[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 100 of about 1529
1. Nakabayashi M, Regan MM, Lifsey D, Kantoff PW, Taplin ME, Sartor O, Oh WK: Efficacy of nilutamide as secondary hormonal therapy in androgen-independent prostate cancer. BJU Int; 2005 Oct;96(6):783-6
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] Efficacy of nilutamide as secondary hormonal therapy in androgen-independent prostate cancer.
  • OBJECTIVE: To evaluate the activity of nilutamide as secondary hormonal therapy in patients with androgen-independent prostate cancer (AIPC), as treatment options are limited for these patients and secondary hormonal therapy with antiandrogens has advantages, including low toxicity, oral administration and high patient acceptance.
  • The decrease in prostate-specific antigen (PSA) levels, side-effects of treatment, and the relationship between baseline characteristics, type and duration of previous therapy and response to nilutamide were assessed.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents / therapeutic use. Imidazolidines / therapeutic use. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Humans. Male. Middle Aged. Prostate-Specific Antigen / blood. Retrospective Studies. Treatment Outcome


2. Aragon-Ching JB, Gillespie J, Price DK, Chuaqui R, Rodriguez-Canales J, Steinberg SM, Dahut WL, Figg WD: Lack of prognostic significance of prostate biopsies in metastatic androgen independent prostate cancer. BJU Int; 2007 Dec;100(6):1245-8
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Lack of prognostic significance of prostate biopsies in metastatic androgen independent prostate cancer.
  • OBJECTIVE: To assess the significance of viable tumour in the prostate of patients with metastatic androgen-independent prostate cancer (AIPC).
  • PATIENTS AND METHODS: We evaluated the clinicopathological features, including follow-up, of 40 men with metastatic AIPC who had a transrectal biopsy of the prostate.
  • RESULTS: Prostate biopsies (median three cores per biopsy) showed viable tumour in 19 of 40 patients (48%).
  • CONCLUSIONS: Taking prostate biopsies at the time of documented metastatic AIPC yielded tumour in about half the patients.
  • A previous history of RT was not associated with a negative prostate biopsy; the latter appears to have no influence on the prognosis.
  • [MeSH-major] Androgens / metabolism. Neoplasms, Hormone-Dependent / pathology. Prostate / pathology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Biopsy, Needle. Follow-Up Studies. Humans. Male. Middle Aged. Neoplasm Metastasis. Prognosis. Prostate-Specific Antigen / blood

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17850370.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


3. Dillard PR, Lin MF, Khan SA: Androgen-independent prostate cancer cells acquire the complete steroidogenic potential of synthesizing testosterone from cholesterol. Mol Cell Endocrinol; 2008 Nov 25;295(1-2):115-20
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] Androgen-independent prostate cancer cells acquire the complete steroidogenic potential of synthesizing testosterone from cholesterol.
  • The proliferation and differentiation of normal prostate epithelial cells depends upon the action of androgens produced by the testis.
  • Prostate cancers retain the ability to respond to androgens in the initial stages of cancer development, but progressively become independent of exogenous androgens in advanced stages of the disease while maintaining the expression of functional androgen receptor (AR).
  • In the present study, we have determined the potential of prostate cancer cells to synthesize androgens from cholesterol which may be involved in intracrine regulation of AR in advanced stages of the disease.
  • Established androgen-independent prostate cancer cell lines, PC3 and DU145 cells, expressed mRNA and proteins for scavenger receptor type B1 (SRB1), steroidogenic acute regulatory (StAR) protein, cytochrome P450 cholesterol side chain cleavage (P450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and other enzymes involved in androgen biosynthesis.
  • Expression of all these proteins and enzymes was significantly higher in the androgen-independent derivative of LNCaP prostate cancer cells (C81) than in the androgen-dependent cell line (C33).
  • In serum-free cultures, the androgen-independent C81 cells secreted approximately 5-fold higher testosterone than C33 cells as determined in the conditioned media by immunoassays.
  • These results for the first time show that prostate cancer cells in advanced stages of the disease could synthesize androgens from cholesterol and hence are not dependent upon testicular and/or adrenal androgens.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cholesterol.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • 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] Annu Rev Physiol. 2001;63:193-213 [11181954.001]
  • [Cites] Endocrinology. 1999 Mar;140(3):1481-91 [10067877.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] J Clin Oncol. 2002 Jul 1;20(13):3001-15 [12089231.001]
  • [Cites] Prostate. 2003 Mar 1;54(4):249-57 [12539223.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5622-8 [14500404.001]
  • [Cites] Am J Pathol. 2004 Jan;164(1):217-27 [14695335.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Clin Cancer Res. 2004 Jan 15;10(2):440-8 [14760063.001]
  • [Cites] J Clin Endocrinol Metab. 2004 May;89(5):2434-41 [15126575.001]
  • [Cites] Mol Cell Endocrinol. 2004 Sep 30;224(1-2):29-39 [15353178.001]
  • [Cites] Cancer Res. 2004 Oct 1;64(19):7156-68 [15466214.001]
  • [Cites] Surg Gynecol Obstet. 1969 Jan;128(1):117 [5774991.001]
  • [Cites] J Clin Endocrinol Metab. 1972 Jan;34(1):177-84 [5061771.001]
  • [Cites] Steroids. 1997 Jan;62(1):148-58 [9029730.001]
  • [Cites] Endocr Relat Cancer. 2005 Mar;12(1):101-7 [15788642.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4653-7 [16000557.001]
  • [Cites] JAMA. 2005 Sep 14;294(10):1255-9 [16160134.001]
  • [Cites] Arthritis Res Ther. 2005;7(5):R938-48 [16207335.001]
  • [Cites] Minerva Endocrinol. 2006 Mar;31(1):1-12 [16498360.001]
  • [Cites] Cancer Res. 2006 Mar 1;66(5):2815-25 [16510604.001]
  • [Cites] Oncogene. 2006 Jun 22;25(26):3719-34 [16449965.001]
  • [Cites] Oncogene. 2007 Mar 8;26(11):1606-15 [16964290.001]
  • [Cites] Prostate. 2007 Apr 1;67(5):557-71 [17221842.001]
  • [Cites] Cancer Res. 2007 May 15;67(10):5033-41 [17510436.001]
  • [Cites] Proc Natl Acad Sci U S A. 1997 Aug 5;94(16):8462-7 [9237999.001]
  • [Cites] Eur Urol. 1997;32 Suppl 3:24-40 [9267783.001]
  • [Cites] Endocrinology. 1997 Nov;138(11):4876-82 [9348218.001]
  • [Cites] Prostate. 2002 Mar 1;50(4):222-35 [11870800.001]
  • (PMID = 18782595.001).
  • [ISSN] 0303-7207
  • [Journal-full-title] Molecular and cellular endocrinology
  • [ISO-abbreviation] Mol. Cell. Endocrinol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA088184; United States / NCRR NIH HHS / RR / G12 RR003062-225542; United States / NCRR NIH HHS / RR / G12RR003062; United States / NCI NIH HHS / CA / R01 CA088184-09; United States / NCI NIH HHS / CA / CA88184; United States / NCRR NIH HHS / RR / G12 RR003062; United States / NCI NIH HHS / CA / CA088184-09; United States / NCRR NIH HHS / RR / RR003062-225542
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Messenger; 3XMK78S47O / Testosterone; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ NIHMS79430; NLM/ PMC2802176
  •  go-up   go-down


Advertisement
4. Fang YF, Liu T, Cao J: [DMF induces apoptosis in human androgen-independent prostate cancer PC3 cells in vitro]. Zhejiang Da Xue Xue Bao Yi Xue Ban; 2007 May;36(3):255-60
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] [DMF induces apoptosis in human androgen-independent prostate cancer PC3 cells in vitro].
  • OBJECTIVE: To evaluate the antiproliferative activity of 3-(2-chlorophenyl)-1-(2-hydroxy-4, 6-dimethoxy-3-((ethyl(methyl) amino) methyl) phenyl) prop-2-en-1-one (DMF) against human androgen-independent prostate cancer PC3 cells in vitro and its underlying mechanisms.

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17571308.001).
  • [ISSN] 1008-9292
  • [Journal-full-title] Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences
  • [ISO-abbreviation] Zhejiang Da Xue Xue Bao Yi Xue Ban
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / 3-(2-chlorophenyl)-1-(2-hydroxy-4, 6-dimethoxy-3-((ethyl(methyl) amino)methyl)phenyl)prop-2-en-1-one; 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Chlorobenzenes; 0 / Flavonoids; 0 / Growth Inhibitors; 0 / Piperidines; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; 45AD6X575G / alvocidib; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 3
  •  go-up   go-down


5. Chau CH, Permenter MG, Steinberg SM, Retter AS, Dahut WL, Price DK, Figg WD: Polymorphism in the hypoxia-inducible factor 1alpha gene may confer susceptibility to androgen-independent prostate cancer. Cancer Biol Ther; 2005 Nov;4(11):1222-5
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism in the hypoxia-inducible factor 1alpha gene may confer susceptibility to androgen-independent prostate cancer.
  • The hypoxia-inducible factor 1alpha (HIF-1alpha) plays a major role in cancer progression.
  • The role of this transcription factor in prostate cancer development and its transition to a metastatic and androgen refractory state remains to be elucidated.
  • Previous reports have identified the existence of single nucleotide polymorphisms (SNPs) in the oxygen-dependent degradation domain of the HIF-1alpha gene in renal cell carcinoma, head and neck squamous cell carcinoma, and androgen-independent prostate cancer (AIPC).
  • Studies in prostate cancer, however, are variable and limited in the number of cases assessed.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16205110.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / DNA, Neoplasm; 0 / Hypoxia-Inducible Factor 1
  •  go-up   go-down


6. Figg WD, Li H, Sissung T, Retter A, Wu S, Gulley JL, Arlen P, Wright JJ, Parnes H, Fedenko K, Latham L, Steinberg SM, Jones E, Chen C, Dahut W: Pre-clinical and clinical evaluation of estramustine, docetaxel and thalidomide combination in androgen-independent prostate cancer. BJU Int; 2007 May;99(5):1047-55
Hazardous Substances Data Bank. THALIDOMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pre-clinical and clinical evaluation of estramustine, docetaxel and thalidomide combination in androgen-independent prostate cancer.
  • OBJECTIVE: To evaluate the combination of docetaxel plus estramustine (which prolongs survival in patients with androgen-independent prostate cancer, AIPC), and thalidomide (that also adds to docetaxel activity), both pre-clinically and clinically in AIPC.
  • Clinically, the progression-free time was 7.2 months with this combination; 18 of 20 patients had a decline of half or more in prostate-specific antigen level and two of 10 patients with soft-tissue lesions had a partial response on computed tomography.
  • The combination of estramustine, docetaxel and thalidomide is an advantageous treatment in pre-clinical models of prostate cancer and is a safe, tolerable and active regimen in patients with AIPC.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17437439.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; 4Z8R6ORS6L / Thalidomide; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP1B1 protein, human; EC 1.14.14.1 / Cyp1b1 protein, mouse; EC 1.14.14.1 / Cytochrome P-450 CYP1B1
  •  go-up   go-down


7. Wagmiller JA, Griggs JJ, Dick AW, Sahasrabudhe DM: Individualized strategy for dosing luteinizing hormone-releasing hormone agonists for androgen-independent prostate cancer: identification of outcomes and costs. J Oncol Pract; 2006 Mar;2(2):57-66
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Individualized strategy for dosing luteinizing hormone-releasing hormone agonists for androgen-independent prostate cancer: identification of outcomes and costs.
  • PURPOSE: Continuing androgen suppression is the current standard in men with androgen-independent prostate cancer (AIPC).
  • The model accounted for direct costs of androgen suppression.
  • In cost analysis, lifetime per-patient costs for androgen suppression were estimated to be $5,694 for individualized LH-RHa dosing and $9,157 for fixed LH-RHa dosing.
  • Applied to the total population, a strategy of individualized LH-RHa dosing would cost $170 million for androgen suppression, compared with $274 million for fixed LH-RHa dosing.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20871718.001).
  • [ISSN] 1554-7477
  • [Journal-full-title] Journal of oncology practice
  • [ISO-abbreviation] J Oncol Pract
  • [Language] eng
  • [Grant] United States / AHRQ HHS / HS / T32 HS000044
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2794621
  •  go-up   go-down


8. Sella A, Sternberg C, Kovel S, Yarom N, Skoneczna I: Progression after docetaxel-based chemotherapy in androgen-independent prostate cancer. BJU Int; 2007 Sep;100(3):533-5
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] Progression after docetaxel-based chemotherapy in androgen-independent prostate cancer.
  • OBJECTIVE: To assess the clinical pattern of progression and prostate-specific antigen doubling time (PSA-DT) after exposure to docetaxel-based chemotherapy in patients with androgen-independent prostate cancer (AIPC).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Disease Progression. Estramustine / administration & dosage. Humans. Male. Middle Aged. Prednisone / administration & dosage. Prostate-Specific Antigen / blood. Retrospective Studies. Survival Analysis. Taxoids / administration & dosage. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. PREDNISONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17559560.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; EC 3.4.21.77 / Prostate-Specific Antigen; VB0R961HZT / Prednisone
  •  go-up   go-down


9. Tu SM, Kim J, Pagliaro LC, Vakar-Lopez F, Wong FC, Wen S, General R, Podoloff DA, Lin SH, Logothetis CJ: Therapy tolerance in selected patients with androgen-independent prostate cancer following strontium-89 combined with chemotherapy. J Clin Oncol; 2005 Nov 1;23(31):7904-10
Hazardous Substances Data Bank. DOXORUBICIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Therapy tolerance in selected patients with androgen-independent prostate cancer following strontium-89 combined with chemotherapy.
  • We assessed the rate of bone marrow failure in patients with prostate cancer who had received a dose of strontium-89.
  • PATIENTS AND METHODS: This subgroup analysis involved 34 patients with androgen-independent prostate cancer who had been given a dose of strontium-89 and six weekly doses of doxorubicin after response to induction chemotherapy.
  • The clinical role and safety profile of radiopharmaceuticals combined with chemotherapy in prostate cancer therapy deserve further exploration.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16258090.001).
  • [ISSN] 0732-183X
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 86342; United States / NCI NIH HHS / CA / P50 CA 90270
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Strontium Radioisotopes; 80168379AG / Doxorubicin
  •  go-up   go-down


10. Ohlmann CH, Markert E, Gerharz M, Pfister D, Dienes HP, Engelmann U, Heidenreich A: [Feasibility of targeted therapy based on immunohistochemical expression analysis in androgen-independent prostate cancer]. Urologe A; 2008 Sep;47(9):1218-23
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.
  • [Title] [Feasibility of targeted therapy based on immunohistochemical expression analysis in androgen-independent prostate cancer].
  • Targeted therapies present an interesting treatment option in prostate cancer.
  • The aim of our study was to analyze the expression profile of several molecular markers that are candidates for targeted therapy in patients with progressive androgen-independent prostate cancer (AIPC).
  • Based on the expression profile, the efficacy of a combination therapy with a signal transduction inhibitor (STI) and docetaxel was evaluated.Tumor tissue obtained from biopsy of the prostate or lymph node and visceral metastasis was analyzed for the immunohistochemical expression of epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor beta (PDGFRbeta), Her-2/neu, c-KIT, and vascular endothelial growth factor (VEGF).
  • Four of the eight patients (50%) showed a decline in prostate-specific antigen of > or =50%, and median survival time was 13.5 months at a median follow-up of 23.6 (11-35) months.The results show that expression of molecular targets is found in about 90% of patients with AIPC.
  • [MeSH-major] Antibodies, Monoclonal / administration & dosage. Antineoplastic Combined Chemotherapy Protocols / administration & dosage. Biomarkers, Tumor / genetics. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / genetics. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / genetics. Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Androgen / genetics. Taxoids / administration & dosage
  • [MeSH-minor] Antibodies, Monoclonal, Humanized. Benzamides. Bevacizumab. Biopsy. Cetuximab. Disease Progression. Drug Resistance, Neoplasm. Gene Expression Profiling. Humans. Imatinib Mesylate. Lymph Nodes / pathology. Male. Piperazines / administration & dosage. Piperazines / adverse effects. Prospective Studies. Prostate / pathology. Prostate-Specific Antigen / blood. Pyrimidines / administration & dosage. Pyrimidines / adverse effects. Trastuzumab

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. Trastuzumab .
  • Hazardous Substances Data Bank. CETUXIMAB .
  • Hazardous Substances Data Bank. IMATINIB MESYLATE .
  • 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
  • [Cites] Clin Cancer Res. 2000 Dec;6(12):4885-92 [11156248.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2643-7 [11555574.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1918-25 [11106683.001]
  • [Cites] Prostate. 2008 Jun 15;68(9):919-23 [18409189.001]
  • [Cites] Br J Cancer. 2004 Jan 26;90(2):449-54 [14735192.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Pathol Res Pract. 2005;201(8-9):593-8 [16259113.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):2053-63 [10815932.001]
  • [Cites] Clin Cancer Res. 2005 Mar 1;11(5):1983-9 [15756024.001]
  • [Cites] J Clin Oncol. 2007 Jan 1;25(1):118-45 [17159189.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Clin Cancer Res. 2003 Mar;9(3):1087-97 [12631612.001]
  • [Cites] J Urol. 2001 Oct;166(4):1514-9 [11547123.001]
  • [Cites] Clin Cancer Res. 2001 Jul;7(7):1888-93 [11448901.001]
  • [Cites] Semin Oncol. 2004 Dec;31(6 Suppl 17):3-9 [15696024.001]
  • [Cites] Mol Cancer Res. 2007 Mar;5(3):203-20 [17374728.001]
  • [Cites] Prostate. 2005 Feb 1;62(2):115-22 [15389797.001]
  • [Cites] J Clin Oncol. 2008 Jun 1;26(16):2745-53 [18509184.001]
  • [Cites] Am J Surg Pathol. 2006 Jun;30(6):705-12 [16723847.001]
  • [Cites] Am J Pathol. 1999 Oct;155(4):1271-9 [10514409.001]
  • [Cites] Clin Cancer Res. 2002 Nov;8(11):3438-44 [12429632.001]
  • [Cites] Clin Cancer Res. 2007 Oct 1;13(19):5816-24 [17908974.001]
  • [Cites] J Clin Oncol. 2004 Feb 1;22(3):537-56 [14752077.001]
  • [Cites] N Engl J Med. 2006 Dec 14;355(24):2542-50 [17167137.001]
  • (PMID = 18679646.001).
  • [ISSN] 0340-2592
  • [Journal-full-title] Der Urologe. Ausg. A
  • [ISO-abbreviation] Urologe A
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Benzamides; 0 / Biomarkers, Tumor; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Androgen; 0 / Taxoids; 15H5577CQD / docetaxel; 2S9ZZM9Q9V / Bevacizumab; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 3.4.21.77 / Prostate-Specific Antigen; P188ANX8CK / Trastuzumab; PQX0D8J21J / Cetuximab
  •  go-up   go-down


11. Sella A, Sternberg CN, Skoneczna I, Kovel S: Prostate-specific antigen flare phenomenon with docetaxel-based chemotherapy in patients with androgen-independent prostate cancer. BJU Int; 2008 Dec;102(11):1607-9
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] Prostate-specific antigen flare phenomenon with docetaxel-based chemotherapy in patients with androgen-independent prostate cancer.
  • OBJECTIVE: To evaluate the prostate-specific antigen (PSA) 'flare' phenomenon in patients with androgen-independent prostate cancer (AIPC) treated with docetaxel, as flare is a known effect of androgen-deprivation therapy in hormone-dependent prostate cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Prostate-Specific Antigen / metabolism. Prostatic Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. PREDNISONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18990177.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; EC 3.4.21.77 / Prostate-Specific Antigen; VB0R961HZT / Prednisone
  •  go-up   go-down


12. Miyazaki T, Bub JD, Iwamoto Y: c-Jun NH(2)-terminal kinase mediates leptin-stimulated androgen-independent prostate cancer cell proliferation via signal transducer and activator of transcription 3 and Akt. Biochim Biophys Acta; 2008 Oct;1782(10):593-604
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] c-Jun NH(2)-terminal kinase mediates leptin-stimulated androgen-independent prostate cancer cell proliferation via signal transducer and activator of transcription 3 and Akt.
  • Obesity is associated with advanced prostate cancer.
  • Here we demonstrate that in mouse prostate cancer TRAMP-C1 cells epididymal fat extracts from high-fat diet-fed obese mice stimulate androgen-independent cell growth more significantly than those from low-fat diet-fed lean mice or genetically obese leptin-deficient ob/ob mice in correlation with leptin concentrations.
  • This result suggests that obesity promotes androgen-independent prostate cancer cell growth via adipose leptin.
  • We have reported that added leptin stimulates androgen-independent prostate cancer cell proliferation through c-Jun NH(2)-terminal kinase (JNK).
  • As with JNK, signal transducer and activator of transcription 3 (STAT3) and Akt are implicated in androgen-independent prostate cancer.
  • In this study, we identify novel interaction of these three molecules in leptin-stimulated androgen-independent cell proliferation.
  • These findings together indicate that JNK mediates leptin-stimulated androgen-independent prostate cancer cell proliferation via STAT3 and Akt.


