-62 [15388790.001]
  • [Cites] Curr Med Chem Anticancer Agents. 2005 Jan;5(1):15-27 [15720258.001]
  • [Cites] Gynecol Oncol. 2005 Apr;97(1):110-7 [15790446.001]
  • [Cites] Mol Cell Probes. 2005 Aug;19(4):261-6 [15979276.001]
  • [Cites] Gene. 2005 Nov 21;361:89-100 [16181749.001]
  • [Cites] Mol Cell Proteomics. 2005 Nov;4(11):1686-96 [16048908.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2815-25 [16510604.001]
  • [Cites] Mol Cell Endocrinol. 2006 Mar 27;248(1-2):182-91 [16417966.001]
  • [Cites] J Biol Chem. 2006 Apr 14;281(15):9882-90 [16495225.001]
  • [Cites] Mol Pharmacol. 2006 May;69(5):1662-72 [16478829.001]
  • [Cites] Anticancer Res. 2006 Jul-Aug;26(4B):2949-55 [16886619.001]
  • [Cites] Annu Rev Pharmacol Toxicol. 2007;47:263-92 [16970545.001]
  • [Cites] Biochem Pharmacol. 2008 Jan 15;75(2):414-26 [17945194.001]
  • [Cites] J Steroid Biochem Mol Biol. 2008 Feb;108(3-5):181-5 [17933521.001]
  • [Cites] J Biochem. 2008 May;143(5):675-83 [18281297.001]
  • [Cites] Haematologica. 2008 Oct;93(10):1580-2 [18698089.001]
  • [Cites] J Biol Chem. 2009 Jan 30;284(5):3136-47 [19047043.001]
  • [Cites] Ann N Y Acad Sci. 2009 Feb;1155:33-42 [19250190.001]
  • [Cites] Gene. 2009 May 15;437(1-2):39-44 [19236911.001]
  • (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
  •  go-up   go-down


25. Nagpal S, Na S, Rathnachalam R: Noncalcemic actions of vitamin D receptor ligands. Endocr Rev; 2005 Aug;26(5):662-87
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • 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

  • MedlinePlus Health Information. consumer health - Vitamin D.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


26. 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
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Kidney cancer.
  • Genetic Alliance. consumer health - Transplantation.
  • MedlinePlus Health Information. consumer health - Kidney Transplantation.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • Hazardous Substances Data Bank. CYCLOSPORIN A .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16434506.001).
  • [ISSN] 1046-6673
  • [Journal-full-title] Journal of the American Society of Nephrology : JASN
  • [ISO-abbreviation] J. Am. Soc. Nephrol.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Immunosuppressive Agents; 83HN0GTJ6D / Cyclosporine; W36ZG6FT64 / Sirolimus
  •  go-up   go-down






Advertisement