13. Jatoi A, Burch P, Hillman D, Vanyo JM, Dakhil S, Nikcevich D, Rowland K, Morton R, Flynn PJ, Young C, Tan W, North Central Cancer Treatment Group: A tomato-based, lycopene-containing intervention for androgen-independent prostate cancer: results of a Phase II study from the North Central Cancer Treatment Group. Urology; 2007 Feb;69(2):289-94
ClinicalTrials.gov. clinical trials - ClinicalTrials.gov .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A tomato-based, lycopene-containing intervention for androgen-independent prostate cancer: results of a Phase II study from the North Central Cancer Treatment Group.
  • This study explored the efficacy of a lycopene-rich tomato product in androgen-independent prostate cancer and the reasons patients participated in an "alternative medicine" study.
  • METHODS: This Phase II study evaluated 46 patients with androgen-independent prostate cancer.
  • All were asymptomatic and had serum prostate-specific antigen elevation despite hormonal manipulation.
  • RESULTS: One patient manifested a tumor response with a 50% or greater confirmed decline in serum prostate-specific antigen level, yielding a response rate of 2%.
  • Lycopene was well tolerated, but 1 patient died of a cancer-related hemorrhage, and 1 had grade 4 diarrhea.
  • CONCLUSIONS: Lycopene, as prescribed in our study, did not appear effective for androgen-independent prostate cancer.
  • [MeSH-major] Androgens / metabolism. Carotenoids / therapeutic use. Dietary Supplements. Prostate-Specific Antigen / blood. Prostatic Neoplasms / therapy

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Dietary Supplements.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17320666.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-15083; United States / NCI NIH HHS / CA / CA-25224; United States / NCI NIH HHS / CA / CA-35101; United States / NCI NIH HHS / CA / CA-35103; United States / NCI NIH HHS / CA / CA-35113; United States / NCI NIH HHS / CA / CA-35119; United States / NCI NIH HHS / CA / CA-35195; United States / NCI NIH HHS / CA / CA-35267; United States / NCI NIH HHS / CA / CA-35269; United States / NCI NIH HHS / CA / CA-37404; United States / NCI NIH HHS / CA / CA-37417; United States / NCI NIH HHS / CA / CA-52352; United States / NCI NIH HHS / CA / CA-60276; United States / NCI NIH HHS / CA / CA-63826
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Anticarcinogenic Agents; 36-88-4 / Carotenoids; EC 3.4.21.77 / Prostate-Specific Antigen; SB0N2N0WV6 / lycopene
  •  go-up   go-down


14. Furutani T, Takeyama K, Koutoku H, Ito S, Taniguchi N, Suzuki E, Kudoh M, Shibasaki M, Shikama H, Kato S: A role of androgen receptor protein in cell growth of an androgen-independent prostate cancer cell line. Biosci Biotechnol Biochem; 2005 Nov;69(11):2236-9
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] A role of androgen receptor protein in cell growth of an androgen-independent prostate cancer cell line.
  • Prostate cancer, which develops due to androgen and is initially responsive to androgen deprivation therapy, often comes to acquire androgen deprivation therapy resistance in short order.
  • We investigated the role of androgen receptor (AR) protein in an androgen-independent prostate cancer cell line using AR ligands and AR siRNA.
  • Although the androgen-independent cell line scarcely responded to AR ligands, their growth was attenuated by ablation of AR protein by siRNA.
  • [MeSH-major] Androgens / pharmacology. Prostatic Neoplasms / pathology. Receptors, Androgen / physiology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16306710.001).
  • [ISSN] 0916-8451
  • [Journal-full-title] Bioscience, biotechnology, and biochemistry
  • [ISO-abbreviation] Biosci. Biotechnol. Biochem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Androgens; 0 / Ligands; 0 / RNA, Small Interfering; 0 / Receptors, Androgen
  •  go-up   go-down


15. Krainer M, Tomek S, Elandt K, Horak P, Albrecht W, Eisenmenger M, Höltl W, Schramek P, Stackl W, Zielinski C, Reibenwein J: A prospective, open label, randomized phase II trial of weekly docetaxel versus weekly vinorelbine as first line chemotherapy in patients with androgen independent prostate cancer. J Urol; 2007 Jun;177(6):2141-5; discussion 2145
Hazardous Substances Data Bank. VINBLASTINE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A prospective, open label, randomized phase II trial of weekly docetaxel versus weekly vinorelbine as first line chemotherapy in patients with androgen independent prostate cancer.
  • PURPOSE: In previous phase I to III studies docetaxel and vinorelbine have shown promising activity in androgen independent prostate cancer.
  • In the present trial we assessed the efficacy and tolerability of single agent low dose docetaxel vs vinorelbine in patients with advanced androgen independent prostate cancer.
  • MATERIALS AND METHODS: A total of 40 chemotherapy naive patients with histologically proven androgen independent prostate cancer, adequate androgen ablation, and clinical and/or biochemical progression were randomly assigned to receive either 25 mg/m(2) docetaxel (arm A) or 25 mg/m(2) vinorelbine (arm B) weekly.
  • Secondary end points included prostate specific antigen response rates in sequential treatment, analgesic response and toxicity.
  • The proportion of patients with a greater than 50% prostate specific antigen decrease on first line therapy was significantly higher in arm A (62.5%) compared to arm B (11.1%) (p = 0.0033).
  • After progression to docetaxel second line vinorelbine yielded a greater than 50% prostate specific antigen response rate of 28.6% vs 62.5% for second line docetaxel.
  • CONCLUSIONS: While weekly application of both cytotoxic agents was well tolerated, this study demonstrates the superiority of docetaxel vs vinorelbine as monotherapy in the treatment of androgen independent prostate cancer.
  • [MeSH-minor] Aged. Aged, 80 and over. Drug Administration Schedule. Humans. Male. Middle Aged. Prospective Studies. Prostate-Specific Antigen / blood. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. VINORELBINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17509302.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Taxoids; 15H5577CQD / docetaxel; 5V9KLZ54CY / Vinblastine; EC 3.4.21.77 / Prostate-Specific Antigen; Q6C979R91Y / vinorelbine
  •  go-up   go-down


16. Singh AP, Bafna S, Chaudhary K, Venkatraman G, Smith L, Eudy JD, Johansson SL, Lin MF, Batra SK: Genome-wide expression profiling reveals transcriptomic variation and perturbed gene networks in androgen-dependent and androgen-independent prostate cancer cells. Cancer Lett; 2008 Jan 18;259(1):28-38
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] Genome-wide expression profiling reveals transcriptomic variation and perturbed gene networks in androgen-dependent and androgen-independent prostate cancer cells.
  • Previously, we have developed a unique in vitro LNCaP cell model, which includes androgen-dependent (LNCaP-C33), androgen-independent (LNCaP-C81) and an intermediate phenotype (LNCaP-C51) cell lines resembling the stages of prostate cancer progression to hormone independence.
  • This model is advantageous in overcoming the heterogeneity associated with the prostate cancer up to a certain extent.
  • We characterized and compared the gene expression profiles in LNCaP-C33 (androgen-dependent) and LNCaP-C81 (androgen-independent) cells using Affymetrix GeneChip array analyses.
  • Multiple genes were identified exhibiting differential expression during androgen-independent progression.
  • Among the important genes upregulated in androgen-independent cells were PCDH7, TPTE, TSPY, EPHA3, HGF, MET, EGF, TEM8, etc., whereas many candidate tumor suppressor genes (HTATIP2, CDKN2A, CDKN2B, CDKN1C, TP53, TP73, ICAM1, SOCS1/2, SPRY2, PPP2CA, PPP3CA, etc.) were decreased.
  • Pathway prediction analysis identified important gene networks associated with growth-promoting and apoptotic signaling that were perturbed during androgen-independent progression.
  • Further investigation of one of the genes, PPP2CA, which encodes the catalytic subunit of a serine phosphatase PP2A, a potent tumor suppressor, revealed that its expression was decreased in prostate cancer compared to adjacent normal/benign tissue.
  • Future studies on the identified differentially expressed genes and signaling pathways may be helpful in understanding the biology of prostate cancer progression and prove useful in developing novel prognostic biomarkers and therapy for androgen-refractory prostate cancer.


17. Mimeault M, Venkatraman G, Johansson SL, Moore E, Henichart JP, Depreux P, Lin MF, Batra SK: Novel combination therapy against metastatic and androgen-independent prostate cancer by using gefitinib, tamoxifen and etoposide. Int J Cancer; 2007 Jan 1;120(1):160-9
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] Novel combination therapy against metastatic and androgen-independent prostate cancer by using gefitinib, tamoxifen and etoposide.
  • In this study, we evaluated, for the first time, the antiproliferative and cytotoxic effects induced by a combination of a selective epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, gefitinib, with other chemotherapeutic drugs including estrogen receptor-beta (ER-beta) antagonist (tamoxifen) and topoisomerase II inhibitor (etoposide) on some metastatic prostate cancer (PC) cell lines.
  • Immunohistochemial analyses revealed that EGFR expression was enhanced in 38% of primary prostatic adenocarcinomas (Gleason scores 4-10) as compared to the corresponding normal tissues of the same prostate gland from 32 PC patients.
  • The RT-PCR and Western blot data have also indicated the higher expression levels of EGFR and ER-beta transcripts and proteins in metastatic LNCaP, DU145 and PC3 cells relative to nonmalignant normal prostate cells.
  • Moreover, the results from MTT and FACS analyses revealed that the drugs, alone or in combination at lower concentrations, inhibited the growth of 17beta-estradiol (E2) plus EGF and serum-stimulated androgen-responsive LNCaP-C33 and androgen-independent LNCaP-C81, DU145 and PC3 cells.
  • [MeSH-minor] Blotting, Western. Caspases / metabolism. Cell Proliferation / drug effects. Cells, Cultured. Ceramides / metabolism. Cytochromes c / metabolism. Drug Synergism. Epidermal Growth Factor / antagonists & inhibitors. Etoposide / administration & dosage. Flow Cytometry. Humans. Immunoenzyme Techniques. Male. Membrane Potential, Mitochondrial / drug effects. Prostate / drug effects. Prostate / metabolism. Quinazolines / administration & dosage. RNA, Messenger / genetics. RNA, Messenger / metabolism. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Reverse Transcriptase Polymerase Chain Reaction. Tamoxifen / administration & dosage

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • 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 = 17013895.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / Quinazolines; 0 / RNA, Messenger; 094ZI81Y45 / Tamoxifen; 62229-50-9 / Epidermal Growth Factor; 6PLQ3CP4P3 / Etoposide; 9007-43-6 / Cytochromes c; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.4.22.- / Caspases; S65743JHBS / gefitinib
  •  go-up   go-down


18. Venkataraman S, Jiang X, Weydert C, Zhang Y, Zhang HJ, Goswami PC, Ritchie JM, Oberley LW, Buettner GR: Manganese superoxide dismutase overexpression inhibits the growth of androgen-independent prostate cancer cells. Oncogene; 2005 Jan 6;24(1):77-89
Hazardous Substances Data Bank. HYDROGEN PEROXIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Manganese superoxide dismutase overexpression inhibits the growth of androgen-independent prostate cancer cells.
  • This study investigates the role of the antioxidant enzyme manganese superoxide dismutase (MnSOD) in androgen-independent human prostate cancer (PC-3) cells' growth rate in vitro and in vivo.
  • MnSOD levels were found to be lower in parental PC-3 cells compared to nonmalignant, immortalized human prostate epithelial cells (P69SV40T).
  • To unravel the role of MnSOD in the prostate cancer phenotype, PC-3 cells were stably transfected with MnSOD cDNA plasmid.
  • These cell lines showed elongated cell doubling time, reduced anchorage-independent growth in soft agar compared to parental PC-3 (Wt) cells, and reduced growth rate of PC-3 tumor xenografts in athymic nude mice.
  • Our results are consistent with MnSOD being a tumor suppressor gene in human prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15543233.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 66081; United States / NCI NIH HHS / CA / CA 81090
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; BBX060AN9V / Hydrogen Peroxide; EC 1.15.1.1 / Superoxide Dismutase
  •  go-up   go-down


19. Marra M, Santini D, Meo G, Vincenzi B, Zappavigna S, Baldi A, Rosolowski M, Tonini G, Loeffler M, Lupu R, Addeo SR, Abbruzzese A, Budillon A, Caraglia M: Cyr61 downmodulation potentiates the anticancer effects of zoledronic acid in androgen-independent prostate cancer cells. Int J Cancer; 2009 Nov 1;125(9):2004-13
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] Cyr61 downmodulation potentiates the anticancer effects of zoledronic acid in androgen-independent prostate cancer cells.
  • We have analyzed the gene modulation induced by zoledronic acid (ZOL) in androgen-resistant prostate cancer PC3 cells with cDNA microarray platform to identify new molecular targets of ZOL in prostate cancer.

  • 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
  • [Copyright] (c) 2009 UICC.
  • (PMID = 19530242.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CYR61 protein, human; 0 / Cysteine-Rich Protein 61; 0 / Diphosphonates; 0 / Imidazoles; 6XC1PAD3KF / zoledronic acid
  •  go-up   go-down


20. Narita S, So A, Ettinger S, Hayashi N, Muramaki M, Fazli L, Kim Y, Gleave ME: GLI2 knockdown using an antisense oligonucleotide induces apoptosis and chemosensitizes cells to paclitaxel in androgen-independent prostate cancer. Clin Cancer Res; 2008 Sep 15;14(18):5769-77
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] GLI2 knockdown using an antisense oligonucleotide induces apoptosis and chemosensitizes cells to paclitaxel in androgen-independent prostate cancer.
  • PURPOSE: GLI transcription factors mediate hedgehog signaling and have been implicated in several human malignancies, including prostate cancer.
  • The objectives of this study were to characterize GLI2 expression levels in human prostate cancer cell lines and tissues to test the effect of antisense oligonucleotide (ASO) targeting GLI2 on androgen-independent (AI) prostate cancer cell lines.
  • EXPERIMENTAL DESIGN: A tissue microarray was used to characterize differences in GLI2 expression in benign prostate hyperplasia, prostate cancer treated by neoadjuvant hormonal therapy and AI prostate cancer.
  • RESULTS: The expression of GLI2 was significantly higher in prostate cancer than in benign prostate hyperplasia, decreased after androgen ablation in a time-dependent fashion, but became highly expressed again in AI prostate cancer.
  • CONCLUSIONS: These findings suggest that increased levels of GLI2 correlates with AI progression and that GLI2 may be a therapeutic target in castrate-resistant prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • 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 = 18794086.001).
  • [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 / Antineoplastic Agents, Phytogenic; 0 / GLI2 protein, human; 0 / Kruppel-Like Transcription Factors; 0 / MRL1 protein, S cerevisiae; 0 / Membrane Proteins; 0 / Nuclear Proteins; 0 / Oligonucleotides, Antisense; 0 / Saccharomyces cerevisiae Proteins; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


21. Wang Q, Li W, Zhang Y, Yuan X, Xu K, Yu J, Chen Z, Beroukhim R, Wang H, Lupien M, Wu T, Regan MM, Meyer CA, Carroll JS, Manrai AK, Jänne OA, Balk SP, Mehra R, Han B, Chinnaiyan AM, Rubin MA, True L, Fiorentino M, Fiore C, Loda M, Kantoff PW, Liu XS, Brown M: Androgen receptor regulates a distinct transcription program in androgen-independent prostate cancer. Cell; 2009 Jul 23;138(2):245-56
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] Androgen receptor regulates a distinct transcription program in androgen-independent prostate cancer.
  • The evolution of prostate cancer from an androgen-dependent state to one that is androgen-independent marks its lethal progression.
  • The androgen receptor (AR) is essential in both, though its function in androgen-independent cancers is poorly understood.
  • We have defined the direct AR-dependent target genes in both androgen-dependent and -independent cancer cells by generating AR-dependent gene expression profiles and AR cistromes.
  • In contrast to what is found in androgen-dependent cells, AR selectively upregulates M-phase cell-cycle genes in androgen-independent cells, including UBE2C, a gene that inactivates the M-phase checkpoint.
  • We find that epigenetic marks at the UBE2C enhancer, notably histone H3K4 methylation and FoxA1 transcription factor binding, are present in androgen-independent cells and direct AR-enhancer binding and UBE2C activation.
  • Thus, the role of AR in androgen-independent cancer cells is not to direct the androgen-dependent gene expression program without androgen, but rather to execute a distinct program resulting in androgen-independent growth.


22. Laidler P, Dulińska J, Lekka M, Lekki J: Expression of prostate specific membrane antigen in androgen-independent prostate cancer cell line PC-3. Arch Biochem Biophys; 2005 Mar 1;435(1):1-14
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] Expression of prostate specific membrane antigen in androgen-independent prostate cancer cell line PC-3.
  • During the progression of prostate cancer from androgen-dependence or sensitivity to androgen-independence, the overall expression of prostate specific membrane antigen (PSMA) increases with its appearance in plasma membrane.
  • However, surprisingly some androgen-independent metastatic prostate cancer cell lines do not express this protein.
  • Estradiol (E2) and basic fibroblast growth factor (bFGF) due to their recognized and strong involvement in prostate growth, development, and pathology were selected with the aim of restoring the expression of PSMA in markedly dedifferentiated prostate cancer PC-3 cells and in Du 145.
  • [MeSH-major] Androgens / metabolism. Estradiol / pharmacology. Fibroblast Growth Factor 2 / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Membrane Proteins / metabolism. Prostate-Specific Antigen / metabolism. Prostatic Neoplasms / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • Hazardous Substances Data Bank. ESTRADIOL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15680901.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Membrane Proteins; 103107-01-3 / Fibroblast Growth Factor 2; 4TI98Z838E / Estradiol; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


23. Dhupkar P, Dowling M, Cengel K, Chen B: Effects of anti-EGFR antibody cetuximab on androgen-independent prostate cancer cells. Anticancer Res; 2010 Jun;30(6):1905-10
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] Effects of anti-EGFR antibody cetuximab on androgen-independent prostate cancer cells.
  • This study examined the effects of anti-EGFR antibody cetuximab on two human androgen-independent prostate carcinoma cell lines, Du145 and PC-3.
  • Cetuximab was not able to inhibit Akt phosphorylation in either prostate cancer cell line.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. CETUXIMAB .
  • 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 = 20651333.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.1.3.48 / PTEN protein, human; EC 3.1.3.67 / PTEN Phosphohydrolase; PQX0D8J21J / Cetuximab
  •  go-up   go-down


24. Jennbacken K, Gustavsson H, Tesan T, Horn M, Vallbo C, Welén K, Damber JE: The prostatic environment suppresses growth of androgen-independent prostate cancer xenografts: an effect influenced by testosterone. Prostate; 2009 Aug 1;69(11):1164-75
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 prostatic environment suppresses growth of androgen-independent prostate cancer xenografts: an effect influenced by testosterone.
  • BACKGROUND: Interactions between prostate cancer cells and their surrounding stroma play an important role in the growth and maintenance of prostate tumors.
  • To elucidate this further, we investigated how growth of androgen-dependent (AD) LNCaP and androgen-independent (AI) LNCaP-19 prostate tumors was affected by different microenvironments and androgen levels.
  • RESULTS: The results showed that LNCaP-19 tumors grew more rapidly at the subcutaneous site than in the prostate, where tumors were obviously inhibited.
  • In contrast to LNCaP-19, the LNCaP cells grew rapidly in the prostate and castration reduced tumor development.
  • Data indicate that the androgen-stimulated prostatic environment limits growth of orthotopic AI tumors through induction of genes that inhibit tumor growth and suppression of genes that promote cell adhesion and metastasis.
  • [MeSH-major] Adenocarcinoma / pathology. Androgens / physiology. Cell Proliferation / drug effects. Prostate / physiology. Prostatic Neoplasms / pathology. Testosterone / pharmacology. Transplantation, Heterologous / pathology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. TESTOSTERONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19399749.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Cadherins; 0 / Cell Adhesion Molecules; 0 / NRCAM protein, human; 0 / RGS Proteins; 0 / RGS2 protein, human; 3XMK78S47O / Testosterone; EC 3.4.24.- / ADAM Proteins; EC 3.4.24.- / ADAMTS1 protein, human
  •  go-up   go-down


25. Coleman IM, Kiefer JA, Brown LG, Pitts TE, Nelson PS, Brubaker KD, Vessella RL, Corey E: Inhibition of androgen-independent prostate cancer by estrogenic compounds is associated with increased expression of immune-related genes. Neoplasia; 2006 Oct;8(10):862-78
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] Inhibition of androgen-independent prostate cancer by estrogenic compounds is associated with increased expression of immune-related genes.
  • The clinical utility of estrogens for treating prostate cancer (CaP) was established in the 1940s by Huggins.
  • The classic model of the anti-CaP activity of estrogens postulates an indirect mechanism involving the suppression of androgen production.
  • However, clinical and preclinical studies have shown that estrogens exert growth-inhibitory effects on CaP under low-androgen conditions, suggesting additional modes whereby estrogens affect CaP cells and/or the microenvironment.
  • Here we have investigated the activity of 17beta estradiol (E2) against androgen-independent CaP and identified molecular alterations in tumors exposed to E2.
  • E2 treatment inhibited the growth of all four androgen-independent CaP xenografts studied (LuCaP 35V, LuCaP 23.1AI, LuCaP 49, and LuCaP 58) in castrated male mice.
  • Of particular interest are changes in transcripts encoding proteins that mediate immune responses and regulate androgen receptor signaling.
  • In conclusion, our data show that estrogens have powerful inhibitory effects on CaP in vivo in androgen-depleted environments and suggest novel mechanisms of estrogen-mediated antitumor activity.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Nuclear Receptor Signaling Atlas (NURSA). supplemental materials - Curated dataset for this article .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • SciCrunch. Nuclear Receptor Signaling Atlas: Data: Gene Expression .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1994 Mar 1;54(5):1190-3 [8118804.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Dec 7;289(3):692-9 [11726203.001]
  • [Cites] J Urol. 1995 Dec;154(6):1991-8 [7500443.001]
  • [Cites] JAMA. 1996 Apr 17;275(15):1153 [8609673.001]
  • [Cites] Cancer. 1996 May 1;77(9):1862-72 [8646686.001]
  • [Cites] Int J Cancer. 1996 Sep 17;67(6):785-90 [8824549.001]
  • [Cites] Mol Cell Biochem. 1997 Feb;167(1-2):169-77 [9059994.001]
  • [Cites] Prostate. 1997 Dec 1;33(4):233-9 [9397194.001]
  • [Cites] Clin Cancer Res. 1996 Jun;2(6):1039-48 [9816265.001]
  • [Cites] Nucleic Acids Res. 1999 Jan 1;27(1):204-8 [9847181.001]
  • [Cites] Carcinogenesis. 2005 Jun;26(6):1109-16 [15731164.001]
  • [Cites] J Endocrinol Invest. 2005;28(3 Suppl):65-75 [16044582.001]
  • [Cites] Carcinogenesis. 2005 Sep;26(9):1527-35 [15878912.001]
  • [Cites] Prostate. 2005 Oct 1;65(2):141-50 [15924336.001]
  • [Cites] Nucleic Acids Res. 2000 Jan 1;28(1):212-3 [10592228.001]
  • [Cites] J Pathol. 2000 Feb;190(2):169-76 [10657015.001]
  • [Cites] Nat Genet. 2000 May;25(1):25-9 [10802651.001]
  • [Cites] Cancer Res. 2000 Jun 15;60(12):3175-82 [10866308.001]
  • [Cites] Cancer Res. 2000 Jul 15;60(14):3904-8 [10919667.001]
  • [Cites] J Neurooncol. 2000 Jul;48(3):225-32 [11100820.001]
  • [Cites] Blood. 2001 Jan 1;97(1):192-7 [11133760.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499.001]
  • [Cites] Mol Cell Endocrinol. 2001 Jun 10;178(1-2):47-50 [11403893.001]
  • [Cites] Endocrinology. 2002 Jan;143(1):313-9 [11751623.001]
  • [Cites] Nucleic Acids Res. 2002 Jan 1;30(1):218-20 [11752298.001]
  • [Cites] J Interferon Cytokine Res. 2002 Jan;22(1):39-47 [11846974.001]
  • [Cites] Clin J Oncol Nurs. 2002 Mar-Apr;6(2):88-93 [11889683.001]
  • [Cites] J Urol. 2002 Feb;167(2 Pt 2):948-51; discussion 952 [11905923.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1003-7 [11948106.001]
  • [Cites] Int J Cancer. 2002 May 1;99(1):149-53 [11948506.001]
  • [Cites] Nihon Hinyokika Gakkai Zasshi. 2002 May;93(4):532-8 [12056037.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3649-53 [12097269.001]
  • [Cites] Am J Pathol. 2002 Aug;161(2):705-15 [12163395.001]
  • [Cites] Genome Biol. 2002 Jun 14;3(7):RESEARCH0032 [12184806.001]
  • [Cites] Genome Biol. 2002 Jun 18;3(7):RESEARCH0034 [12184808.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11890-5 [12185249.001]
  • [Cites] Int J Urol. 2002 Aug;9(8):431-4 [12225339.001]
  • [Cites] Cancer Res. 2002 Sep 15;62(18):5365-9 [12235008.001]
  • [Cites] BJU Int. 2002 Nov;90(7):748-53 [12410760.001]
  • [Cites] J Natl Cancer Inst. 2002 Nov 6;94(21):1641-7 [12419791.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Mar 28;303(1):219-22 [12646190.001]
  • [Cites] Prostate. 2003 Jun 1;55(4):239-46 [12712403.001]
  • [Cites] Prostate. 2003 Jun 15;56(1):13-22 [12746842.001]
  • [Cites] Mol Cancer Ther. 2004 May;3(5):587-95 [15141016.001]
  • [Cites] Am J Pathol. 2004 Jun;164(6):2003-12 [15161636.001]
  • [Cites] Urology. 2004 Oct;64(4):814-20 [15491740.001]
  • [Cites] Surg Gynecol Obstet. 1967 May;124(5):1011-7 [6022476.001]
  • [Cites] J Urol. 1967 Oct;98(4):516-22 [4862213.001]
  • [Cites] Br Med J. 1968 Jan 6;1(5583):28-30 [5636740.001]
  • [Cites] JAMA. 1969 Nov 10;210(6):1074-5 [5394427.001]
  • [Cites] Cancer. 1970 Aug;26(2):257-61 [4916020.001]
  • [Cites] Urol Res. 1982;10(3):119-22 [6890254.001]
  • [Cites] Cancer. 1986 Aug 15;58(4):985-93 [3719562.001]
  • [Cites] Mol Endocrinol. 1988 Jul;2(7):650-7 [3137456.001]
  • [Cites] NCI Monogr. 1988;(7):165-70 [3050535.001]
  • [Cites] Cancer Res. 1991 Sep 1;51(17):4712-5 [1873815.001]
  • [Cites] Cancer Res. 1991 Dec 1;51(23 Pt 1):6372-80 [1933900.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517.001]
  • [Cites] BJU Int. 2006 Apr;97(4):691-7 [16536755.001]
  • [Cites] Am J Pathol. 2001 Jul;159(1):79-92 [11438457.001]
  • [Cites] Cancer Res. 2001 Jul 15;61(14):5331-5 [11454669.001]
  • [Cites] Cancer Res. 2001 Oct 1;61(19):7142-7 [11585747.001]
  • [Cites] Microsc Res Tech. 1995 Mar 1;30(4):293-304 [7541676.001]
  • (PMID = 17032503.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA085859; United States / NCI NIH HHS / CA / P50 CA097186; United States / NCI NIH HHS / CA / CA85859; United States / NCI NIH HHS / CA / CA97186
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 4TI98Z838E / Estradiol
  • [Other-IDs] NLM/ PMC1715921
  •  go-up   go-down


26. Culine S, El Demery M, Lamy PJ, Iborra F, Avancès C, Pinguet F: Docetaxel and cisplatin in patients with metastatic androgen independent prostate cancer and circulating neuroendocrine markers. J Urol; 2007 Sep;178(3 Pt 1):844-8; discussion 848
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] Docetaxel and cisplatin in patients with metastatic androgen independent prostate cancer and circulating neuroendocrine markers.
  • PURPOSE: A link between neuroendocrine cell differentiation and resistance to androgen deprivation has been observed in prostate cancer, suggesting the possible efficacy of specific treatments.
  • We assessed the efficacy and toxicity of a chemotherapy regimen combining docetaxel and cisplatin in men with androgen independent prostatic adenocarcinoma and circulating neuroendocrine markers.
  • The prostate specific antigen response rate was 48%.


27. Fina F, Muracciole X, Rocchi P, Nanni-Métellus I, Delfino C, Daniel L, Dussert C, Ouafik L', Martin PM: Molecular profile of androgen-independent prostate cancer xenograft LuCaP 23.1. J Steroid Biochem Mol Biol; 2005 Sep;96(5):355-65
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] Molecular profile of androgen-independent prostate cancer xenograft LuCaP 23.1.
  • After castration or therapeutic hormone deprivation, most cancer of the prostate (CaP) cells develop androgen-independent (AI) growth.
  • In this work, we studied the effect of androgen depletion (castration) on the growth of experimental model LuCaP 23.1 xenograft.
  • The progressive tumors FG-P, and some tumors of SG-P subgroup, presented significantly high levels of HER1, epidermal growth factor receptor type 2 (HER2), TS, uPA, TP, tumor necrosis factor superfamily member 6 (FAS) and peptidylglycine alpha-amidating mono-oxygenase (PAM) mRNA all of which correlated with androgen receptor (AR) mRNA.
  • [MeSH-minor] Adrenomedullin. Animals. Castration. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Peptides / metabolism. Prostate-Specific Antigen / metabolism. Thymidine Phosphorylase / metabolism. Tumor Necrosis Factors / metabolism. Vascular Endothelial Growth Factor A / metabolism


28. Mellado B, Codony J, Ribal MJ, Visa L, Gascón P: Molecular biology of androgen-independent prostate cancer: the role of the androgen receptor pathway. Clin Transl Oncol; 2009 Jan;11(1):5-10
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] Molecular biology of androgen-independent prostate cancer: the role of the androgen receptor pathway.
  • Prostate cancer (PC) cells express the androgen receptor (AR) and need the presence of androgens to survive.
  • Androgen suppression is the gold standard first-line therapy for metastatic disease.
  • Several mechanisms that enhance AR signalling in an androgen-depleted environment have been elucidated:.
  • (1) AR mutations that allow activation by low androgen levels or by other endogenous steroids, (2) AR amplification and/or overexpression, (3) increased local intracrine synthesis of androgens, (4) changes in AR cofactors and (5) cross-talk with cytokines and growth factors.
  • [MeSH-major] Drug Resistance, Neoplasm / genetics. Prostatic Neoplasms / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Signal Transduction / physiology
  • [MeSH-minor] Androgen Antagonists / therapeutic use. Humans. Male. Molecular Biology / trends

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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 = 19155198.001).
  • [ISSN] 1699-048X
  • [Journal-full-title] Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico
  • [ISO-abbreviation] Clin Transl Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Spain
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Receptors, Androgen
  • [Number-of-references] 42
  •  go-up   go-down


29. Sun T, Wang Q, Balk S, Brown M, Lee GS, Kantoff P: The role of microRNA-221 and microRNA-222 in androgen-independent prostate cancer cell lines. Cancer Res; 2009 Apr 15;69(8):3356-63
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] The role of microRNA-221 and microRNA-222 in androgen-independent prostate cancer cell lines.
  • Androgen-dependent prostate cancer typically progresses to castration-resistant prostate cancer (CRPC) after the androgen deprivation therapy.
  • Recent studies have shown that miR expression patterns are significantly different in normal and neoplastic prostate epithelial cells.
  • By performing genome-wide expression profiling of miRs, we found that expression levels of several miRs, in particular miR-221 and miR-222, were significantly increased in CRPC cells (the LNCaP-derived cell line LNCaP-Abl), compared with those in the androgen-dependent prostate cancer cell line (LNCaP).
  • Overexpression of miR-221 or miR-222 in LNCaP or another androgen-dependent cell line, LAPC-4, significantly reduced the level of the dihydrotestosterone (DHT) induced up-regulation of prostate-specific antigen (PSA) expression and increased androgen-independent growth of LNCaP cells.
  • Knocking down the expression level of miR-221 and miR-222 with antagonist miRs in the LNCaP-Abl cell line restored the response to the DHT induction of PSA transcription and also increased the growth response of the LNCaP-Abl cells to the androgen treatment.
  • Changing the expression level of p27/kip1, a known target of miR-221 and miR-222, alone in LNCaP cells affected the DHT-independent cell growth but did not significantly influence the response of PSA transcription to the DHT treatment.

  • Genetic Alliance. consumer health - Prostate 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 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] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Jan;8(1):23-36 [17183358.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6130-5 [17616669.001]
  • [Cites] J Biol Chem. 2007 Aug 10;282(32):23716-24 [17569667.001]
  • [Cites] Mol Cell. 2007 Aug 3;27(3):380-92 [17679089.001]
  • [Cites] EMBO J. 2007 Aug 8;26(15):3699-708 [17627278.001]
  • [Cites] Annu Rev Cell Dev Biol. 2007;23:175-205 [17506695.001]
  • [Cites] Cell Cycle. 2007 Nov 15;6(22):2742-9 [17986865.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 11;104(50):19983-8 [18056640.001]
  • [Cites] Cell. 2007 Dec 28;131(7):1273-86 [18155131.001]
  • [Cites] RNA. 2008 Mar;14(3):417-24 [18174313.001]
  • [Cites] Nat Rev Cancer. 2008 Apr;8(4):253-67 [18354415.001]
  • [Cites] Cancer Res. 2008 Apr 15;68(8):2773-80 [18413744.001]
  • [Cites] Oncogene. 2008 Jun 19;27(27):3845-55 [18246122.001]
  • [Cites] Science. 2008 Jun 20;320(5883):1643-7 [18566288.001]
  • [Cites] Cell Cycle. 2008 Aug 15;7(16):2570-83 [18719369.001]
  • [Cites] Oncogene. 2008 Sep 25;27(43):5651-61 [18521080.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Oct 21;105(42):16230-5 [18852463.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] J Urol. 2002 Jul;168(1):9-12 [12050481.001]
  • [Cites] Oncogene. 2004 Aug 26;23(39):6684-92 [15221013.001]
  • [Cites] Prog Clin Biol Res. 1980;37:115-32 [7384082.001]
  • [Cites] Nat Med. 1997 Apr;3(4):402-8 [9095173.001]
  • [Cites] Mol Endocrinol. 1998 Jul;12(7):941-53 [9658399.001]
  • [Cites] Br J Cancer. 1999 Sep;81(2):242-51 [10496349.001]
  • [Cites] Nature. 2005 Jun 9;435(7043):834-8 [15944708.001]
  • [Cites] Mol Cell. 2005 Sep 2;19(5):631-42 [16137620.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 13;102(50):18081-6 [16330772.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19075-80 [16365291.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460.001]
  • [Cites] Cancer Cell. 2006 Mar;9(3):189-98 [16530703.001]
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] Dev Cell. 2006 Oct;11(4):441-50 [17011485.001]
  • [Cites] J Clin Oncol. 2006 Oct 10;24(29):4677-84 [16966691.001]
  • [Cites] Blood. 2006 Nov 1;108(9):3068-71 [16849646.001]
  • (PMID = 19351832.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P50 CA090381; United States / NCI NIH HHS / CA / P50 CA090381-06; United States / NCI NIH HHS / CA / 2 P50 CA090381-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / MIRN221 microRNA, human; 0 / MIRN222 microRNA, human; 0 / MicroRNAs; 0 / Receptors, Androgen; 08J2K08A3Y / Dihydrotestosterone
  • [Other-IDs] NLM/ NIHMS97177; NLM/ PMC2703812
  •  go-up   go-down


30. Terracciano D, Mazzarella C, Di Carlo A, Mariano A, Ferro M, Di Lorenzo G, Giordano A, Altieri V, De Placido S, Macchia V: Effects of the ErbB1/ErbB2 kinase inhibitor GW2974 on androgen-independent prostate cancer PC-3 cell line growth and NSE, chromogranin A and osteopontin content. Oncol Rep; 2010 Jul;24(1):213-7
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] Effects of the ErbB1/ErbB2 kinase inhibitor GW2974 on androgen-independent prostate cancer PC-3 cell line growth and NSE, chromogranin A and osteopontin content.
  • Prostate cancer is one of the most frequently diagnosed cancer in men.
  • Treatment by radical prostatectomy, radiotherapy and anti-androgen drugs is successful in patients with localized cancer.
  • However, prolonged androgen deprivation often leads to hormone refractory condition, associated with disease relapse.
  • ErbB1 and ErbB2 activity has been correlated with androgen-independence.
  • We determined the effects of GW2974, a dual inhibitor of ErbB-1 and ErbB-2 tyrosine kinase activity, on growth, NSE, chromogranin A and osteopontin cytosol content in the androgen-independent prostate cancer cell line PC-3.
  • The present data may have clinical implications for the treatment of advanced prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20514464.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; 0 / Carrier Proteins; 0 / Chromogranin A; 0 / GW2974; 0 / NSE1 protein, human; 0 / Quinazolines; 106441-73-0 / Osteopontin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, ErbB-2
  •  go-up   go-down


31. Yan X, Shen H, Jiang H, Zhang C, Hu D, Wang J, Wu X: External Qi of Yan Xin Qigong induces G2/M arrest and apoptosis of androgen-independent prostate cancer cells by inhibiting Akt and NF-kappa B pathways. Mol Cell Biochem; 2008 Mar;310(1-2):227-34
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] External Qi of Yan Xin Qigong induces G2/M arrest and apoptosis of androgen-independent prostate cancer cells by inhibiting Akt and NF-kappa B pathways.
  • In order to understand the molecular mechanisms underlying the antitumor effects of YXQG-EQ, we investigate the effects of YXQG-EQ on growth and apoptosis in androgen-independent prostate cancer PC3 cells.
  • These results indicate that YXQG-EQ has profound effects on growth and apoptosis of prostate cancer cells by targeting survival pathways including the Akt and NF-kappa B pathways.


32. Gravina GL, Festuccia C, Millimaggi D, Dolo V, Tombolini V, de Vito M, Vicentini C, Bologna M: Chronic azacitidine treatment results in differentiating effects, sensitizes against bicalutamide in androgen-independent prostate cancer cells. Prostate; 2008 May 15;68(7):793-801
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] Chronic azacitidine treatment results in differentiating effects, sensitizes against bicalutamide in androgen-independent prostate cancer cells.
  • BACKGROUND: About 20-30% of hormone-independent PCa are characterized by the extensive loss of AR expression that appears to occur at the transcriptional level.
  • Here, we investigate the effect of Aza-CR administered both acutely and chronically on AR expression, PSA expression, cell survival, and proliferation in androgen-independent/AR-negative PCa cells.
  • METHODS: The in vitro effect of Aza-CR as single agent and its ability to induce AR expression and to augment the efficacy to bicalutamide were assessed using two androgen-independent and AR-negative cell lines (PC3 and DU145).
  • Furthermore, following Aza-CR chronic treatment the formerly androgen-independent PC3 and DU145 cells increase their susceptibility to the apoptotic effects of bicalutamide.
  • CONCLUSIONS: Aza-CR acute treatment has modest effects on androgen-independent and AR-negative PCa cell survival and proliferation, but chronic administration results in profound decrease in proliferation and in sensitization to antiandrogen agents.
  • All these effects seem, in some measure, dependent on a partial restoration of androgen regulation.
  • [MeSH-major] Androgen Antagonists / pharmacology. Anilides / pharmacology. Antineoplastic Agents / pharmacology. Azacitidine / pharmacology. Nitriles / pharmacology. Prostatic Neoplasms / drug therapy. Tosyl Compounds / pharmacology
  • [MeSH-minor] Androgens / metabolism. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. Gene Silencing. Humans. Male. Prostate-Specific Antigen / metabolism. RNA, Small Interfering / metabolism. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Repressor Proteins / genetics. Repressor Proteins / metabolism

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • 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
  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18324645.001).
  • [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 / Androgen Antagonists; 0 / Androgens; 0 / Anilides; 0 / Antineoplastic Agents; 0 / DMAP1 protein, human; 0 / Nitriles; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 0 / Repressor Proteins; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide; EC 3.4.21.77 / Prostate-Specific Antigen; M801H13NRU / Azacitidine
  •  go-up   go-down


33. Shaw G, Prowse DM: Inhibition of androgen-independent prostate cancer cell growth is enhanced by combination therapy targeting Hedgehog and ErbB signalling. Cancer Cell Int; 2008;8:3
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] Inhibition of androgen-independent prostate cancer cell growth is enhanced by combination therapy targeting Hedgehog and ErbB signalling.
  • BACKGROUND: Prostate cancer is a leading cause of male cancer specific mortality.
  • When cure by radical prostatectomy is not possible the next line of prostate cancer treatment is androgen deprivation.
  • However prolonged androgen deprivation often results in relapse and androgen-independent prostate cancer that is inevitably fatal despite optimal chemotherapy.
  • The Hedgehog signalling pathway has recently been implicated in prostate cancer development and metastasis.
  • EGFR or ErbB2 expression has been also correlated with androgen independence, shorter survival and metastasis.
  • RESULTS: We determined that the Hedgehog and ErbB signalling pathways are active in circulating tumour cells isolated from androgen-independent prostate cancer patients and in the androgen-independent prostate cancer cell line LNCaP C4-2B.
  • Androgen-independent prostate cancer cell growth was inhibited by a SMO inhibitor (cyclopamine) which blocks Hedgehog signalling and by ErbB inhibitors (gefitinib and lapatinib).
  • CONCLUSION: Androgen-independent prostate cancer cell proliferation was associated with activity of the Hedgehog and ErbB signalling pathways.
  • Cyclopamine, gefitinib or lapatinib treatment significantly decreased the proliferation of androgen-independent prostate cancer cells.
  • The Hedgehog pathway therefore represents a promising new therapeutic target in androgen-independent prostate cancer.
  • This study may have clinical implications for improving the treatment of advanced 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
  • [Cites] Prostate. 2004 Sep 1;60(4):332-7 [15264245.001]
  • [Cites] Oncol Rep. 2004 Jun;11(6):1273-9 [15138566.001]
  • [Cites] Nature. 2004 Oct 7;431(7009):707-12 [15361885.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Mol Cancer. 2004 Oct 13;3:29 [15482598.001]
  • [Cites] Br J Cancer. 2005 Jan 17;92(1):36-40 [15570307.001]
  • [Cites] J Clin Oncol. 2005 Jan 20;23(3):455-60 [15659491.001]
  • [Cites] Int J Cancer. 2005 Jul 1;115(4):630-40 [15700310.001]
  • [Cites] J Clin Oncol. 2005 Mar 1;23(7):1420-30 [15735118.001]
  • [Cites] Urology. 2005 Apr;65(4):713-8 [15833514.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3404-9 [15833875.001]
  • [Cites] Int J Cancer. 2006 Feb 15;118(4):1022-31 [16108016.001]
  • [Cites] Carcinogenesis. 2006 Jan;27(1):1-22 [16195239.001]
  • [Cites] Cell Mol Life Sci. 2006 Feb;63(4):435-48 [16389455.001]
  • [Cites] Prostate. 2006 Sep 15;66(13):1437-44 [16741920.001]
  • [Cites] N C Med J. 2006 Mar-Apr;67(2):122-7 [16752715.001]
  • [Cites] Urology. 2006 Jul;68(1):110-5 [16806433.001]
  • [Cites] Mol Cell Biol. 2006 Aug;26(16):6283-98 [16880536.001]
  • [Cites] Int J Cancer. 2007 Jan 1;120(1):160-9 [17013895.001]
  • [Cites] BJU Int. 2007 May;99(5):1056-65 [17346277.001]
  • [Cites] Adv Enzyme Regul. 1984;22:27-55 [6382953.001]
  • [Cites] In Vivo. 1994 May-Jun;8(3):439-43 [7803731.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2577-81 [8168083.001]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2861-4 [8187068.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3550-5 [11325816.001]
  • [Cites] J Urol. 2001 Oct;166(4):1514-9 [11547123.001]
  • [Cites] J Clin Endocrinol Metab. 2003 Jul;88(7):2972-82 [12843129.001]
  • [Cites] Prostate. 2003 Nov 1;57(3):205-25 [14518029.001]
  • [Cites] Clin Chem. 2004 May;50(5):826-35 [14988224.001]
  • [Cites] Int J Cancer. 2004 Oct 20;112(1):78-86 [15305378.001]
  • (PMID = 18348720.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2311276
  •  go-up   go-down


34. Luo Y, Ling Y, Guo W, Pang J, Liu W, Fang Y, Wen X, Wei K, Gao X: Docetaxel loaded oleic acid-coated hydroxyapatite nanoparticles enhance the docetaxel-induced apoptosis through activation of caspase-2 in androgen independent prostate cancer cells. J Control Release; 2010 Oct 15;147(2):278-88
Hazardous Substances Data Bank. HYDROXYAPATITE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Docetaxel loaded oleic acid-coated hydroxyapatite nanoparticles enhance the docetaxel-induced apoptosis through activation of caspase-2 in androgen independent prostate cancer cells.
  • Docetaxel (Dtxl) remains the preferred choice of improving the survival of patients with hormone refractory prostate cancer (HRPC), but many patients suffer from modest drug response and significant toxicity.
  • The Dtxl-NPs exhibited significantly more cytotoxicity in both prostate cancer cell lines (PC3 and DU145) compared with Dtxl in vitro and increased the Dtxl-induced apoptosis in the PC3 cells.

  • Genetic Alliance. consumer health - Prostate cancer.
  • Hazardous Substances Data Bank. OLEIC ACID .
  • Hazardous Substances Data Bank. DOCETAXEL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • (PMID = 20655966.001).
  • [ISSN] 1873-4995
  • [Journal-full-title] Journal of controlled release : official journal of the Controlled Release Society
  • [ISO-abbreviation] J Control Release
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Drug Carriers; 0 / RNA, Small Interfering; 0 / Taxoids; 15H5577CQD / docetaxel; 2UMI9U37CP / Oleic Acid; 91D9GV0Z28 / Durapatite; EC 3.4.22.- / CASP2 protein, human; EC 3.4.22.- / Caspase 2; EC 3.4.22.- / Cysteine Endopeptidases
  •  go-up   go-down


35. Lee DI, Sumbilla C, Lee M, Natesavelalar C, Klein MG, Ross DD, Inesi G, Hussain A: Mechanisms of resistance and adaptation to thapsigargin in androgen-independent prostate cancer PC3 and DU145 cells. Arch Biochem Biophys; 2007 Aug 1;464(1):19-27
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] Mechanisms of resistance and adaptation to thapsigargin in androgen-independent prostate cancer PC3 and DU145 cells.
  • Thus, novel TG-specific resistance mechanisms are recruited by these cancer cells.

  • Genetic Alliance. consumer health - Prostate cancer.
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17475205.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Enzyme Inhibitors; 0 / RNA, Small Interfering; 67526-95-8 / Thapsigargin; EC 3.6.3.8 / ATP2A2 protein, human; EC 3.6.3.8 / Sarcoplasmic Reticulum Calcium-Transporting ATPases; SY7Q814VUP / Calcium
  •  go-up   go-down


36. Gill C, Walsh SE, Morrissey C, Fitzpatrick JM, Watson RW: Resveratrol sensitizes androgen independent prostate cancer cells to death-receptor mediated apoptosis through multiple mechanisms. Prostate; 2007 Nov 1;67(15):1641-53
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] Resveratrol sensitizes androgen independent prostate cancer cells to death-receptor mediated apoptosis through multiple mechanisms.
  • BACKGROUND: A critical factor in prostate cancer development and progression is the altered expression of apoptotic regulatory proteins which renders cells resistant to both hormone- and chemo-therapies.
  • Resveratrol, a dietary component with chemopreventive properties has been reported to resensitize a variety of cancer cell types to apoptosis.
  • In the current study, the ability of resveratrol pre-treatment to sensitize hormone refractory prostate cancer cell lines (PC-3 and DU145) to apoptosis and the mechanisms involved were investigated.
  • CONCLUSION: Altering apoptotic susceptibility in advanced androgen independent disease requires manipulation of a broad signaling pathway.
  • Use of resveratrol or inhibition of Akt phosphorylation may represent an important therapeutic approach in combination with conventional therapies for the treatment of prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. RESVERATROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17823925.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / BIRC2 protein, human; 0 / Chromones; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / Inhibitor of Apoptosis Proteins; 0 / Morpholines; 0 / RNA, Small Interfering; 0 / Receptors, Death Domain; 0 / Stilbenes; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 6.3.2.19 / Ubiquitin-Protein Ligases; Q369O8926L / resveratrol
  •  go-up   go-down


37. Gu YH, Sivam G: Cytotoxic effect of oyster mushroom Pleurotus ostreatus on human androgen-independent prostate cancer PC-3 cells. J Med Food; 2006;9(2):196-204
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] Cytotoxic effect of oyster mushroom Pleurotus ostreatus on human androgen-independent prostate cancer PC-3 cells.
  • Twenty species of edible mushrooms and three purified mushroom polysaccharides were screened for their antitumor potential on human androgen-independent cancer PC-3 cells.
  • Interestingly, PC-3 cells appeared to be more sensitive to POE in anchorage-independent growth condition.

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16822205.001).
  • [ISSN] 1096-620X
  • [Journal-full-title] Journal of medicinal food
  • [ISO-abbreviation] J Med Food
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / T32-AT00815
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  •  go-up   go-down


38. Quayle SN, Hare H, Delaney AD, Hirst M, Hwang D, Schein JE, Jones SJ, Marra MA, Sadar MD: Novel expressed sequences identified in a model of androgen independent prostate cancer. BMC Genomics; 2007;8:32
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Novel expressed sequences identified in a model of androgen independent prostate cancer.
  • BACKGROUND: Prostate cancer is the most frequently diagnosed cancer in American men, and few effective treatment options are available to patients who develop hormone-refractory prostate cancer.
  • The molecular changes that occur to allow prostate cells to proliferate in the absence of androgens are not fully understood.
  • RT-PCR experiments confirmed that the 6 sequences tested were expressed in specific human tissues, as well as in clinical samples of prostate cancer.
  • The tissue-specific expression of 4 of the 6 clones tested indicates the expression of these novel transcripts is tightly regulated, and future work will determine the possible role(s) these novel transcripts may play in the progression of prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Pathol. 2004 Jan;164(1):217-27 [14695335.001]
  • [Cites] Nature. 2005 Sep 15;437(7057):376-80 [16056220.001]
  • [Cites] Genome Res. 2004 Mar;14(3):331-42 [14993201.001]
  • [Cites] BMC Genomics. 2004 Apr 27;5(1):26 [15113399.001]
  • [Cites] PLoS Biol. 2004 Jun;2(6):e162 [15103394.001]
  • [Cites] Mol Cancer Ther. 2004 Aug;3(8):921-32 [15299075.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Proc Natl Acad Sci U S A. 1988 Dec;85(23):8998-9002 [2461560.001]
  • [Cites] Science. 1995 Oct 20;270(5235):484-7 [7570003.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):6025-30 [8650213.001]
  • [Cites] Anal Biochem. 1996 Aug 15;240(1):90-7 [8811883.001]
  • [Cites] Cell. 1999 Apr 2;97(1):17-27 [10199399.001]
  • [Cites] Am J Pathol. 1999 May;154(5):1335-43 [10329586.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D121-4 [15608160.001]
  • [Cites] Int J Cancer. 2001 Oct 15;94(2):178-84 [11668495.001]
  • [Cites] Cancer Pract. 2001 Nov-Dec;9(6):295-306 [11879332.001]
  • [Cites] Nat Biotechnol. 2002 May;20(5):508-12 [11981567.001]
  • [Cites] Prostate. 2002 Jun 1;51(4):247-55 [11987153.001]
  • [Cites] Genome Res. 2002 Jun;12(6):996-1006 [12045153.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12257-62 [12213963.001]
  • [Cites] Mol Cancer Ther. 2002 Jun;1(8):629-37 [12479223.001]
  • [Cites] Biol Chem. 2006 Mar;387(3):243-9 [16542144.001]
  • [Cites] Genomics. 2006 May;87(5):633-7 [16439095.001]
  • [Cites] Cell. 2006 Jun 30;125(7):1215-20 [16814704.001]
  • [Cites] BMC Genomics. 2006;7:246 [17010196.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14523-8 [10588738.001]
  • [Cites] Cancer Res. 2000 Mar 15;60(6):1677-82 [10749139.001]
  • [Cites] J Pathol. 2001 Jan;193(1):73-9 [11169518.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1563-8 [11245466.001]
  • [Cites] Cancer Res. 2001 Sep 1;61(17):6331-4 [11522620.001]
  • [Cites] Nucleic Acids Res. 2005 Jan 1;33(Database issue):D447-53 [15608235.001]
  • [Cites] Science. 2004 Dec 24;306(5705):2242-6 [15539566.001]
  • [Cites] CA Cancer J Clin. 2005 Jan-Feb;55(1):10-30 [15661684.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2846-53 [15805286.001]
  • [Cites] Bioinformatics. 2005 Apr 15;21(8):1393-400 [15591356.001]
  • [Cites] Genomics. 2005 Jun;85(6):739-51 [15885500.001]
  • [Cites] Science. 2005 May 20;308(5725):1149-54 [15790807.001]
  • [Cites] Genome Res. 2005 Aug;15(8):1034-50 [16024819.001]
  • [Cites] Science. 2005 Sep 2;309(5740):1570-3 [16141075.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • (PMID = 17257419.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ DQ668378/ DQ668379/ DQ668380/ DQ668381/ DQ668382/ DQ668383/ DQ668384/ DQ668385/ DQ668386/ DQ668387/ DQ668388/ DQ668389/ DQ668390/ DQ668391/ DQ668392/ DQ668393/ DQ668394/ DQ668395/ DQ668396/ DQ668397/ DQ668398/ DQ668399/ DQ668400/ DQ668401/ DQ668402/ DQ668403/ EC093848/ EC093849/ EC093850/ EC093851/ EC093852/ EC093853/ EC093854/ EC093855/ EC093856/ EC093857/ EC093858/ EC093859/ EC093860/ EC093861/ EC093862/ EC093863/ EC093864/ EC093865/ EC093866/ EC093867/ EC093868/ EC093869/ EC093870/ EC093871/ EC093872/ EC093873/ EC093874/ EC093875/ EC093876/ EC093877/ EC093878/ EC093879/ EC093880/ EC093881/ EC093882/ EC093883/ EC093884/ EC093885/ EC093886/ EC093887/ EC093888/ EC093889/ EC093890/ EC093891/ EC093892/ EC093893/ EC093894/ EC093895/ EC093896/ EC093897/ EC093898/ EC093899/ EC093900/ EC093901/ EC093902/ EC093903/ EC093904/ EC093905/ EC093906/ EC093907/ EC093908/ EC093909/ EC093910/ EC093911/ EC093912/ EC093913/ EC093914/ EC093915/ EC093916/ EC093917/ EC093918/ EC093919/ EC093920/ EC093921/ EC093922/ EC093923/ EC093924/ EC093925/ EC093926/ EC093927/ EC093928/ EC093929/ EC093930/ EC093931/ EC093932/ EC093933/ EC093934/ EC093935/ EC093936/ EC093937/ EC093938/ EC093939/ EC093940/ EC093941/ EC093942/ EC093943/ EC093944/ EC093945/ EC093946/ EC093947/ EC093948/ EC093949/ EC093950/ EC093951/ EC093952/ EC093953/ EC093954/ EC093955/ EC093956/ EC093957/ EC093958/ EC093959/ EC093960/ EC093961/ EC093962/ EC093963/ EC093964/ EC093965/ EC093966/ EC093967/ EC093968/ EC093969/ EC093970/ EC093971/ EC093972/ EC093973/ EC093974/ EC093975/ EC093976/ EC093977/ EC093978/ EC093979/ EC093980/ EC093981/ EC093982/ EC093983/ EC093984/ EC093985/ EC093986/ EC093987/ EC093988/ EC093989/ EC093990/ EC093991/ EC093992/ EC093993/ EC093994/ EC093995/ EC093996/ EC093997/ EC093998/ EC093999/ EC094000/ EC094001/ EC094002/ EC094003/ EC094004/ EC094005/ EC094006/ EC094007/ EC094008/ EC094009/ EC094010/ EC094011/ EC094012/ EC094013/ EC094014/ EC094015/ EC094016/ EC094017/ EC094018/ EC094019/ EC094020/ EC094021/ EC094022/ EC094023/ EC094024/ EC094025/ EC094026/ EC094027/ EC094028/ EC094029/ EC094030/ EC094031/ EC094032/ EC094033/ EC094034/ EC094035/ EC094036/ EC094037/ EC094038/ EC094039/ EC094040/ EC094041/ EC094042/ EC094043/ EC094044/ EC094045/ EC094046/ EC094047/ EC094048/ EC094049/ EC094050/ EC094051/ EC094052/ EC094053/ EC094054/ EC094055/ EC094056/ EC094057/ EH613608/ EH613609/ EH613610
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Messenger; 0 / Untranslated Regions
  • [Other-IDs] NLM/ PMC1790899
  •  go-up   go-down


39. Wang P, Ma Q, Luo J, Liu B, Tan F, Zhang Z, Chen Z: Nkx3.1 and p27(KIP1) cooperate in proliferation inhibition and apoptosis induction in human androgen-independent prostate cancer cells. Cancer Invest; 2009 May;27(4):369-75
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] Nkx3.1 and p27(KIP1) cooperate in proliferation inhibition and apoptosis induction in human androgen-independent prostate cancer cells.
  • Prostate cancer (PC), which responds well to androgen ablation initially, invariably progresses to treatment resistance.
  • The so-called androgen-independent PC is also a concern, since there is no effective therapy so far.
  • Nkx3.1 is a putative prostate tumor suppressor that is expressed exclusively in the prostate under the regulation of androgen, and p27(KIP1) functions as a cell proliferation inhibitor and apoptosis trigger by disrupting the cyclin-dependent kinase (CDK)-cyclin complex.
  • Here, we show that endogenous expressions of both Nkx3.1 and p27(KIP1) are lost in the androgen-independent PC3 PC cells, while remaining intact in LNCaP PC cells, which contain functional androgen receptor (AR) and are hormone-responsive.
  • Our findings thus reveal the crucial relevance of the combined antiproliferative and proapoptotic activities of Nkx3.1 and p27(KIP1) in androgen-independent PC cells, and further suggest that a combined, rather than single gene manipulation may be of clinical value for hormone-refractory PC.


40. Shi GH, Ye DW, Yao XD, Zhang SL, Dai B, Zhang HL, Shen YJ, Zhu Y, Zhu YP, Xiao WJ, Ma CG: Involvement of microRNA-21 in mediating chemo-resistance to docetaxel in androgen-independent prostate cancer PC3 cells. Acta Pharmacol Sin; 2010 Jul;31(7):867-73
Hazardous Substances Data Bank. DOCETAXEL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Involvement of microRNA-21 in mediating chemo-resistance to docetaxel in androgen-independent prostate cancer PC3 cells.
  • AIM: To investigate whether microRNA-21 was involved in mediating the chemoresistance of prostate cancer cells to docetaxel.
  • RESULTS: A docetaxel-resistant prostate cancer PC3 cell line (PC3R) was established .
  • CONCLUSION: Our findings suggest that miR-21 contributed to the resistance of PC3 cells to docetaxel, and that targeting miR-21 may offer a promising therapeutic approach in sensitizing prostate cancer to docetaxel treatment.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Rev Cancer. 2006 Apr;6(4):259-69 [16557279.001]
  • [Cites] Oncogene. 2006 Oct 5;25(45):6101-12 [16682950.001]
  • [Cites] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945.001]
  • [Cites] J Immunol. 2006 Dec 1;177(11):8095-102 [17114484.001]
  • [Cites] J Biol Chem. 2007 May 11;282(19):14328-36 [17363372.001]
  • [Cites] Gastroenterology. 2007 Aug;133(2):647-58 [17681183.001]
  • [Cites] Oncogene. 2008 Apr 3;27(15):2128-36 [17968323.001]
  • [Cites] Mol Biol Cell. 2008 Aug;19(8):3272-82 [18508928.001]
  • [Cites] Oncogene. 2008 Aug 7;27(34):4712-23 [18408758.001]
  • [Cites] BJU Int. 2008 Aug 5;102(5):622-7 [18494832.001]
  • [Cites] Biochem Biophys Res Commun. 2008 Dec 5;377(1):114-9 [18834855.001]
  • [Cites] Cancer Res. 2009 Apr 1;69(7):3148-56 [19318582.001]
  • [Cites] Biochem Soc Trans. 2009 Aug;37(Pt 4):918-25 [19614619.001]
  • [Cites] Cancer Res. 2009 Sep 15;69(18):7165-9 [19738047.001]
  • [Cites] Oncogene. 2009 Nov 19;28(46):4065-74 [19734943.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):14037-42 [10570194.001]
  • [Cites] Oncogene. 2001 Feb 8;20(6):669-76 [11314000.001]
  • [Cites] Oncogene. 2003 Jun 12;22(24):3712-20 [12802278.001]
  • [Cites] J Pathol. 2003 Aug;200(5):640-6 [12898601.001]
  • [Cites] Cell. 2004 Jan 23;116(2):281-97 [14744438.001]
  • [Cites] Mol Cell Biol. 2004 May;24(9):3894-906 [15082783.001]
  • [Cites] Nat Rev Genet. 2004 Jul;5(7):522-31 [15211354.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Oncogene. 2004 Oct 21;23(49):8135-45 [15361828.001]
  • [Cites] Cancer Treat Rev. 1993 Oct;19(4):351-86 [8106152.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6029-33 [16024602.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6034-41 [16024603.001]
  • [Cites] Cancer Res. 2005 Aug 15;65(16):7065-70 [16103053.001]
  • [Cites] Mol Cell Biol. 2006 Feb;26(4):1297-306 [16449643.001]
  • (PMID = 20581857.001).
  • [ISSN] 1745-7254
  • [Journal-full-title] Acta pharmacologica Sinica
  • [ISO-abbreviation] Acta Pharmacol. Sin.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Lipids; 0 / Lipofectamine; 0 / MIRN21 microRNA, human; 0 / MicroRNAs; 0 / PDCD4 protein, human; 0 / RNA-Binding Proteins; 0 / Taxoids; 15H5577CQD / docetaxel
  • [Other-IDs] NLM/ PMC4007720
  •  go-up   go-down


41. Wu M, Bai X, Xu G, Wei J, Zhu T, Zhang Y, Li Q, Liu P, Song A, Zhao L, Gang C, Han Z, Wang S, Zhou J, Lu Y, Ma D: Proteome analysis of human androgen-independent prostate cancer cell lines: variable metastatic potentials correlated with vimentin expression. Proteomics; 2007 Jun;7(12):1973-83
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] Proteome analysis of human androgen-independent prostate cancer cell lines: variable metastatic potentials correlated with vimentin expression.
  • To better understand the molecular mechanisms of prostate cancer (PCA) dissemination and to develop new anti-metastasis therapies, key regulatory molecules involved in PCA metastasis were identified in two human androgen-independent PCA cell lines, highly metastatic 1E8-H and lowly metastatic 2B4-L cells.
  • To our knowledge, this study is the first to demonstrate that up-regulation of VIM expression positively correlates with the invasion and metastasis of androgen-independent PCA.


42. Filleur S, Hirsch J, Wille A, Schön M, Sell C, Shearer MH, Nelius T, Wieland I: INTS6/DICE1 inhibits growth of human androgen-independent prostate cancer cells by altering the cell cycle profile and Wnt signaling. Cancer Cell Int; 2009;9:28
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] INTS6/DICE1 inhibits growth of human androgen-independent prostate cancer cells by altering the cell cycle profile and Wnt signaling.
  • BACKGROUND: The gene encoding integrator complex subunit 6 (INTS6), previously known as deleted in cancer cells 1 (DICE1, OMIM 604331) was found to be frequently affected by allelic deletion and promoter hypermethylation in prostate cancer specimens and cell lines.
  • A missense mutation has been detected in prostate cancer cell line LNCaP.
  • Together, these results suggest INTS6/DICE1 as a putative tumor suppressor gene in prostate cancer.
  • In this study, we examined the growth inhibitory effects of INTS6/DICE1 on prostate cancer cells.
  • RESULTS: Markedly decreased INTS6/DICE1 mRNA levels were detected in prostate cancer cell lines LNCaP, DU145 and PC3 as well as CPTX1532 as compared to a cell line derived from normal prostate tissue, NPTX1532.
  • Exogenous re-expression of INTS6/DICE1 cDNA in androgen-independent PC3 and DU145 cell lines substantially suppressed their ability to form colonies in vitro.
  • Rather, prostate cancer cells arrested in G1 phase of the cell cycle.

  • COS Scholar Universe. author profiles.
  • 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] Anal Biochem. 1987 Apr;162(1):156-9 [2440339.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Jan 20;106(3):755-60 [19136632.001]
  • [Cites] Oncogene. 1996 Mar 21;12(6):1231-8 [8649825.001]
  • [Cites] Mol Cell Biol. 1997 Jan;17(1):427-35 [8972223.001]
  • [Cites] Cancer Res. 1997 Mar 1;57(5):995-1002 [9041206.001]
  • [Cites] Exp Cell Res. 1998 Feb 1;238(2):359-70 [9473344.001]
  • [Cites] Oncogene. 1999 Aug 12;18(32):4530-7 [10467397.001]
  • [Cites] Mol Cell Biol. 2001 Jan;21(1):330-42 [11113207.001]
  • [Cites] J Biol Chem. 2001 Sep 7;276(36):33608-15 [11445567.001]
  • [Cites] Oncogene. 2001 Aug 16;20(36):4942-50 [11526479.001]
  • [Cites] Methods. 2001 Dec;25(4):402-8 [11846609.001]
  • [Cites] Oncol Res. 2001;12(11-12):491-500 [11939413.001]
  • [Cites] Mol Biol Cell. 2002 Oct;13(10):3369-87 [12388743.001]
  • [Cites] Oncogene. 2003 Jan 16;22(2):314-8 [12527901.001]
  • [Cites] J Pathol. 2004 Jan;202(1):50-9 [14694521.001]
  • [Cites] Oncol Rep. 2004 Aug;12(2):207-11 [15254679.001]
  • [Cites] Arch Dermatol Res. 2004 Jul;296(2):59-66 [15278364.001]
  • [Cites] Oncogene. 2005 Oct 6;24(44):6667-75 [16007164.001]
  • [Cites] Cancer Res. 2005 Aug 1;65(15):6864-73 [16061670.001]
  • [Cites] Cell. 2005 Oct 21;123(2):265-76 [16239144.001]
  • [Cites] Cancer Res. 2005 Nov 1;65(21):9762-70 [16266997.001]
  • [Cites] Cancer Genet Cytogenet. 2005 Nov;163(1):91-2 [16271964.001]
  • [Cites] Clin Cancer Res. 2006 Mar 15;12(6):1665-71 [16551847.001]
  • [Cites] BMC Mol Biol. 2008;9:83 [18828910.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 15;90(18):8392-6 [7690960.001]
  • (PMID = 19906297.001).
  • [ISSN] 1475-2867
  • [Journal-full-title] Cancer cell international
  • [ISO-abbreviation] Cancer Cell Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2779787
  •  go-up   go-down


43. Ting HJ, Bao BY, Reeder JE, Messing EM, Lee YF: Increased expression of corepressors in aggressive androgen-independent prostate cancer cells results in loss of 1alpha,25-dihydroxyvitamin D3 responsiveness. Mol Cancer Res; 2007 Sep;5(9):967-80
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] Increased expression of corepressors in aggressive androgen-independent prostate cancer cells results in loss of 1alpha,25-dihydroxyvitamin D3 responsiveness.
  • Vitamin D has antiproliferative activity in prostate cancer; however, resistance to vitamin D-mediated growth inhibition occurs.
  • To investigate the mechanisms of vitamin D resistance, we screened two prostate cancer sublines of CWR22rv1, CWR22R-1, and CWR22R-2, with differential sensitivity to vitamin D.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • 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 = 17855664.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Receptors, Calcitriol; FXC9231JVH / Calcitriol; Q0OZ0D9223 / seocalcitol
  •  go-up   go-down


44. Shamaladevi N, Lyn DA, Escudero DO, Lokeshwar BL: CXC receptor-1 silencing inhibits androgen-independent prostate cancer. Cancer Res; 2009 Nov 1;69(21):8265-74
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] CXC receptor-1 silencing inhibits androgen-independent prostate cancer.
  • The function of CXCR1 in prostate cancer was investigated by silencing its expression, using RNA interference.
  • Other IL-8-expressing prostate cancer cell lines also exhibited similar phenotypes when CXCR1 was depleted by CXCR1 shRNA transfection.

  • 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 .
  • 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] Clin Cancer Res. 2000 May;6(5):2104-19 [10815938.001]
  • [Cites] Clin Cancer Res. 2004 Dec 1;10(23):8037-47 [15585639.001]
  • [Cites] Cytokine Growth Factor Rev. 2001 Dec;12(4):375-91 [11544106.001]
  • [Cites] Pharmacol Ther. 2001 Oct;92(1):57-70 [11750036.001]
  • [Cites] Int J Cancer. 2002 Mar 10;98(2):297-309 [11857423.001]
  • [Cites] Prostate. 2005 Jun 15;64(1):40-9 [15651067.001]
  • [Cites] Am J Pathol. 2005 Jun;166(6):1807-15 [15920165.001]
  • [Cites] Clin Cancer Res. 2005 Jun 1;11(11):4117-27 [15930347.001]
  • [Cites] Angiogenesis. 2005;8(1):63-71 [16132619.001]
  • [Cites] Am J Clin Pathol. 2006 Feb;125(2):209-16 [16393674.001]
  • [Cites] Nat Methods. 2006 Sep;3(9):677-81 [16929311.001]
  • [Cites] Prostate. 2006 Dec 1;66(16):1721-8 [16941672.001]
  • [Cites] Lung Cancer. 2007 Apr;56(1):25-33 [17175059.001]
  • [Cites] Cancer Res. 2007 Jul 15;67(14):6854-62 [17638896.001]
  • [Cites] Mol Cancer Res. 2007 Jul;5(7):737-48 [17606477.001]
  • [Cites] Urol Oncol. 2007 Sep-Oct;25(5):413-9 [17826663.001]
  • [Cites] Exp Cell Res. 2008 Jan 15;314(2):352-65 [17996233.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4111-8 [18593988.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3003-6 [18725993.001]
  • [Cites] Oncogene. 2008 Oct 20;27(48):6194-206 [18931687.001]
  • [Cites] Clin Cancer Res. 2008 Nov 1;14(21):6735-41 [18980965.001]
  • [Cites] Exp Cell Res. 2000 Apr 10;256(1):58-66 [10739652.001]
  • [Cites] J Biol Chem. 2003 Mar 7;278(10):8508-15 [12496258.001]
  • [Cites] Biochem Pharmacol. 2003 Mar 1;65(5):813-21 [12628493.001]
  • [Cites] Oncogene. 2004 Mar 18;23(12):2197-205 [14767470.001]
  • [Cites] Technol Cancer Res Treat. 2004 Oct;3(5):411 [15453805.001]
  • [Cites] Control Clin Trials. 1990 Apr;11(2):116-28 [2161310.001]
  • [Cites] Science. 1991 Sep 13;253(5025):1278-80 [1840701.001]
  • [Cites] Science. 1991 Sep 13;253(5025):1280-3 [1891716.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6682-6 [8692878.001]
  • [Cites] J Biol Chem. 1996 Aug 23;271(34):20545-50 [8702798.001]
  • [Cites] Annu Rev Immunol. 1997;15:675-705 [9143704.001]
  • [Cites] J Biol Chem. 1998 Sep 11;273(37):23830-6 [9726994.001]
  • [Cites] J Urol. 1998 Oct;160(4):1220-9 [9751323.001]
  • [Cites] Am J Pathol. 1999 Feb;154(2):375-84 [10027396.001]
  • [Cites] Nat Med. 1999 Mar;5(3):280-5 [10086382.001]
  • [Cites] Haematologica. 1999 Mar;84(3):208-11 [10189383.001]
  • [Cites] Am J Pathol. 1999 May;154(5):1503-12 [10329603.001]
  • [Cites] Genes Dev. 1999 Aug 1;13(15):1899-911 [10444588.001]
  • [Cites] Prostate. 1999 Oct 1;41(2):78-88 [10477904.001]
  • [Cites] Curr Cancer Drug Targets. 2004 Nov;4(7):569-76 [15578914.001]
  • [Cites] Neoplasia. 2001 Jan-Feb;3(1):33-42 [11326314.001]
  • (PMID = 19861539.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA061038-10A1; United States / NCCIH NIH HHS / AT / R01AT003544; United States / NCI NIH HHS / CA / 2R01CA61038; United States / NCCIH NIH HHS / AT / R01 AT003544-01A1; United States / NCI NIH HHS / CA / R01 CA156776; United States / NCCIH NIH HHS / AT / AT003544-01A1; United States / NCI NIH HHS / CA / R01 CA061038; United States / NCCIH NIH HHS / AT / R01 AT003544; United States / NCI NIH HHS / CA / R01 CA061038-10A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Interleukin-8; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, Interleukin-8A; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS140244; NLM/ PMC2788615
  •  go-up   go-down


45. Terry S, Queires L, Gil-Diez-de-Medina S, Chen MW, de la Taille A, Allory Y, Tran PL, Abbou CC, Buttyan R, Vacherot F: Protocadherin-PC promotes androgen-independent prostate cancer cell growth. Prostate; 2006 Jul 1;66(10):1100-13
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] Protocadherin-PC promotes androgen-independent prostate cancer cell growth.
  • BACKGROUND: Protocadherin-PC (PCDH-PC) expression is upregulated in apoptosis-resistant sublines of the LNCaP human prostate cancer (CaP) cell line.
  • Here, we assess the role of PCDH-PC in CaP cells and its mRNA expression in human prostate tissues.
  • METHODS: LNCaP cells transfected with PCDH-PC were tested for their ability to grow in vitro and in vivo in androgen-deprived conditions.
  • RESULTS: PCDH-PC expression induced Wnt signaling in CaP cells and permitted androgen-independent growth of hormone-sensitive CaP cells.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2005 Wiley-Liss, Inc.
  • [Cites] Nature. 2000 May 18;405(6784):354-60 [10830965.001]
  • [Cites] Cancer. 2004 Sep 15;101(6):1345-56 [15316903.001]
  • [Cites] Mamm Genome. 2000 Oct;11(10):906-14 [11003707.001]
  • [Cites] Prostate. 2000 Dec 1;45(4):323-34 [11102958.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4575-80 [11287641.001]
  • [Cites] Oncogene. 2001 Apr 12;20(16):1981-9 [11360182.001]
  • [Cites] Mol Cell Biol. 2001 Dec;21(24):8385-97 [11713275.001]
  • [Cites] Cancer Res. 2001 Dec 15;61(24):8664-7 [11751382.001]
  • [Cites] Genome Biol. 2002;3(1):REVIEWS3001 [11806834.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Genes Chromosomes Cancer. 2002 May;34(1):9-16 [11921277.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1168-71 [11948129.001]
  • [Cites] Oncogene. 2002 Apr 18;21(17):2679-94 [11965541.001]
  • [Cites] Cell. 2002 Oct 18;111(2):241-50 [12408868.001]
  • [Cites] Oncogene. 2002 Nov 7;21(51):7861-71 [12420223.001]
  • [Cites] J Cell Sci. 2002 Dec 15;115(Pt 24):4809-18 [12432069.001]
  • [Cites] Clin Cancer Res. 2003 May;9(5):1801-7 [12738737.001]
  • [Cites] J Cancer Res Clin Oncol. 2003 Apr;129(4):199-221 [12707770.001]
  • [Cites] Nature. 2003 May 22;423(6938):409-14 [12717450.001]
  • [Cites] Cell. 2003 Jun 27;113(7):841-52 [12837243.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100 Suppl 1:11830-5 [12913119.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Prostate. 2004 Jul 1;60(2):91-7 [15162375.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5489-95 [15289359.001]
  • [Cites] Oncogene. 2006 Jun 8;25(24):3436-44 [16474850.001]
  • [Cites] Biochemistry. 1979 Nov 27;18(24):5294-9 [518835.001]
  • [Cites] Prostate. 1981;2(1):35-49 [7279811.001]
  • [Cites] Cancer. 1987 Aug 1;60(3 Suppl):589-601 [3297288.001]
  • [Cites] Prog Clin Biol Res. 1987;243A:1-19 [3309968.001]
  • [Cites] Prog Clin Biol Res. 1987;243A:21-31 [3309971.001]
  • [Cites] Cancer Res. 1990 Jun 15;50(12):3748-53 [2340521.001]
  • [Cites] Prog Clin Biol Res. 1990;350:129-40 [2201039.001]
  • [Cites] N Engl J Med. 1991 Jan 24;324(4):236-45 [1985245.001]
  • [Cites] Cancer Res. 1992 Aug 15;52(16):4313-9 [1353702.001]
  • [Cites] J Natl Cancer Inst. 1993 Oct 20;85(20):1657-69 [7692074.001]
  • [Cites] Am J Pathol. 1995 Jun;146(6):1368-75 [7778676.001]
  • [Cites] J Urol. 1995 Aug;154(2 Pt 1):414-21 [7609105.001]
  • [Cites] Cancer Res. 1995 Oct 1;55(19):4438-45 [7671257.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 1994;59:653-9 [7587126.001]
  • [Cites] Cancer Res. 1998 Jun 15;58(12):2520-3 [9635571.001]
  • [Cites] Am J Pathol. 1998 Jul;153(1):141-8 [9665474.001]
  • [Cites] Science. 1998 Sep 4;281(5382):1509-12 [9727977.001]
  • [Cites] Hum Pathol. 1998 Sep;29(9):1005-12 [9744319.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1603-8 [9990071.001]
  • [Cites] Nature. 1999 Apr 1;398(6726):422-6 [10201372.001]
  • [Cites] CA Cancer J Clin. 1999 Jan-Feb;49(1):8-31, 1 [10200775.001]
  • [Cites] Curr Opin Cell Biol. 1999 Apr;11(2):233-40 [10209158.001]
  • [Cites] Am J Pathol. 1999 May;154(5):1335-43 [10329586.001]
  • [Cites] Cancer Res. 1999 Aug 15;59(16):4030-4 [10463603.001]
  • [Cites] Cancer Res. 1999 Oct 1;59(19):5030-6 [10519419.001]
  • [Cites] Int J Oncol. 2005 Apr;26(4):1033-40 [15753999.001]
  • [Cites] Cancer Res. 2005 Jun 15;65(12):5263-71 [15958572.001]
  • [Cites] Genomics. 1999 Dec 15;62(3):540-3 [10644456.001]
  • [Cites] Cell. 1999 Oct 29;99(3):335-45 [10555149.001]
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1837-51 [10921899.001]
  • (PMID = 16637074.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA111618-04; United States / NCI NIH HHS / CA / R01 CA111618; United States / NCI NIH HHS / CA / CA111618; United States / NCI NIH HHS / CA / R01 CA111618-04
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Cadherins; 0 / PCDH11Y protein, human; 0 / RNA, Messenger; 0 / TCF Transcription Factors; 0 / Wnt Proteins
  • [Other-IDs] NLM/ NIHMS88547; NLM/ PMC2660890
  •  go-up   go-down


46. Madan RA, Lieberman R, Gulley JL, Dahut W, Arlen PM: Significant prostate-specific antigen (PSA) response to low-dose ketoconazole in a patient with non-metastatic androgen-independent prostate cancer (AIPC) and a review of the literature. Am J Ther; 2007 May-Jun;14(3):310-3
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] Significant prostate-specific antigen (PSA) response to low-dose ketoconazole in a patient with non-metastatic androgen-independent prostate cancer (AIPC) and a review of the literature.
  • Although there are a variety of treatment options for nonmetastatic androgen-independent prostate cancer (AIPC), they have limited benefits.
  • Ultimately, sequential therapeutics can be used to minimize symptomatic progression and control the underlying disease, as determined by prostate-specific antigen (PSA) levels.
  • [MeSH-major] Ketoconazole / therapeutic use. Prostate-Specific Antigen / drug effects. Prostatic Neoplasms / drug therapy


47. Drewa T: Re: Fritz H. Schröder. Progress in understanding androgen-independent prostate cancer (AIPC): a review of potential endocrine-mediated mechanisms. Eur Urol 2008;53:1129-37. Eur Urol; 2009 Jan;55(1):e6-7; author reply e8-9
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] Re: Fritz H. Schröder. Progress in understanding androgen-independent prostate cancer (AIPC): a review of potential endocrine-mediated mechanisms. Eur Urol 2008;53:1129-37.
  • [MeSH-major] Androgens / physiology. Prostatic Neoplasms / physiopathology. Prostatic Neoplasms / therapy. Receptors, Androgen / physiology

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Eur Urol. 2008 Jun;53(6):1129-37 [18262723.001]
  • (PMID = 18603349.001).
  • [ISSN] 1873-7560
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  •  go-up   go-down


48. Hååg P, Bektic J, Bartsch G, Klocker H, Eder IE: Androgen receptor down regulation by small interference RNA induces cell growth inhibition in androgen sensitive as well as in androgen independent prostate cancer cells. J Steroid Biochem Mol Biol; 2005 Aug;96(3-4):251-8
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] Androgen receptor down regulation by small interference RNA induces cell growth inhibition in androgen sensitive as well as in androgen independent prostate cancer cells.
  • We investigated the effects of androgen receptor (AR) down regulation with a small interference RNA molecule (siRNA_AR(start)) on androgen sensitive LNCaP and androgen independent LNCaPabl prostate cancer cells, the latter representing an in vitro model for the development of therapy resistance in prostate cancer.
  • Although LNCaPabl cells express increased levels of AR in comparison with androgen sensitive LNCaP cells, the protein was significantly down regulated in response to siRNA_AR(start) treatment.
  • By contrast, DU-145 prostate cancer cells, which lack AR expression, were not inhibited by the siRNA_AR(start).
  • In summary, we found that AR inhibition with siRNA induces cell growth retardation in androgen sensitive as well as in androgen independent prostate cancer cells and thus may represent an interesting approach to combat hormone-refractory prostate cancer.
  • [MeSH-major] Androgen Receptor Antagonists. Prostatic Neoplasms / therapy. RNA Interference
  • [MeSH-minor] Androgens / metabolism. Cell Cycle Proteins / metabolism. Cell Proliferation / drug effects. Cyclin D1 / metabolism. Cyclin-Dependent Kinase Inhibitor p21. Down-Regulation. Gene Expression Regulation, Neoplastic. Humans. Male. RNA, Small Interfering / genetics. Receptors, Androgen / genetics. Receptors, Androgen / metabolism. Transfection. Tumor Cells, Cultured. Up-Regulation

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • 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
  • (PMID = 15982869.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Androgens; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / RNA, Small Interfering; 0 / Receptors, Androgen; 136601-57-5 / Cyclin D1
  •  go-up   go-down


49. Shazer RL, Jain A, Galkin AV, Cinman N, Nguyen KN, Natale RB, Gross M, Green L, Bender LI, Holden S, Kaplan L, Agus DB: Raloxifene, an oestrogen-receptor-beta-targeted therapy, inhibits androgen-independent prostate cancer growth: results from preclinical studies and a pilot phase II clinical trial. BJU Int; 2006 Apr;97(4):691-7
Hazardous Substances Data Bank. RALOXIFENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Raloxifene, an oestrogen-receptor-beta-targeted therapy, inhibits androgen-independent prostate cancer growth: results from preclinical studies and a pilot phase II clinical trial.
  • OBJECTIVES: To determine, in preclinical in vivo animal and in clinical studies, whether raloxifene (a selective oestrogen-receptor (ER) modulator that targets ER-beta and induces apoptosis in vitro in androgen-independent prostate cancer, AIPC cells) affects prostate cell differentiation, proliferation and carcinogenesis, and in the pilot phase II clinical trial, the response rate and duration of patients with AIPC treated with a daily oral dose of raloxifene.
  • PATIENTS, MATERIALS AND METHODS: Tumour proliferation rate in response to raloxifene treatment, and molecular markers of cell cycle and apoptosis, were evaluated in established ER-beta-positive androgen-dependent (AD) CWR22 and AI CWRSA9 human xenograft prostate cancer models.
  • [MeSH-minor] Aged. Aged, 80 and over. Animals. Humans. Immunohistochemistry. Male. Mice. Middle Aged. Pilot Projects. Prostate-Specific Antigen / blood. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16536755.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Selective Estrogen Receptor Modulators; 4F86W47BR6 / Raloxifene Hydrochloride; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


50. Alaoui-Jamali MA Sr, Gupta A, Szarek WA, Bismar TA, Gheorghe R, Schipper HM: A novel selective therapeutic targeting heme oxygenase-1 revealed a potent antimetastatic activity in androgen-refractory human prostate cancer models. J Clin Oncol; 2009 May 20;27(15_suppl):e16090

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel selective therapeutic targeting heme oxygenase-1 revealed a potent antimetastatic activity in androgen-refractory human prostate cancer models.
  • : e16090 Prostate cancer is a highly prevalent disease.
  • Despite a significant improvement in the overall survival attributed in part to early detection and introduction of novel therapeutic modalities, many cancer patients at primary diagnosis present advanced disease or experience recurrence of the cancer.
  • The progression of prostate cancer (PCA) to hormone-refractory phenotype (HRPCA) and to metastasis is an ominous event in patients with advanced PCA.
  • In this study, we identified heme oxygenase 1 (HO-1) to be significantly upregulated in epithelial PCA cells, but not in surrounding stromal cells, from hormone refractory prostate cancer cases compared to hormone-responsive prostate cancer and to benign tissues.
  • Specifically, inhibition of HO-1 gene in androgen-independent and highly invasive prostate cancer cells, PC3M, decreased HO-1 activity, oxidative stress, MAPKs activation, cell proliferation, and cell migration and invasion in vitro, as well as inhibition of prostate tumor growth and lymph nodes and lung metastases in vivo.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963085.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


51. Zi X, Guo Y, Simoneau AR, Hope C, Xie J, Holcombe RF, Hoang BH: Expression of Frzb/secreted Frizzled-related protein 3, a secreted Wnt antagonist, in human androgen-independent prostate cancer PC-3 cells suppresses tumor growth and cellular invasiveness. Cancer Res; 2005 Nov 1;65(21):9762-70
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] Expression of Frzb/secreted Frizzled-related protein 3, a secreted Wnt antagonist, in human androgen-independent prostate cancer PC-3 cells suppresses tumor growth and cellular invasiveness.
  • Here, we examined the biological effects of Frzb/sFRP3 on an androgen-independent prostate cancer cell model.
  • Together, these data suggest that Frzb/sFRP3 and DN-LRP5 exhibit antitumor activity through the reversal of epithelial-to-mesenchymal transition and inhibition of MMP activities in a subset of prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 16266997.001).
  • [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 / Cadherins; 0 / LDL-Receptor Related Proteins; 0 / LRP5 protein, human; 0 / Low Density Lipoprotein Receptor-Related Protein-5; 0 / Lrp5 protein, mouse; 0 / Matrix Metalloproteinase Inhibitors; 0 / Proteins; 0 / Wnt Proteins; 0 / beta Catenin; 0 / frizzled related protein-3; 68238-35-7 / Keratins; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
  •  go-up   go-down


52. Beer TM, Lalani AS, Lee S, Mori M, Eilers KM, Curd JG, Henner WD, Ryan CW, Venner P, Ruether JD, Chi KN, ASCENT Investigators: C-reactive protein as a prognostic marker for men with androgen-independent prostate cancer: results from the ASCENT trial. Cancer; 2008 Jun;112(11):2377-83
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] C-reactive protein as a prognostic marker for men with androgen-independent prostate cancer: results from the ASCENT trial.
  • BACKGROUND: Studies of cancer risk and molecular carcinogenesis suggest a role for inflammation in cancer development and progression.
  • The authors sought to determine whether specific blood proteins associated with inflammation predict for outcomes in men with metastatic androgen-independent prostate cancer (AIPC) who are initiating docetaxel-based chemotherapy.
  • Logistic regression was used for analyses of associations with prostate-specific antigen (PSA) decline.
  • [MeSH-minor] Aged. Aged, 80 and over. Humans. Male. Middle Aged. Neoplasm Staging. Placebos. Prognosis. Prostate-Specific Antigen / blood. Survival Rate

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2008 American Cancer Society.
  • [CommentIn] Cancer. 2009 Mar 1;115(5):1132 [19156910.001]
  • (PMID = 18428198.001).
  • [ISSN] 1097-0142
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Calcium Channel Agonists; 0 / Placebos; 0 / Taxoids; 15H5577CQD / docetaxel; 9007-41-4 / C-Reactive Protein; EC 3.4.21.77 / Prostate-Specific Antigen; FXC9231JVH / Calcitriol
  •  go-up   go-down


53. Tiffany NM, Ryan CW, Garzotto M, Wersinger EM, Beer TM: High dose pulse calcitriol, docetaxel and estramustine for androgen independent prostate cancer: a phase I/II study. J Urol; 2005 Sep;174(3):888-92
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] High dose pulse calcitriol, docetaxel and estramustine for androgen independent prostate cancer: a phase I/II study.
  • PURPOSE: We determined the safety and preliminary efficacy of the combination of high dose pulse calcitriol (1,25-dihydroxycholecalciferol) with a standard regimen of docetaxel plus estramustine in patients with metastatic androgen independent prostate cancer.
  • RESULTS: A total of 24 patients, including 11 who were chemotherapy naïve and 13 who had previously been treated with docetaxel, were evaluable for toxicity and 22 for prostate specific antigen decrease data.
  • Six of 11 evaluable, chemotherapy naïve patients (55%) met prostate specific antigen response criteria.
  • [MeSH-minor] Administration, Oral. Aged. Calcitriol / administration & dosage. Calcitriol / toxicity. Disease Progression. Dose-Response Relationship, Drug. Drug Administration Schedule. Estramustine / administration & dosage. Estramustine / toxicity. Follow-Up Studies. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / pathology. Prostate-Specific Antigen / blood. Taxoids / administration & dosage. Taxoids / toxicity. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • 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 = 16093981.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 3M01RR00334-33S2
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; 35LT29625A / Estramustine; EC 3.4.21.77 / Prostate-Specific Antigen; FXC9231JVH / Calcitriol
  •  go-up   go-down


54. Figg WD, Liu Y, Arlen P, Gulley J, Steinberg SM, Liewehr DJ, Cox MC, Zhai S, Cremers S, Parr A, Yang X, Chen CC, Jones E, Dahut WL: A randomized, phase II trial of ketoconazole plus alendronate versus ketoconazole alone in patients with androgen independent prostate cancer and bone metastases. J Urol; 2005 Mar;173(3):790-6
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 randomized, phase II trial of ketoconazole plus alendronate versus ketoconazole alone in patients with androgen independent prostate cancer and bone metastases.
  • Ketoconazole (KT) has demonstrated activity in androgen independent prostate cancer (AIPC).
  • Prostate specific antigen (PSA) consensus criteria and radiographic scans were used to determine the proportion of patients with a PSA decrease, time to progression and response duration.


55. Montgomery RB, Nelson PS, Lin D, Ryan CW, Garzotto M, Beer TM: Diethylstilbestrol and docetaxel: a Phase II study of tubulin active agents in patients with metastatic, androgen-independent prostate cancer. Cancer; 2007 Sep 1;110(5):996-1002
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] Diethylstilbestrol and docetaxel: a Phase II study of tubulin active agents in patients with metastatic, androgen-independent prostate cancer.
  • BACKGROUND: The addition of diethylstilbestrol to docetaxel modified tubulin composition and improved the response of prostate cancer to chemotherapy in preclinical models.
  • METHODS: Twenty-nine patients with progressive, metastatic, chemotherapy-naive androgen-independent prostate cancer were treated with diethylstilbestrol 1 mg daily and 5 mg on the day before docetaxel and docetaxel 36 mg/m(2) intravenously weekly for 3 weeks of a 4-week cycle.
  • Patients were assessed by prostate-specific antigen (PSA) monthly and computed tomography (CT) and bone scans every 3 cycles.
  • [MeSH-minor] Administration, Oral. Aged. Aged, 80 and over. Diarrhea / chemically induced. Diethylstilbestrol / administration & dosage. Diethylstilbestrol / adverse effects. Drug Administration Schedule. Humans. Infusions, Intravenous. Male. Middle Aged. Neoplasm Metastasis. Paclitaxel / administration & dosage. Paclitaxel / adverse effects. Prospective Studies. Prostate-Specific Antigen / blood. Treatment Outcome. Tubulin Modulators / administration & dosage. Tubulin Modulators / adverse effects. Venous Thrombosis / chemically induced

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. DIETHYLSTILBESTROL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17639587.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA97186
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tubulin Modulators; 731DCA35BT / Diethylstilbestrol; EC 3.4.21.77 / Prostate-Specific Antigen; P88XT4IS4D / Paclitaxel
  •  go-up   go-down


56. Sharifi N, Farrar WL: Androgen receptor as a therapeutic target for androgen independent prostate cancer. Am J Ther; 2006 Mar-Apr;13(2):166-70
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] Androgen receptor as a therapeutic target for androgen independent prostate cancer.
  • Prostate cancer is the leading cause of nonskin malignancy and the second leading cause of cancer death in men.
  • Androgen deprivation therapy is the first-line of systemic therapy against advanced prostate cancer.
  • All advanced prostate cancers eventually grow despite castrate levels of testosterone.
  • We review the evidence that androgen independent prostate cancer continues to require androgen receptor activity for growth, the mechanisms of androgen receptor activation in the castrate setting, and possible points of intervention for novel therapies targeting the androgen receptor and prostate cancer.
  • [MeSH-major] Androgens / physiology. Prostatic Neoplasms / drug therapy. Receptors, Androgen / physiology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16645434.001).
  • [ISSN] 1075-2765
  • [Journal-full-title] American journal of therapeutics
  • [ISO-abbreviation] Am J Ther
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / /
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  • [Number-of-references] 42
  •  go-up   go-down


57. Schellhammer PF, Hershberg RM: Immunotherapy with autologous antigen presenting cells for the treatment of androgen independent prostate cancer. World J Urol; 2005 Feb;23(1):47-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immunotherapy with autologous antigen presenting cells for the treatment of androgen independent prostate cancer.
  • Prostate cancer is an excellent target for an active vaccine-based approach based on the fact that prostate cancer cells express unique proteins which serve as highly specific targets.
  • Clinical trial outcomes have demonstrated activity in patients with androgen independent prostate cancer.
  • [MeSH-minor] Acid Phosphatase. Cancer Vaccines / therapeutic use. Disease Progression. Follow-Up Studies. Humans. Male. Protein Tyrosine Phosphatases / metabolism. T-Lymphocytes / immunology. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Immunol. 2001 Apr;2(4):293-9 [11276199.001]
  • [Cites] Nat Immunol. 2004 May;5(5):508-15 [15064759.001]
  • [Cites] Cancer Res. 2001 Jul 1;61(13):5161-7 [11431355.001]
  • [Cites] Cancer Immun. 2003 Feb 14;3:2 [12747744.001]
  • [Cites] J Natl Cancer Inst. 2002 Oct 2;94(19):1458-68 [12359855.001]
  • [Cites] J Clin Oncol. 2003 Apr 1;21(7):1232-7 [12663709.001]
  • [Cites] Cancer Res. 2001 Jun 15;61(12):4756-60 [11406548.001]
  • (PMID = 15647927.001).
  • [ISSN] 0724-4983
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article; Randomized Controlled Trial
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgens; 0 / Autoantigens; 0 / Cancer Vaccines; EC 3.1.3.2 / Acid Phosphatase; EC 3.1.3.2 / prostatic acid phosphatase; EC 3.1.3.48 / Protein Tyrosine Phosphatases
  •  go-up   go-down


58. Li Y, Wang L, Zhang M, Melamed J, Liu X, Reiter R, Wei J, Peng Y, Zou X, Pellicer A, Garabedian MJ, Ferrari A, Lee P: LEF1 in androgen-independent prostate cancer: regulation of androgen receptor expression, prostate cancer growth, and invasion. Cancer Res; 2009 Apr 15;69(8):3332-8
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] LEF1 in androgen-independent prostate cancer: regulation of androgen receptor expression, prostate cancer growth, and invasion.
  • A major obstacle in treating prostate cancer is the development of androgen-independent disease.
  • In this study, we examined LEF1 expression in androgen-independent cancer as well as its regulation of androgen receptor (AR) expression, prostate cancer growth, and invasion in androgen-independent prostate cancer cells.
  • Affymetrix microarray analysis of LNCaP and LNCaP-AI (androgen-independent variant LNCaP) cells revealed 100-fold increases in LEF1 expression in LNCaP-AI cells.
  • Thus, we identified LEF1 as a potential marker for androgen-independent disease and as a key regulator of AR expression and prostate cancer growth and invasion.
  • LEF1 is highly expressed in androgen-independent prostate cancer, potentially serving as a marker for androgen-independent disease.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • 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] Oncogene. 2006 Jun 8;25(24):3436-44 [16474850.001]
  • [Cites] J Cell Biochem. 2006 Oct 1;99(2):402-10 [16741972.001]
  • [Cites] J Mol Endocrinol. 2006 Oct;37(2):283-300 [17032745.001]
  • [Cites] Nat Clin Pract Oncol. 2007 Apr;4(4):236-44 [17392714.001]
  • [Cites] Endocrinology. 2007 Sep;148(9):4334-43 [17540719.001]
  • [Cites] Cancer Res. 2008 Feb 15;68(4):1128-35 [18281488.001]
  • [Cites] BMC Cell Biol. 2008;9:4 [18218096.001]
  • [Cites] J Androl. 2008 Mar-Apr;29(2):207-12 [17916567.001]
  • [Cites] Cancer Res. 2008 Apr 15;68(8):2678-88 [18413735.001]
  • [Cites] J Cell Mol Med. 2008 Dec;12(6B):2790-8 [18266956.001]
  • [Cites] Cancer Res. 1999 Nov 1;59(21):5483-7 [10554023.001]
  • [Cites] Genes Dev. 2000 Aug 1;14(15):1837-51 [10921899.001]
  • [Cites] Cancer Res. 2000 Sep 1;60(17):4709-13 [10987273.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1918-25 [11106683.001]
  • [Cites] Cancer Res. 2000 Dec 15;60(24):6841-5 [11156376.001]
  • [Cites] Biochem Biophys Res Commun. 2001 Apr 27;283(1):179-87 [11322786.001]
  • [Cites] Cancer Res. 2001 May 1;61(9):3550-5 [11325816.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4315-9 [11389051.001]
  • [Cites] J Urol. 2001 Oct;166(4):1514-9 [11547123.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7544-51 [11606392.001]
  • [Cites] Nat Rev Cancer. 2001 Oct;1(1):34-45 [11900250.001]
  • [Cites] Biol Chem. 2002 Feb;383(2):255-61 [11934263.001]
  • [Cites] J Biol Chem. 2002 Jun 7;277(23):20702-10 [11916967.001]
  • [Cites] J Cancer Res Clin Oncol. 2003 Apr;129(4):199-221 [12707770.001]
  • [Cites] Br J Cancer. 2003 Oct 20;89(8):1566-73 [14562033.001]
  • [Cites] Nat Med. 2004 Jan;10(1):33-9 [14702632.001]
  • [Cites] Oncogene. 2004 Jul 1;23(30):5175-84 [15156193.001]
  • [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]
  • [Cites] Cancer Res. 1994 Jun 1;54(11):2861-4 [8187068.001]
  • [Cites] J Biol Chem. 1994 Oct 14;269(41):25655-9 [7929269.001]
  • [Cites] Cell Growth Differ. 1994 Nov;5(11):1243-51 [7848925.001]
  • [Cites] N Engl J Med. 1995 May 25;332(21):1393-8 [7723794.001]
  • [Cites] Nat Genet. 1995 Apr;9(4):401-6 [7795646.001]
  • [Cites] Mol Cell Endocrinol. 1996 May 17;119(1):83-93 [8793857.001]
  • [Cites] Oncol Res. 1995;7(10-11):545-58 [8866667.001]
  • [Cites] Cancer Res. 1997 Jan 15;57(2):314-9 [9000575.001]
  • [Cites] Cancer Res. 1998 Oct 15;58(20):4640-5 [9788616.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):279-84 [9927031.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):7777-83 [10075669.001]
  • [Cites] Nat Med. 1999 Mar;5(3):280-5 [10086382.001]
  • [Cites] J Cell Physiol. 1999 Jun;179(3):336-46 [10228952.001]
  • [Cites] Endocrinology. 1999 Sep;140(9):4056-64 [10465276.001]
  • [Cites] Biochim Biophys Acta. 1999 Oct 29;1424(2-3):M23-37 [10528152.001]
  • [Cites] Cell Res. 2005 Jan;15(1):28-32 [15686623.001]
  • [Cites] Nature. 2005 Apr 14;434(7035):843-50 [15829953.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2005;8(2):119-26 [15809669.001]
  • [Cites] Mol Endocrinol. 2005 Jul;19(7):1792-802 [15731171.001]
  • [Cites] Endocr Rev. 2005 Dec;26(7):898-915 [16126938.001]
  • [Cites] Exp Cell Res. 2006 Apr 1;312(6):831-43 [16413016.001]
  • [Cites] Clin Cancer Res. 2006 Mar 15;12(6):1665-71 [16551847.001]
  • (PMID = 19351848.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK058024; United States / NCRR NIH HHS / RR / UL1 RR025741; United States / NIDDK NIH HHS / DK / DK058024
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / LEF1 protein, human; 0 / Lymphoid Enhancer-Binding Factor 1; 0 / RNA, Messenger; 0 / Receptors, Androgen
  • [Other-IDs] NLM/ NIHMS97236; NLM/ PMC3182465
  •  go-up   go-down


59. Erlich S, Tal-Or P, Liebling R, Blum R, Karunagaran D, Kloog Y, Pinkas-Kramarski R: Ras inhibition results in growth arrest and death of androgen-dependent and androgen-independent prostate cancer cells. Biochem Pharmacol; 2006 Aug 14;72(4):427-36
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] Ras inhibition results in growth arrest and death of androgen-dependent and androgen-independent prostate cancer cells.
  • Prostate cancer is one of the most frequently diagnosed cancers in human males.
  • Progression of these tumors is facilitated by autocrine/paracrine growth factors which activate critical signaling cascades that promote prostate cancer cell growth, survival and migration.
  • Here we examined the effect of the Ras inhibitor S-trans, trans-farnesylthiosalicylic acid (FTS), on growth and viability of androgen-dependent and androgen-independent prostate cancer cells.
  • Consequently the anchorage-dependent and anchorage-independent growth of LNCaP and PC3 cells were inhibited.
  • Our study demonstrated that androgen-dependent and androgen-independent prostate cancer cells require active Ras for growth and survival.
  • FTS may be qualified as a potential agent for the treatment of prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • Hazardous Substances Data Bank. FARNESOL .
  • 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 .
  • 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 = 16780807.001).
  • [ISSN] 0006-2952
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Androgens; 0 / Antineoplastic Agents; 0 / Cell Cycle Proteins; 0 / E2F1 Transcription Factor; 0 / Salicylates; 0 / Serine Proteinase Inhibitors; 0 / butyloxycarbonyl-aspartyl-fluoromethyl ketone; 0 / farnesylthiosalicylic acid; 136601-57-5 / Cyclin D1; 4602-84-0 / Farnesol; EC 2.7.1.- / CDC42BPB protein, human; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.11.1 / Myotonin-Protein Kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.6.5.2 / ras Proteins
  •  go-up   go-down


60. Katsogiannou M, El Boustany C, Gackiere F, Delcourt P, Athias A, Mariot P, Dewailly E, Jouy N, Lamaze C, Bidaux G, Mauroy B, Prevarskaya N, Slomianny C: Caveolae contribute to the apoptosis resistance induced by the alpha(1A)-adrenoceptor in androgen-independent prostate cancer cells. PLoS One; 2009;4(9):e7068
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] Caveolae contribute to the apoptosis resistance induced by the alpha(1A)-adrenoceptor in androgen-independent prostate cancer cells.
  • BACKGROUND: During androgen ablation prostate cancer cells' growth and survival become independent of normal regulatory mechanisms.
  • These androgen-independent cells acquire the remarkable ability to adapt to the surrounding microenvironment whose factors, such as neurotransmitters, influence their survival.
  • Although findings are becoming evident about the expression of alpha(1A)-adrenoceptors in prostate cancer epithelial cells, their exact functional role in androgen-independent cells has yet to be established.
  • Previous work has demonstrated that membrane lipid rafts associated with key signalling proteins mediate growth and survival signalling pathways in prostate cancer cells.
  • METHODOLOGY/PRINCIPAL FINDINGS: In order to analyze the membrane topology of the alpha(1A)-adrenoceptor we explored its presence by a biochemical approach in purified detergent resistant membrane fractions of the androgen-independent prostate cancer cell line DU145.
  • Further, immunohistofluorescence revealed the relation between high levels of alpha(1A)-adrenoceptor and caveolin-1 expression with advanced stage prostate cancer.
  • CONCLUSIONS/SIGNIFICANCE: In conclusion, we propose that alpha(1A)-adrenoceptor stimulation in androgen-independent prostate cancer cells via caveolae constitutes one of the mechanisms contributing to their protection from TG-induced apoptosis.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. CHOLESTEROL .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Semin Oncol. 1988 Aug;15(4):371-89 [3043671.001]
  • [Cites] Prostate Suppl. 1989;2:5-16 [2619992.001]
  • [Cites] Prostate Suppl. 1992;4:129-38 [1574453.001]
  • [Cites] Nature. 1994 Sep 22;371(6495):346-7 [8090205.001]
  • [Cites] J Biol Chem. 1994 Dec 30;269(52):32848-57 [7806510.001]
  • [Cites] Br J Urol. 1994 Nov;74(5):585-9 [7530122.001]
  • [Cites] Cell. 1995 Jan 27;80(2):249-57 [7834744.001]
  • [Cites] Cell. 1995 Jun 2;81(5):801-9 [7774019.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8655-9 [7567992.001]
  • [Cites] FEBS Lett. 2000 Jan 21;466(1):6-10 [10648802.001]
  • [Cites] J Biol Chem. 2000 Apr 14;275(15):11470-7 [10753965.001]
  • [Cites] Cancer Res. 2000 Aug 15;60(16):4550-5 [10969806.001]
  • [Cites] Clin Biochem. 2000 Oct;33(7):541-7 [11124339.001]
  • [Cites] J Urol. 2001 Mar;165(3):1033-6 [11176535.001]
  • [Cites] Cancer Res. 2001 May 15;61(10):3882-5 [11358800.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4386-92 [11389065.001]
  • [Cites] Nat Rev Mol Cell Biol. 2000 Oct;1(1):31-9 [11413487.001]
  • [Cites] Mol Cell. 2001 Mar;7(3):661-71 [11463390.001]
  • [Cites] J Urol. 1995 Dec;154(6):2096-9 [7500467.001]
  • [Cites] Br J Pharmacol. 1995 Jul;115(5):781-6 [8548177.001]
  • [Cites] Br J Pharmacol. 1996 Nov;119(5):797-803 [8922723.001]
  • [Cites] Prostate. 1997 Feb 15;30(3):202-15 [9122046.001]
  • [Cites] Nature. 1997 Jun 5;387(6633):569-72 [9177342.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 1998 Feb;357(2):100-10 [9521482.001]
  • [Cites] Clin Cancer Res. 1998 Aug;4(8):1873-80 [9717814.001]
  • [Cites] Nat Med. 1998 Sep;4(9):1062-4 [9734401.001]
  • [Cites] J Biol Chem. 1998 Dec 11;273(50):33533-9 [9837934.001]
  • [Cites] Annu Rev Cell Dev Biol. 1998;14:111-36 [9891780.001]
  • [Cites] Cancer Res. 1999 Jan 15;59(2):279-84 [9927031.001]
  • [Cites] Eur Urol. 1999;36 Suppl 1:31-4; discussion 65 [10393470.001]
  • [Cites] J Urol. 1999 Oct;162(4):1537-42 [10492251.001]
  • [Cites] Mol Cell Biol. 1999 Nov;19(11):7289-304 [10523618.001]
  • [Cites] J Biol Chem. 1957 May;226(1):497-509 [13428781.001]
  • [Cites] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078.001]
  • [Cites] Ann Med. 2004;36(8):584-95 [15768830.001]
  • [Cites] Mol Biol Cell. 2005 May;16(5):2234-47 [15728718.001]
  • [Cites] Prostate. 2005 Sep 1;64(4):408-18 [15789364.001]
  • [Cites] J Cell Biochem. 2006 Jan 1;97(1):18-32 [16216007.001]
  • [Cites] Biochim Biophys Acta. 2005 Dec 30;1746(3):234-51 [16368465.001]
  • [Cites] Cancer Res. 2006 Feb 15;66(4):2038-47 [16489003.001]
  • [Cites] Cell Calcium. 2006 Apr;39(4):357-66 [16442617.001]
  • [Cites] Endocr Relat Cancer. 2006 Mar;13(1):181-95 [16601287.001]
  • [Cites] Prostate. 2006 May 15;66(7):761-7 [16425183.001]
  • [Cites] J Mol Cell Cardiol. 2006 Jul;41(1):17-25 [16730745.001]
  • [Cites] Br J Pharmacol. 2007 Feb;150(3):261-70 [17179950.001]
  • [Cites] Circulation. 2007 Feb 13;115(6):763-72 [17283256.001]
  • [Cites] Cytometry A. 2007 Mar;71(3):125-31 [17252584.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Mar;8(3):185-94 [17318224.001]
  • [Cites] Prostate. 2007 May 1;67(6):614-22 [17299799.001]
  • [Cites] Apoptosis. 2007 May;12(5):887-96 [17453158.001]
  • [Cites] Neuropathol Appl Neurobiol. 2007 Jun;33(3):317-27 [17493012.001]
  • [Cites] Biochim Biophys Acta. 2007 Aug;1773(8):1213-26 [17112607.001]
  • [Cites] Nat Rev Mol Cell Biol. 2008 Jan;9(1):47-59 [18097445.001]
  • [Cites] Eur J Pharmacol. 2008 Jan 14;578(2-3):349-58 [17936747.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Jan 8;105(1):124-8 [18172219.001]
  • [Cites] J Biol Chem. 2008 Feb 1;283(5):2973-85 [18048357.001]
  • [Cites] J Biol Chem. 2008 Apr 11;283(15):10162-73 [18230611.001]
  • [Cites] Cancer Metastasis Rev. 2008 Dec;27(4):715-35 [18506396.001]
  • [Cites] J Mol Biol. 2005 Mar 4;346(4):1109-20 [15701521.001]
  • [Cites] Cardiovasc Res. 2001 Sep;51(4):709-16 [11530104.001]
  • [Cites] Science. 2001 Sep 28;293(5539):2449-52 [11498544.001]
  • [Cites] J Urol. 2002 Mar;167(3):1458-63 [11832770.001]
  • [Cites] Endocr Relat Cancer. 2002 Mar;9(1):61-73 [11914183.001]
  • [Cites] Biophys J. 2002 May;82(5):2526-35 [11964241.001]
  • [Cites] Curr Urol Rep. 2000 Aug;1(2):89-96 [12084321.001]
  • [Cites] Arterioscler Thromb Vasc Biol. 2002 Aug 1;22(8):1267-72 [12171786.001]
  • [Cites] J Urol. 2002 Oct;168(4 Pt 1):1589-96 [12352463.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2002;5(2):88-95 [12496995.001]
  • [Cites] Cancer Res. 2003 May 1;63(9):2037-41 [12727816.001]
  • [Cites] J Clin Invest. 2003 Jun;111(11):1691-701 [12782672.001]
  • [Cites] Sci STKE. 2004 Jan 20;2004(216):re2 [14734786.001]
  • [Cites] J Mol Endocrinol. 2004 Apr;32(2):325-38 [15072542.001]
  • [Cites] J Cell Biol. 1973 May;57(2):551-65 [4121290.001]
  • (PMID = 19763272.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ADRA1A protein, human; 0 / Neurotransmitter Agents; 0 / Receptors, Adrenergic, alpha-1; 0 / Sphingomyelins; 67526-95-8 / Thapsigargin; 97C5T2UQ7J / Cholesterol
  • [Other-IDs] NLM/ PMC2742726
  •  go-up   go-down


61. Tamura T, Chiba J: STEAP4 regulates focal adhesion kinase activation and CpG motifs within STEAP4 promoter region are frequently methylated in DU145, human androgen-independent prostate cancer cells. Int J Mol Med; 2009 Nov;24(5):599-604
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] STEAP4 regulates focal adhesion kinase activation and CpG motifs within STEAP4 promoter region are frequently methylated in DU145, human androgen-independent prostate cancer cells.
  • The possible roles of STEAP4 in cancer progression have not been reported.
  • In this study, we report that STEAP4 expression is able to inhibit anchorage-independent cell growth.
  • Furthermore, we show that CpG sequences in STEAP4 promoter region were frequently methylated in DU145, androgen-independent prostate cancer cells.
  • Demethylation treatment induced STEAP4 expression in DU145, suggesting the possibility that STEAP4 expression in cancer cells is in part epigenetically regulated.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19787193.001).
  • [ISSN] 1791-244X
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Androgens; 0 / Membrane Proteins; 21820-51-9 / Phosphotyrosine; EC 1.- / Oxidoreductases; EC 1.16.1.- / STEAP4 protein, human; EC 2.7.10.2 / Focal Adhesion Protein-Tyrosine Kinases
  •  go-up   go-down


62. Chua CW, Lee DT, Ling MT, Zhou C, Man K, Ho J, Chan FL, Wang X, Wong YC: FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer. Int J Cancer; 2005 Dec 20;117(6):1039-48
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] FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer.
  • Our study evaluates the therapeutic potential of FTY720 in the treatment of androgen-independent prostate cancer using a human prostate cancer xenograft in nude mice.
  • CWR22R, an androgen-independent human prostate tumor xenograft was inoculated into castrated nude mice and the animals were administrated with either normal saline or FTY720 (10 mg/kg) through intraperitoneal (i.p.) injection for 20 days.
  • Body weight and tumor volume were recorded every 2 days, and serum prostate specific antigen (PSA) levels were also measured before and after the treatment.
  • In addition, the potential inhibitory effect of FTY720 on prostate cancer angiogenesis and metastasis was investigated by immunostaining of CD31, VEGF, E-cadherin and beta-catenin.
  • Our results suggest a potential novel agent in the suppression of androgen-independent prostate cancer.
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Apoptosis / drug effects. Body Weight. Cadherins / analysis. Caspase 3. Caspases / analysis. Cell Division / drug effects. Fingolimod Hydrochloride. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Neoplasm Metastasis / prevention & control. Neoplasm Transplantation. Neovascularization, Pathologic / prevention & control. Orchiectomy. Prostate-Specific Antigen / blood. Proto-Oncogene Proteins c-bcl-2 / analysis. Sphingosine / analogs & derivatives. Vascular Endothelial Growth Factor A / analysis. beta Catenin / analysis

  • Genetic Alliance. consumer health - Prostate 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 .
  • 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
  • [Copyright] Copyright 2005 Wiley-Liss, Inc
  • (PMID = 15986440.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antigens, CD31; 0 / Cadherins; 0 / Propylene Glycols; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vascular Endothelial Growth Factor A; 0 / beta Catenin; EC 3.4.21.77 / Prostate-Specific Antigen; EC 3.4.22.- / CASP3 protein, human; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; EC 3.4.22.- / Caspases; G926EC510T / Fingolimod Hydrochloride; NGZ37HRE42 / Sphingosine
  •  go-up   go-down


63. Sissung TM, Baum CE, Deeken J, Price DK, Aragon-Ching J, Steinberg SM, Dahut W, Sparreboom A, Figg WD: ABCB1 genetic variation influences the toxicity and clinical outcome of patients with androgen-independent prostate cancer treated with docetaxel. Clin Cancer Res; 2008 Jul 15;14(14):4543-9
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] ABCB1 genetic variation influences the toxicity and clinical outcome of patients with androgen-independent prostate cancer treated with docetaxel.
  • PURPOSE: Polymorphisms that are associated with ABCB1 expression and function may be linked to treatment efficacy and the development of neutropenia and neurotoxicity in patients with androgen-independent prostate cancer receiving docetaxel.
  • EXPERIMENTAL DESIGN: Patients with androgen-independent prostate cancer treated with docetaxel alone (n = 23) or docetaxel and thalidomide (n = 50) were genotyped for the ABCB1 1236C>T, 2677 G>T/A, and 3435 C>T alleles by direct sequencing, and diplotypes were constructed using an EM algorithm.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. THALIDOMIDE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Jpn J Cancer Res. 1999 Dec;90(12):1380-6 [10665657.001]
  • [Cites] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392.001]
  • [Cites] Muscle Nerve. 2001 Aug;24(8):1050-7 [11439380.001]
  • [Cites] Acta Otolaryngol. 2001 Sep;121(6):735-42 [11678173.001]
  • [Cites] Eur J Cancer. 2002 Mar;38(4):497-504 [11872341.001]
  • [Cites] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585.001]
  • [Cites] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7735-8 [2444983.001]
  • [Cites] Proc Natl Acad Sci U S A. 1989 Jan;86(2):695-8 [2563168.001]
  • [Cites] Cell. 1991 Jul 12;66(1):85-94 [1712673.001]
  • [Cites] Blood. 1992 Dec 1;80(11):2729-34 [1360266.001]
  • [Cites] Cancer Treat Rev. 1993 Oct;19(4):351-86 [8106152.001]
  • [Cites] Cell. 1994 May 20;77(4):491-502 [7910522.001]
  • [Cites] J Chromatogr B Biomed Sci Appl. 1997 Jun 6;693(2):437-41 [9210450.001]
  • [Cites] Neurosci Lett. 1997 Aug 22;232(1):41-4 [9292887.001]
  • [Cites] Recent Results Cancer Res. 1998;144:93-115 [9304712.001]
  • [Cites] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):854-9 [16467099.001]
  • [Cites] Cancer Chemother Pharmacol. 2006 May;57(5):599-606 [16136308.001]
  • [Cites] J Clin Pharmacol. 2006 Mar;46(3):373-9 [16490813.001]
  • [Cites] Clin Pharmacol Ther. 2006 Jun;79(6):570-80 [16765145.001]
  • [Cites] Clin Cancer Res. 2006 Jul 1;12(13):4127; author reply 4127-9 [16818714.001]
  • [Cites] Clin Cancer Res. 2006 Oct 1;12(19):5786-93 [17020985.001]
  • [Cites] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):6204 [17062699.001]
  • [Cites] Eur J Cancer. 2006 Nov;42(17):2893-6 [16950614.001]
  • [Cites] Pharmacogenet Genomics. 2006 Dec;16(12):855-61 [17108809.001]
  • [Cites] Science. 2007 Jan 26;315(5811):525-8 [17185560.001]
  • [Cites] Expert Opin Pharmacother. 2007 Feb;8(2):119-27 [17257083.001]
  • [Cites] Clin Cancer Res. 2008 Jun 1;14(11):3312-8 [18519758.001]
  • [Cites] BJU Int. 2008 Aug 5;102(5):617-21 [18537956.001]
  • [Cites] Prostate. 2004 Apr 1;59(1):77-90 [14991868.001]
  • [Cites] Clin Pharmacokinet. 2004;43(9):553-76 [15217301.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2532-9 [15226321.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3473-8 [10716719.001]
  • (PMID = 18628469.001).
  • [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
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010453-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Intramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCB1 protein, human; 0 / Androgens; 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / P-Glycoproteins; 0 / Taxoids; 15H5577CQD / docetaxel; 4Z8R6ORS6L / Thalidomide
  • [Other-IDs] NLM/ NIHMS105257; NLM/ PMC2723795
  •  go-up   go-down


64. Chhipa RR, Wu Y, Mohler JL, Ip C: Survival advantage of AMPK activation to androgen-independent prostate cancer cells during energy stress. Cell Signal; 2010 Oct;22(10):1554-61
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] Survival advantage of AMPK activation to androgen-independent prostate cancer cells during energy stress.
  • Androgen-independent prostate cancer usually develops as a relapse following androgen ablation therapy.
  • Removing androgen systemically causes vascular degeneration and nutrient depletion of the prostate tumor tissue.
  • The fact that the malignancy later evolves to androgen-independence suggests that some cancer cells are able to survive the challenge of energy/nutrient deprivation.
  • The present study was designed to investigate the role of AMPK in contributing to the survival of the androgen-independent phenotype.
  • Most of the experiments were carried out in the androgen-dependent LNCaP cells and the androgen-independent C4-2 cells.
  • The observation that similar results were found in other androgen-independent prostate cancer cell lines, including CW22Rv1 abd VCaP, provided further assurance that AMPK is a facilitator on the road to androgen-independence of prostate cancer cells.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. GLUCOSE .
  • 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 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20570728.001).
  • [ISSN] 1873-3913
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P01 CA126804; United States / NCI NIH HHS / CA / P01 CA126804-03; United States / NCI NIH HHS / CA / P30 CA016056; United States / NCI NIH HHS / CA / P30 CA16056
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; EC 2.7.11.1 / AMP-Activated Protein Kinases; IY9XDZ35W2 / Glucose
  • [Other-IDs] NLM/ NIHMS216272; NLM/ PMC4712644
  •  go-up   go-down


65. Azuma K, Nakashiro K, Sasaki T, Goda H, Onodera J, Tanji N, Yokoyama M, Hamakawa H: Anti-tumor effect of small interfering RNA targeting the androgen receptor in human androgen-independent prostate cancer cells. Biochem Biophys Res Commun; 2010 Jan 1;391(1):1075-9
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] Anti-tumor effect of small interfering RNA targeting the androgen receptor in human androgen-independent prostate cancer cells.
  • Early phase prostate cancer is usually androgen-dependent, with the androgen/androgen receptor (AR) signaling pathway playing a central role.
  • At this stage, the cancer responds well to androgen ablation therapy, but prostate cancers eventually acquire androgen independence and more aggressive phenotypes.
  • To determine if the AR is a plausible therapeutic target, we investigated the anti-tumor effect of small interfering RNAs targeting the AR (siAR) in the human prostate cancer cells, LNCaP and 22Rv1, which express mutated AR.
  • These results suggest that the AR is still a key therapeutic target even in androgen-independent prostate cancer (AIPC).
  • [MeSH-major] Androgen Receptor Antagonists. Prostatic Neoplasms / therapy. RNA Interference. RNA, Small Interfering / genetics
  • [MeSH-minor] Androgens / genetics. Androgens / metabolism. Base Sequence. Cell Line, Tumor. Gene Knockdown Techniques. Humans. Male. Receptors, Androgen / genetics

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • [Copyright] Copyright 2009 Elsevier Inc. All rights reserved.
  • (PMID = 20004643.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Androgens; 0 / RNA, Small Interfering; 0 / Receptors, Androgen
  •  go-up   go-down


66. Veuillen C, Gravis G, Marcy M, Walz J, Bladou F, Salem N, Brunelle S, Olive D: Alterations of natural killer cells in metastatic prostate cancer. J Clin Oncol; 2009 May 20;27(15_suppl):e16131

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alterations of natural killer cells in metastatic prostate cancer.
  • : e16131 Background: Recently, prostate cancer (PCa) has been considered as a potential target for antitumoral immunotherapy and cells such as Natural Killer (NK) cells, with antitumoral activity are a promising candidate.
  • METHODS: Activating and inhibitory receptors were analysed by flow cytometry in peripheral NK cells from 8 patients with metastatic androgen dependent prostate cancer (ADPC), 10 with metastatic androgen independent prostate cancer (AIPC), 7 patients with localized prostate cancer (LPC ) and 15 healthy donors.
  • Moreover, this could constitute a potential mechanism for cancer cells immune escape and a possible target for therapies improving NK functions.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27963371.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


67. Floryk D, Huberman E: Mycophenolic acid-induced replication arrest, differentiation markers and cell death of androgen-independent prostate cancer cells DU145. Cancer Lett; 2006 Jan 8;231(1):20-9
Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mycophenolic acid-induced replication arrest, differentiation markers and cell death of androgen-independent prostate cancer cells DU145.
  • Here, we report that MPA also induces such a differentiation in the androgen-independent prostate cancer derived cell line DU145.
  • The inhibitor also induced the expression of CD55, clusterin, granulophysin, glucose-regulated protein 78, vasoactive intestinal polypeptide and prostate-specific transglutaminase, which are differentiation markers associated with the phenotype of normal prostate cells.
  • We suggest that inosine 5'-monophosphate dehydrogenase inhibitors, which are already used for the treatment of other diseases, may be used as potential differentiation therapy drugs to control prostate cancer.
  • [MeSH-minor] Androgen Antagonists / pharmacology. Biomarkers / analysis. Cell Cycle / drug effects. Cell Proliferation / drug effects. Drug Resistance, Neoplasm. Humans. Male. Phenotype. Tumor Cells, Cultured

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16356827.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 80826
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antibiotics, Antineoplastic; 0 / Biomarkers; HU9DX48N0T / Mycophenolic Acid
  •  go-up   go-down


68. Peng Y, Chen F, Melamed J, Chiriboga L, Wei J, Kong X, McLeod M, Li Y, Li CX, Feng A, Garabedian MJ, Wang Z, Roeder RG, Lee P: Distinct nuclear and cytoplasmic functions of androgen receptor cofactor p44 and association with androgen-independent prostate cancer. Proc Natl Acad Sci U S A; 2008 Apr 1;105(13):5236-41
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] Distinct nuclear and cytoplasmic functions of androgen receptor cofactor p44 and association with androgen-independent prostate cancer.
  • Androgen receptor (AR) mediates transcriptional activation of diverse target genes through interactions with various coactivators that may alter its function and help mediate the switch between prostate cell proliferation and differentiation.
  • We recently identified p44/MEP50 as an AR coactivator and further showed that it is expressed primarily in the nucleus and cytoplasm of benign prostate epithelial and prostate cancer cells, respectively.
  • We also showed that haploinsufficiency in p44(+/-) mice causes prostate epithelial cell proliferation.
  • To establish direct cause-and-effect relationships, we have used p44 fusion proteins that are selectively expressed in the nucleus or cytoplasm of prostate cancer cells (LNCaP), along with RNAi analyses, to examine effects of p44 both in vitro and in vivo (in tumor xenografts).
  • Importantly, we also demonstrate that altered p44 expression is associated with androgen-independent prostate cancer.
  • Our results indicate that nuclear p44 and cytoplasmic p44 have distinct and opposing functions in the regulation of prostate cancer cell proliferation.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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] Cell. 1999 Sep 3;98(5):675-86 [10490106.001]
  • [Cites] J Mol Endocrinol. 2006 Oct;37(2):283-300 [17032745.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11345-53 [16357141.001]
  • [Cites] J Mol Endocrinol. 2006 Jun;36(3):463-83 [16720717.001]
  • [Cites] Clin Cancer Res. 2000 May;6(5):1891-5 [10815912.001]
  • [Cites] Biochem Soc Trans. 2000;28(4):415-8 [10961931.001]
  • [Cites] Cell Growth Differ. 2002 Jan;13(1):1-11 [11801526.001]
  • [Cites] EMBO J. 2002 Feb 15;21(4):736-48 [11847121.001]
  • [Cites] J Biol Chem. 2002 Mar 1;277(9):7076-85 [11751884.001]
  • [Cites] J Biol Chem. 2002 Mar 8;277(10):8243-7 [11756452.001]
  • [Cites] Cancer Metastasis Rev. 2001;20(3-4):207-23 [12085963.001]
  • [Cites] Am J Pathol. 2002 Oct;161(4):1467-74 [12368219.001]
  • [Cites] Crit Rev Eukaryot Gene Expr. 2002;12(3):193-207 [12449343.001]
  • [Cites] Essays Biochem. 2000;36:89-103 [12471905.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 1;31(3):999-1005 [12560496.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):7019-29 [12972618.001]
  • [Cites] J Biol Chem. 2004 Apr 2;279(14):13944-52 [14711828.001]
  • [Cites] Science. 1988 May 13;240(4854):889-95 [3283939.001]
  • [Cites] Cancer Res. 1993 Mar 15;53(6):1304-11 [8443809.001]
  • [Cites] Prostate. 1993;22(2):109-18 [7681204.001]
  • [Cites] Curr Opin Genet Dev. 1999 Apr;9(2):140-7 [10322133.001]
  • [Cites] Biochem Biophys Res Commun. 2006 Jul 7;345(3):1051-8 [16712789.001]
  • [Cites] J Cell Biochem. 2006 Oct 1;99(2):333-44 [16518832.001]
  • [Cites] EMBO Rep. 2005 Jan;6(1):70-6 [15592453.001]
  • (PMID = 18356297.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / DK058024; United States / NIDDK NIH HHS / DK / DK071900; United States / NCRR NIH HHS / RR / UL1 RR025741; United States / NIDDK NIH HHS / DK / R01 DK071900; United States / NIDDK NIH HHS / DK / R01 DK065156; United States / NIDDK NIH HHS / DK / R01 DK058024; United States / NIDDK NIH HHS / DK / DK065156 01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / CCND2 protein, human; 0 / Cyclin D2; 0 / Cyclins; 0 / Receptors, Androgen; 0 / Transcription Factors; 0 / p44 protein, human; EC 2.7.11.22 / Cyclin-Dependent Kinase 6
  • [Other-IDs] NLM/ PMC2278178
  •  go-up   go-down


69. Wagner M, Garzotto M, Lemmon D, Eilers KM, Beer TM: Prostate-specific antigen decline after gonadotropin-releasing hormone antagonist withdrawal in androgen-independent prostate cancer. Urology; 2005 Apr;65(4):799
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Prostate-specific antigen decline after gonadotropin-releasing hormone antagonist withdrawal in androgen-independent prostate cancer.
  • A 66-year-old man with androgen-independent prostate cancer was treated with abarelix, a gonadotropin-releasing hormone antagonist, for 20 weeks in an experimental protocol.
  • He did not respond to therapy, but his serum prostate-specific antigen level dropped from 15.8 ng/mL to a confirmed 0.8 ng/mL after abarelix was stopped.
  • His prostate-specific antigen level did not return to greater than 15.8 ng/mL for 14 months.
  • This is the first report of a withdrawal response after therapy with a gonadotropin-releasing hormone antagonist, a new class of agents for prostate cancer.
  • [MeSH-major] Gonadotropin-Releasing Hormone / antagonists & inhibitors. Oligopeptides / administration & dosage. Prostate-Specific Antigen / blood. Prostatic Neoplasms / blood. Prostatic Neoplasms / drug therapy

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer Screening.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15833548.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Grant] United States / NCRR NIH HHS / RR / 5 M01 RR00334-33S2
  • [Publication-type] Case Reports; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Oligopeptides; 33515-09-2 / Gonadotropin-Releasing Hormone; EC 3.4.21.77 / Prostate-Specific Antigen; W486SJ5824 / abarelix
  •  go-up   go-down


70. Schröder FH: Progress in understanding androgen-independent prostate cancer (AIPC): a review of potential endocrine-mediated mechanisms. Eur Urol; 2008 Jun;53(6):1129-37
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] Progress in understanding androgen-independent prostate cancer (AIPC): a review of potential endocrine-mediated mechanisms.
  • This review is triggered by recent developments that offer new explanations for the mechanism of progression of prostate cancer to androgen independence.
  • A total of seven mechanisms can be identified that relate to progression to androgen independence.
  • Five of those are dependent on the androgen receptor, which is present or over-expressed in androgen-independent prostate cancer tissue.
  • Probably due to selective pressure, AIPC cells have the capability to escape from the effect of castration and antiandrogens; exclusion of the androgen receptor activity by inhibition of dimerisation or inhibition of DNA binding seem to be the logical next steps.
  • Although androgen levels and androgen synthesis are suppressed in prostatic tissues during the phase of response to endocrine treatment, androgen levels and, specifically, 5-alpha-dihydrotestosterone (DHT) were elevated in tissues derived from metastases of AIPC.
  • [MeSH-major] Androgens / physiology. Prostatic Neoplasms / physiopathology. Prostatic Neoplasms / therapy. Receptors, Androgen / physiology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Eur Urol. 2009 Jan;55(1):e6-7; author reply e8-9 [18603349.001]
  • [CommentIn] Eur Urol. 2008 Jun;53(6):1101-3 [18294760.001]
  • (PMID = 18262723.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  • [Number-of-references] 58
  •  go-up   go-down


71. Altundag K, Altundag O, Morandi P, Gunduz M: Imatinib mesylate and zoledronic acid in androgen-independent prostate cancer. Urology; 2005 Jan;65(1):211-2; author reply 212
Hazardous Substances Data Bank. IMATINIB MESYLATE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Imatinib mesylate and zoledronic acid in androgen-independent prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] Urology. 2004 May;63(5):934-9 [15134984.001]
  • (PMID = 15667906.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Benzamides; 0 / Diphosphonates; 0 / Imidazoles; 0 / Neoplasm Proteins; 0 / Piperazines; 0 / Pyrimidines; 6XC1PAD3KF / zoledronic acid; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor
  •  go-up   go-down


72. Pienta KJ, Bradley D: Mechanisms underlying the development of androgen-independent prostate cancer. Clin Cancer Res; 2006 Mar 15;12(6):1665-71
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] Mechanisms underlying the development of androgen-independent prostate cancer.
  • [MeSH-minor] Humans. Male. Models, Biological. Receptors, Androgen / physiology

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16551847.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / P50CA69568
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  • [Number-of-references] 92
  •  go-up   go-down


73. Shimada K, Nakamura M, De Velasco MA, Tanaka M, Ouji Y, Konishi N: Syndecan-1, a new target molecule involved in progression of androgen-independent prostate cancer. Cancer Sci; 2009 Jul;100(7):1248-54
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] Syndecan-1, a new target molecule involved in progression of androgen-independent prostate cancer.
  • In the present study, we focused on the role of syndecan-1 in human prostate cancer.
  • Immunohistochemical analysis revealed either no or rare expression of syndecan-1 in normal secretory glands and prostate cancer cells at hormone naïve status, whereas the expression was significantly increased in viable cancer cells following neo-adjuvant hormonal therapy.
  • Syndecan-1 expression was much higher in the androgen independent prostate cancer cell lines DU145 and PC3, rather than the androgen-dependent LNCaP, but the level in LNCaP was up-regulated in response to long-term culture under androgen deprivation.
  • In conclusion, syndecan-1 might participate in the process of androgen-dependent to -independent conversion, and be a new target molecule for hormone resistant prostate cancer therapy.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19432893.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Small Interfering; 0 / Syndecan-1
  •  go-up   go-down


74. Floryk D, Huberman E: Differentiation of androgen-independent prostate cancer PC-3 cells is associated with increased nuclear factor-kappaB activity. Cancer Res; 2005 Dec 15;65(24):11588-96
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] Differentiation of androgen-independent prostate cancer PC-3 cells is associated with increased nuclear factor-kappaB activity.
  • Recently, we have reported that inosine 5'-monophosphate dehydrogenase inhibitors, such as mycophenolic acid (MPA), induce the differentiation of PC-3 cells, which are derived from a human androgen-independent prostate cancer, into cells with a phenotype resembling maturing prostate secretory cells.
  • Taken together, our results implicate both NF-kappaB-dependent and NF-kappaB-independent genes in the processes leading to PC-3 cell differentiation induced by tributyrin and MPA.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. MYCOPHENOLATE MOFETIL .
  • Hazardous Substances Data Bank. GALLIC ACID .
  • Hazardous Substances Data Bank. APIGENIN .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16357169.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 80826
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antibiotics, Antineoplastic; 0 / Calcium Channel Blockers; 0 / NF-kappa B; 57818-92-5 / 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate; 632XD903SP / Gallic Acid; 7V515PI7F6 / Apigenin; HU9DX48N0T / Mycophenolic Acid
  •  go-up   go-down


75. Stanbrough M, Bubley GJ, Ross K, Golub TR, Rubin MA, Penning TM, Febbo PG, Balk SP: Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer. Cancer Res; 2006 Mar 1;66(5):2815-25
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] Increased expression of genes converting adrenal androgens to testosterone in androgen-independent prostate cancer.
  • Androgen receptor (AR) plays a central role in prostate cancer, and most patients respond to androgen deprivation therapies, but they invariably relapse with a more aggressive prostate cancer that has been termed hormone refractory or androgen independent.
  • To identify proteins that mediate this tumor progression, gene expression in 33 androgen-independent prostate cancer bone marrow metastases versus 22 laser capture-microdissected primary prostate cancers was compared using Affymetrix oligonucleotide microarrays.
  • Multiple genes associated with aggressive behavior were increased in the androgen-independent metastatic tumors (MMP9, CKS2, LRRC15, WNT5A, EZH2, E2F3, SDC1, SKP2, and BIRC5), whereas a candidate tumor suppressor gene (KLF6) was decreased.
  • Consistent with castrate androgen levels, androgen-regulated genes were reduced 2- to 3-fold in the androgen-independent tumors.
  • This was associated with increased expression of AR (5.8-fold) and multiple genes mediating androgen metabolism (HSD3B2, AKR1C3, SRD5A1, AKR1C2, AKR1C1, and UGT2B15).
  • These results indicate that enhanced intracellular conversion of adrenal androgens to testosterone and dihydrotestosterone is a mechanism by which prostate cancer cells adapt to androgen deprivation and suggest new therapeutic targets.
  • [MeSH-minor] 3-Hydroxysteroid Dehydrogenases / biosynthesis. 3-Hydroxysteroid Dehydrogenases / genetics. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Hydroxyprostaglandin Dehydrogenases / biosynthesis. Hydroxyprostaglandin Dehydrogenases / genetics. Hydroxysteroid Dehydrogenases / biosynthesis. Hydroxysteroid Dehydrogenases / genetics. Male. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / metabolism. Receptors, Androgen / biosynthesis. Receptors, Androgen / genetics. Reverse Transcriptase Polymerase Chain Reaction


76. Nabhan C: Is chemotherapy the standard for asymptomatic androgen-independent prostate cancer? J Clin Oncol; 2008 May 10;26(14):2413-4; author reply 2414-5
Hazardous Substances Data Bank. DOCETAXEL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is chemotherapy the standard for asymptomatic androgen-independent prostate cancer?
  • [MeSH-minor] Humans. Male. Neoplasms, Hormone-Dependent / drug therapy. Prostate-Specific Antigen / blood. Taxoids / administration & dosage

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentOn] J Clin Oncol. 2008 Jan 10;26(2):242-5 [18182665.001]
  • (PMID = 18467737.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Comment; Letter
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


77. Shi YF, Tang YQ, Sun XW, Yu DJ, Han BM, Hong Y, Xia SJ: [Targeted degradation of androgen receptors in androgen-independent prostate cancer cells: an experimental study]. Zhonghua Nan Ke Xue; 2009 Dec;15(12):1059-63
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] [Targeted degradation of androgen receptors in androgen-independent prostate cancer cells: an experimental study].
  • OBJECTIVE: To investigate targeted degradation of the androgen receptor (AR) by chimeric molecules (DHT-PROTAC) via the ubiquitin-proteasome pathway in androgen-independent prostate cancer CA-2B cells, and explore the proliferation, secretion and apoptosis of the treated cells.
  • CONCLUSION: The chimeric molecule (DHT-PROTAC) can target the degradation of androgen receptors, reduce the secretion of PSA and repress the in vitro growth of C4-2B cells.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / metabolism. Receptors, Androgen / metabolism
  • [MeSH-minor] Apoptosis. Cell Line, Tumor. Cell Proliferation. Humans. Male. Prostate-Specific Antigen / metabolism

  • 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
  • (PMID = 20180412.001).
  • [ISSN] 1009-3591
  • [Journal-full-title] Zhonghua nan ke xue = National journal of andrology
  • [ISO-abbreviation] Zhonghua Nan Ke Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Antineoplastic Agents; 0 / Receptors, Androgen; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


78. Bellmunt J, Albiol S, Albanell J: Intermittent chemotherapy in metastatic androgen-independent prostate cancer. BJU Int; 2007 Sep;100(3):490-2
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] Intermittent chemotherapy in metastatic androgen-independent prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17669140.001).
  • [ISSN] 1464-4096
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal
  •  go-up   go-down


79. Gul HI, Das U, Pandit B, Li PK: Evaluation of the cytotoxicity of some mono-mannich bases and their corresponding azine derivatives against androgen-independent prostate cancer cells. Arzneimittelforschung; 2006;56(12):850-4
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] Evaluation of the cytotoxicity of some mono-mannich bases and their corresponding azine derivatives against androgen-independent prostate cancer cells.
  • The cytotoxic activity of the compounds was tested against the androgen-independent prostate cancer cell line PC-3.

  • 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 = 17260673.001).
  • [ISSN] 0004-4172
  • [Journal-full-title] Arzneimittel-Forschung
  • [ISO-abbreviation] Arzneimittelforschung
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents; 0 / Hydrazines; 0 / Mannich Bases
  •  go-up   go-down


80. Perez SA, Bisias S, Kallinteris NL, Ardavanis A, Georgakopoulou KG, Apostolikas N, Thanos A, Papamichail M, von Hofe E, Baxevanis CN: Results from the first phase I clinical study of the novel Ii-Key/HER2/neu(776-790) hybrid peptide vaccine in patients with prostate cancer. J Clin Oncol; 2009 May 20;27(15_suppl):3011

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Results from the first phase I clinical study of the novel Ii-Key/HER2/neu(776-790) hybrid peptide vaccine in patients with prostate cancer.
  • Herein, we present the results of the first phase I clinical trial of the Ii-Key/HER-2/neu(776-790) (AE37) vaccine in patients (pts) with prostate cancer.
  • METHODS: Androgen-dependent (AD) and androgen-independent (AI) pts with HER-2/neu+ (IHC: 1-3) prostate adenocarcinomas were eligible.
  • AE37 is also capable of eliciting potent and specific immunologic responses in prostate cancer pts.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 27962063.001).
  • [ISSN] 1527-7755
  • [Journal-full-title] Journal of clinical oncology : official journal of the American Society of Clinical Oncology
  • [ISO-abbreviation] J. Clin. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


81. Petrylak DP: Chemotherapy for androgen-independent prostate cancer. World J Urol; 2005 Feb;23(1):10-3
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Chemotherapy for androgen-independent prostate cancer.
  • The evolution of taxanes as treatment for androgen-independent prostate cancer hes emerged from both the laboratory and clinic.
  • Two randomized trials have proven the superiority of docetaxel based treatment in improving survival in men with androgen-independent prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Ann Oncol. 1999 Jan;10(1):33-8 [10076719.001]
  • [Cites] Clin Prostate Cancer. 2004 Sep;3(2):104-11 [15479494.001]
  • [Cites] Ann Oncol. 2001 Sep;12(9):1273-9 [11697840.001]
  • [Cites] J Clin Oncol. 2001 May 1;19(9):2509-16 [11331330.001]
  • [Cites] J Natl Cancer Inst. 1994 May 4;86(9):688-94 [7908988.001]
  • [Cites] J Urol. 1993 Jun;149(6):1622-5 [8501820.001]
  • [Cites] Br J Urol. 1997 Feb;79(2):196-202 [9052470.001]
  • [Cites] Hematol Oncol Clin North Am. 2001 Jun;15(3):525-45 [11525295.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213.001]
  • [Cites] Cancer. 2000 Jul 15;89(2):431-6 [10918176.001]
  • [Cites] J Clin Oncol. 1999 Oct;17(10):3160-6 [10506613.001]
  • [Cites] Drugs Aging. 1995 Jul;7(1):49-74 [7579781.001]
  • [Cites] Apoptosis. 2003 Jan;8(1):29-37 [12510149.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 17):14-8 [10604263.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] J Clin Oncol. 1999 Aug;17(8):2506-13 [10561316.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2532-9 [15226321.001]
  • [Cites] Semin Oncol. 2001 Aug;28(4 Suppl 15):8-15 [11685723.001]
  • [Cites] J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243.001]
  • [Cites] Semin Oncol. 1999 Oct;26(5 Suppl 17):28-33 [10604266.001]
  • [Cites] Cancer. 1993 Feb 1;71(3 Suppl):1098-109 [7679039.001]
  • [Cites] Cancer. 1993 Oct 15;72(8):2457-60 [8104680.001]
  • [Cites] Cancer Res. 1996 Mar 15;56(6):1253-5 [8640809.001]
  • [Cites] J Clin Oncol. 1999 Mar;17(3):958-67 [10071290.001]
  • [Cites] Pharmacol Ther. 1992 Dec;56(3):323-39 [1301594.001]
  • [Cites] Cancer Res. 1992 Aug 15;52(16):4433-40 [1353706.001]
  • [Cites] Cancer Res. 1993 Oct 1;53(19):4573-81 [8402630.001]
  • (PMID = 15685445.001).
  • [ISSN] 0724-4983
  • [Journal-full-title] World journal of urology
  • [ISO-abbreviation] World J Urol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Androgens; 0 / Antineoplastic Agents
  • [Number-of-references] 29
  •  go-up   go-down


82. Nakabayashi M, Xie W, Regan MM, Jackman DM, Kantoff PW, Oh WK: Response to low-dose ketoconazole and subsequent dose escalation to high-dose ketoconazole in patients with androgen-independent prostate cancer. Cancer; 2006 Sep 1;107(5):975-81
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] Response to low-dose ketoconazole and subsequent dose escalation to high-dose ketoconazole in patients with androgen-independent prostate cancer.
  • BACKGROUND: High-dose ketoconazole (HDK) in combination with steroids has been recognized as an effective secondary hormonal therapy in androgen-independent prostate cancer (AIPC).
  • In addition, patients were identified who received dose escalation to HDK (400 mg orally 3 times daily) after experiencing a rising prostate-specific antigen (PSA) level.
  • A longer duration of primary androgen deprivation therapy and total duration of all previous hormonal therapies was associated with a longer time to progression with LDK (P < .05).
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / administration & dosage. Biomarkers, Tumor / analysis. Disease Progression. Dose-Response Relationship, Drug. Fatigue / chemically induced. Humans. Male. Middle Aged. Neoplasms, Hormone-Dependent / drug therapy. Prostate-Specific Antigen / analysis. Retrospective Studies. Survival Analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16862573.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen; R9400W927I / Ketoconazole
  •  go-up   go-down


83. MacManus CF, Pettigrew J, Seaton A, Wilson C, Maxwell PJ, Berlingeri S, Purcell C, McGurk M, Johnston PG, Waugh DJ: Interleukin-8 signaling promotes translational regulation of cyclin D in androgen-independent prostate cancer cells. Mol Cancer Res; 2007 Jul;5(7):737-48
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] Interleukin-8 signaling promotes translational regulation of cyclin D in androgen-independent prostate cancer cells.
  • We have shown previously that interleukin-8 (IL-8) and IL-8 receptor expression is elevated in tumor cells of human prostate biopsy tissue and correlates with increased cyclin D1 expression.
  • Using PC3 and DU145 cell lines, we sought to determine whether IL-8 signaling regulated cyclin D1 expression in androgen-independent prostate cancer (AIPC) cells and to characterize the signaling pathways underpinning this response and that of IL-8-promoted proliferation.
  • This study provides a molecular basis to support the correlation of IL-8 expression with that of cyclin D1 in human prostate cancer and suggests a mechanism by which this chemokine promotes cell proliferation.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • 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
  • (PMID = 17606477.001).
  • [ISSN] 1541-7786
  • [Journal-full-title] Molecular cancer research : MCR
  • [ISO-abbreviation] Mol. Cancer Res.
  • [Language] eng
  • [Grant] United Kingdom / Wellcome Trust / / 067104/z/02/z
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Androgens; 0 / EIF4EBP1 protein, human; 0 / Interleukin-8; 0 / Phosphoproteins; 136601-57-5 / Cyclin D1; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; EC 2.7.11.13 / PKC-3 protein; EC 2.7.11.13 / Protein Kinase C; EC 3.1.4.4 / Phospholipase D
  •  go-up   go-down


84. Dai Y, Desano J, Tang W, Meng X, Meng Y, Burstein E, Lawrence TS, Xu L: Natural proteasome inhibitor celastrol suppresses androgen-independent prostate cancer progression by modulating apoptotic proteins and NF-kappaB. PLoS One; 2010 Dec 10;5(12):e14153
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Natural proteasome inhibitor celastrol suppresses androgen-independent prostate cancer progression by modulating apoptotic proteins and NF-kappaB.
  • BACKGROUND: Celastrol is a natural proteasome inhibitor that exhibits promising anti-tumor effects in human malignancies, especially the androgen-independent prostate cancer (AIPC) with constitutive NF-κB activation.
  • Celastrol induces apoptosis by means of proteasome inhibition and suppresses prostate tumor growth.
  • Celastrol as an active ingredient of traditional herbal medicine could thus be developed as a new therapeutic agent for hormone-refractory prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell Death Differ. 2006 Aug;13(8):1260-2 [16710358.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3850-5 [10725400.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9636-45 [17018621.001]
  • [Cites] J Natl Cancer Inst. 1999 Nov 17;91(22):1956-60 [10564680.001]
  • [Cites] Cell Death Differ. 2011 Jan;18(1):60-71 [20577262.001]
  • [Cites] Leukemia. 2000 Jul;14(7):1276-83 [10914553.001]
  • [Cites] J Cell Sci. 2002 Jan 1;115(Pt 1):141-51 [11801732.001]
  • [Cites] Biosci Biotechnol Biochem. 2003 Sep;67(9):1883-7 [14519971.001]
  • [Cites] Mol Cancer Ther. 2003 Sep;2(9):835-43 [14555702.001]
  • [Cites] J Cell Biochem. 2004 Jan 1;91(1):100-17 [14689584.001]
  • [Cites] Nat Rev Cancer. 2004 May;4(5):349-60 [15122206.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):392-401 [15122352.001]
  • [Cites] Prostate. 2004 Jul 1;60(2):98-108 [15162376.001]
  • [Cites] Leukemia. 2004 Aug;18(8):1357-63 [15190257.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5036-43 [15289299.001]
  • [Cites] Science. 1995 Aug 4;269(5224):682-5 [7624798.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):344-54 [15531918.001]
  • [Cites] Blood. 2005 Apr 15;105(8):3255-62 [15613543.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6282-93 [16024630.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6294-304 [16024631.001]
  • [Cites] Hepatology. 2005 Sep;42(3):588-97 [16037944.001]
  • [Cites] Blood. 2006 Jan 1;107(1):257-64 [16166592.001]
  • [Cites] Blood. 2006 Mar 15;107(6):2354-63 [16219794.001]
  • [Cites] J Biomed Sci. 2006 Mar;13(2):201-4 [16456709.001]
  • [Cites] Cancer Res. 2006 May 1;66(9):4758-65 [16651429.001]
  • [Cites] Biochem Pharmacol. 2006 Nov 15;72(10):1311-21 [16984800.001]
  • [Cites] Blood. 2007 Apr 1;109(7):2727-35 [17110449.001]
  • [Cites] Cancer Res. 2007 Jun 1;67(11):5418-24 [17545623.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19488-93 [18042711.001]
  • [Cites] Oncogene. 2008 Jan 31;27(6):721-31 [17653083.001]
  • [Cites] Expert Rev Anticancer Ther. 2008 Jul;8(7):1053-72 [18588451.001]
  • [Cites] Mol Cancer Ther. 2008 Jul;7(7):2192-202 [18645028.001]
  • [Cites] Clin Cancer Res. 2008 Dec 1;14(23):7701-10 [19047096.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2009 Jul 15;74(4):1217-25 [19545787.001]
  • [Cites] PLoS One. 2009;4(8):e6816 [19714243.001]
  • [Cites] Chin Med J (Engl). 2009 Jul 20;122(14):1666-73 [19719969.001]
  • [Cites] BMC Cancer. 2009;9:343 [19778460.001]
  • [Cites] BMC Cancer. 2009;9:392 [19895686.001]
  • [Cites] Mol Cancer Res. 2009 Dec;7(12):1946-53 [19934274.001]
  • [Cites] Cancer Res. 2010 Mar 1;70(5):1951-9 [20160026.001]
  • [Cites] Curr Drug Targets. 2010 Jun;11(6):699-707 [20298153.001]
  • [Cites] Bioorg Med Chem. 2010 Jun 1;18(11):3812-22 [20466555.001]
  • [Cites] Autophagy. 2010 Nov;6(8):1201-3 [20930561.001]
  • [Cites] Biochem Pharmacol. 2006 Oct 30;72(9):1132-41 [16965765.001]
  • (PMID = 21170316.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA121830; United States / NCI NIH HHS / CA / P30 CA046592; United States / NCI NIH HHS / CA / 5 P30 CA46592; United States / NCI NIH HHS / CA / R01 CA121830(S1); United States / NCI NIH HHS / CA / R01 CA134655; United States / NCI NIH HHS / CA / R21 CA128220
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Enzyme Inhibitors; 0 / Mcl1 protein, mouse; 0 / Myeloid Cell Leukemia Sequence 1 Protein; 0 / NF-kappa B; 0 / Protease Inhibitors; 0 / Proteasome Inhibitors; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Triterpenes; 34157-83-0 / tripterine
  • [Other-IDs] NLM/ PMC3000808
  •  go-up   go-down


85. Srinivas S, Krishnan AV, Colocci N, Feldman D: Phase II study evaluating oral triamcinolone in patients with androgen-independent prostate cancer. Urology; 2006 May;67(5):1001-6
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] Phase II study evaluating oral triamcinolone in patients with androgen-independent prostate cancer.
  • OBJECTIVES: To assess the effect of triamcinolone administration on the serum prostate-specific antigen (PSA) response and the time to progression in patients with androgen-independent prostate cancer (AIPC).
  • [MeSH-minor] Aged. Aged, 80 and over. Androgen Antagonists / administration & dosage. Disease Progression. Humans. Hydrocortisone / blood. Male. Middle Aged. Point Mutation. Prospective Studies. Prostate-Specific Antigen / blood. Receptors, Androgen / genetics. Receptors, Androgen / metabolism


86. Yee SW, Campbell MJ, Simons C: Inhibition of Vitamin D3 metabolism enhances VDR signalling in androgen-independent prostate cancer cells. J Steroid Biochem Mol Biol; 2006 Mar;98(4-5):228-35
Hazardous Substances Data Bank. KETOCONAZOLE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibition of Vitamin D3 metabolism enhances VDR signalling in androgen-independent prostate cancer cells.
  • Induction of growth arrest and differentiation by 1alpha,25-dihydroxyvitamin D(3) (1,25-(OH)(2)D(3)) occurs in non-malignant cell types but is often reduced in cancer cells.
  • For example, androgen-independent prostate cancer cells, DU-145 and PC-3, are relatively insensitive to the anti-proliferative action of 1,25-(OH)(2)D(3).

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • MedlinePlus Health Information. consumer health - Vitamin D.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16483768.001).
  • [ISSN] 0960-0760
  • [Journal-full-title] The Journal of steroid biochemistry and molecular biology
  • [ISO-abbreviation] J. Steroid Biochem. Mol. Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / GADD45A protein, human; 0 / Nuclear Proteins; 0 / Receptors, Calcitriol; 0 / dihydroxy-vitamin D3; 1406-16-2 / Vitamin D; EC 1.14.- / Steroid Hydroxylases; EC 1.14.13.126 / Vitamin D3 24-Hydroxylase; R9400W927I / Ketoconazole
  •  go-up   go-down


87. Diallo JS, Betton B, Parent N, Péant B, Lessard L, Le Page C, Bertrand R, Mes-Masson AM, Saad F: Enhanced killing of androgen-independent prostate cancer cells using inositol hexakisphosphate in combination with proteasome inhibitors. Br J Cancer; 2008 Nov 18;99(10):1613-22
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] Enhanced killing of androgen-independent prostate cancer cells using inositol hexakisphosphate in combination with proteasome inhibitors.
  • Effective treatments for androgen-independent prostate cancer (AIPCa) are lacking.
  • Inositol hexakisphosphate (IP6) is an orally non-toxic phytochemical that exhibits antitumour activity against several types of cancer including PCa.

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Annu Rev Immunol. 2000;18:621-63 [10837071.001]
  • [Cites] Clin Prostate Cancer. 2004 Dec;3(3):141-3 [15636679.001]
  • [Cites] Cell. 2005 Jul 1;121(7):1085-95 [15989957.001]
  • [Cites] Oncogene. 2005 Jul 21;24(31):4993-9 [15824729.001]
  • [Cites] Curr Opin Cell Biol. 2005 Dec;17(6):617-25 [16243507.001]
  • [Cites] Nat Cell Biol. 2006 Jul;8(7):711-6 [16783363.001]
  • [Cites] Nat Cell Biol. 2006 Jul;8(7):668-76 [16783364.001]
  • [Cites] Prostate. 2006 Sep 1;66(12):1245-56 [16705740.001]
  • [Cites] Mol Cell Biol. 2006 Oct;26(20):7345-57 [16894031.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9636-45 [17018621.001]
  • [Cites] Nat Cell Biol. 2006 Dec;8(12):1348-58 [17115033.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Physiol Rev. 2007 Jan;87(1):99-163 [17237344.001]
  • [Cites] Oncogene. 2007 Mar 15;26(12):1681-92 [16983338.001]
  • [Cites] Mol Cell. 2007 Jun 8;26(5):625-37 [17560369.001]
  • [Cites] Recent Results Cancer Res. 2007;176:165-76 [17607924.001]
  • [Cites] Carcinogenesis. 2000 Dec;21(12):2225-35 [11133812.001]
  • [Cites] J Immunol. 2001 Mar 1;166(5):3130-42 [11207265.001]
  • [Cites] Nat Rev Cancer. 2002 Apr;2(4):301-10 [12001991.001]
  • [Cites] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886.001]
  • [Cites] Science. 2002 Nov 8;298(5596):1241-5 [12424381.001]
  • [Cites] Carcinogenesis. 2002 Dec;23(12):2031-41 [12507926.001]
  • [Cites] Complement Ther Med. 2002 Dec;10(4):229-34 [12594974.001]
  • [Cites] Carcinogenesis. 2003 Mar;24(3):555-63 [12663518.001]
  • [Cites] Mol Biol Cell. 2003 Sep;14(9):3848-56 [12972568.001]
  • [Cites] J Nutr. 2003 Nov;133(11 Suppl 1):3778S-3784S [14608114.001]
  • [Cites] Anticancer Res. 2003 Sep-Oct;23(5A):3855-61 [14666688.001]
  • [Cites] Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):244-50 [14734476.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 May;5(5):392-401 [15122352.001]
  • [Cites] J Clin Oncol. 2004 Jun 1;22(11):2108-21 [15169797.001]
  • [Cites] Cancer Res. 2004 Aug 1;64(15):5036-43 [15289299.001]
  • [Cites] Clin Cancer Res. 2004 Sep 15;10(18 Pt 2):6382S-7S [15448035.001]
  • [Cites] J Gen Virol. 1980 Dec;51(Pt 2):255-61 [6262437.001]
  • [Cites] Biochem Pharmacol. 1987 Jun 1;36(11):1769-73 [3579972.001]
  • [Cites] Science. 1993 Mar 26;259(5103):1912-5 [8096091.001]
  • [Cites] Trends Biochem Sci. 1993 Oct;18(10):366-71 [8256283.001]
  • [Cites] Cell. 1994 Sep 9;78(5):773-85 [8087845.001]
  • [Cites] Science. 1995 Mar 10;267(5203):1485-8 [7878466.001]
  • [Cites] Cell Immunol. 1997 Feb 1;175(2):199-202 [9023426.001]
  • [Cites] FEBS Lett. 1997 Jul 7;411(1):77-82 [9247146.001]
  • [Cites] Trends Cell Biol. 1998 Oct;8(10):397-403 [9789328.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):10976-83 [10500111.001]
  • [Cites] Neoplasia. 2004 Sep-Oct;6(5):646-59 [15548374.001]
  • [Cites] J Biol Chem. 2004 Dec 31;279(53):55633-43 [15489227.001]
  • [Cites] Mol Cancer Ther. 2005 Mar;4(3):443-9 [15767553.001]
  • (PMID = 18941459.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Anticarcinogenic Agents; 0 / Protease Inhibitors; 7IGF0S7R8I / Phytic Acid
  • [Other-IDs] NLM/ PMC2584963
  •  go-up   go-down


88. Scholz M, Jennrich R, Strum S, Brosman S, Johnson H, Lam R: Long-term outcome for men with androgen independent prostate cancer treated with ketoconazole and hydrocortisone. J Urol; 2005 Jun;173(6):1947-52
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] Long-term outcome for men with androgen independent prostate cancer treated with ketoconazole and hydrocortisone.
  • PURPOSE: The combination of high dose ketoconazole and hydrocortisone (HDK) is active against androgen independent prostate cancer (AIPC).
  • RESULTS: The median baseline prostate specific antigen (PSA) before the initiation of HDK was 25.1.
  • Long responses are more likely to occur in men initiating HDK earlier in the course of disease before the cancer burden becomes excessive.
  • [MeSH-minor] Aged. Biomarkers, Tumor / blood. Bone Neoplasms / drug therapy. Bone Neoplasms / mortality. Bone Neoplasms / physiopathology. Bone Neoplasms / secondary. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Follow-Up Studies. Humans. Long-Term Care. Male. Middle Aged. Prostate-Specific Antigen / blood. Retrospective Studies. Survival Analysis

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. HYDROCORTISONE .
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • 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 = 15879788.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Biomarkers, Tumor; EC 3.4.21.77 / Prostate-Specific Antigen; R9400W927I / Ketoconazole; WI4X0X7BPJ / Hydrocortisone
  •  go-up   go-down


89. Pu YS, Hsieh MW, Wang CW, Liu GY, Huang CY, Lin CC, Guan JY, Lin SR, Hour TC: Epidermal growth factor receptor inhibitor (PD168393) potentiates cytotoxic effects of paclitaxel against androgen-independent prostate cancer cells. Biochem Pharmacol; 2006 Mar 14;71(6):751-60
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] Epidermal growth factor receptor inhibitor (PD168393) potentiates cytotoxic effects of paclitaxel against androgen-independent prostate cancer cells.
  • Recent data showed that epidermal growth factor receptor (EGFR) inhibitors, such as ZD1839, alone or in combination with chemotherapeutic agents for androgen-independent prostate cancer (AIPC) did not produce promising results in clinical settings.
  • In results, both the androgen-independent cell lines PC-3 and DU145 expressed higher levels of EGFR than the androgen-dependent MDA PCa 2b and androgen-responsive LNCaP cells by Western blotting.


90. Joshua AM, Nordman I, Venkataswaran R, Clarke S, Stockler MR, Boyer MJ: Weekly docetaxel as second line treatment after mitozantrone for androgen-independent prostate cancer. Intern Med J; 2005 Aug;35(8):468-72
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] Weekly docetaxel as second line treatment after mitozantrone for androgen-independent prostate cancer.
  • BACKGROUND: Two recent phase III trials have shown an improvement in survival with the use of docetaxel in metastatic androgen-independent prostate cancer (AIPC) compared to mitozantrone.
  • End-points included prostate specific antigen response, common toxicity criteria, time to progression and overall survival.
  • CONCLUSIONS: Weekly docetaxel is a safe and active second-line treatment after mitozantrone for androgen-resistant prostate cancer, with similar levels of activity to the first-line setting.
  • [MeSH-minor] Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Infusions, Intravenous. Male. Maximum Tolerated Dose. Middle Aged. Mitoxantrone / adverse effects. Mitoxantrone / therapeutic use. Neoplasm Staging. Neoplasms, Hormone-Dependent. Prognosis. Prospective Studies. Prostate-Specific Antigen / blood. Risk Assessment. Survival Rate. Taxoids / adverse effects. Taxoids / therapeutic use. Treatment Outcome

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. NOVANTRONE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16176469.001).
  • [ISSN] 1444-0903
  • [Journal-full-title] Internal medicine journal
  • [ISO-abbreviation] Intern Med J
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Taxoids; 15H5577CQD / docetaxel; BZ114NVM5P / Mitoxantrone; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


91. Dreicer R, Petrylak D, Agus D, Webb I, Roth B: Phase I/II study of bortezomib plus docetaxel in patients with advanced androgen-independent prostate cancer. Clin Cancer Res; 2007 Feb 15;13(4):1208-15
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] Phase I/II study of bortezomib plus docetaxel in patients with advanced androgen-independent prostate cancer.
  • PURPOSE: To determine the dose-limiting toxicities and maximum tolerated dose, and evaluate the antitumor activity of bortezomib/docetaxel combination therapy in androgen-independent prostate cancer.
  • Antitumor activity was evaluated using prostate-specific antigen (PSA) levels and Response Evaluation Criteria in Solid Tumors guidelines.
  • Further investigations are warranted to determine activity and optimize bortezomib/docetaxel therapy in androgen-independent prostate cancers.
  • [MeSH-minor] Aged. Aged, 80 and over. Androgens / metabolism. Boronic Acids / administration & dosage. Boronic Acids / adverse effects. Bortezomib. Dose-Response Relationship, Drug. Humans. Interleukin-6 / blood. Male. Middle Aged. Neoplasms, Hormone-Dependent / blood. Neoplasms, Hormone-Dependent / drug therapy. Prostate-Specific Antigen / blood. Pyrazines / administration & dosage. Pyrazines / adverse effects. Taxoids / administration & dosage. Taxoids / adverse effects

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. BORTEZOMIB .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17317831.001).
  • [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] Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Boronic Acids; 0 / Interleukin-6; 0 / Pyrazines; 0 / Taxoids; 15H5577CQD / docetaxel; 69G8BD63PP / Bortezomib; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


92. Svatek R, Karakiewicz PI, Shulman M, Karam J, Perrotte P, Benaim E: Pre-treatment nomogram for disease-specific survival of patients with chemotherapy-naive androgen independent prostate cancer. Eur Urol; 2006 Apr;49(4):666-74
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] Pre-treatment nomogram for disease-specific survival of patients with chemotherapy-naive androgen independent prostate cancer.
  • OBJECTIVE: Our objective was to develop a nomogram that predicts the probability of cancer-specific survival in men with untreated androgen-independent prostate cancer (AIPC).
  • Univariate and multivariate Cox regression models were used to test the association between prostate-specific antigen (PSA) level at initiation of androgen deprivation, PSA doubling time (PSADT), PSA nadir on androgen deprivation therapy (ADT), time from ADT to AIPC, and AIPC-specific mortality.
  • In multivariate models, PSADT and time from androgen deprivation to AIPC remained statistically significant (p < or = 0.004).
  • [MeSH-major] Androgen Antagonists / therapeutic use. Nomograms. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / mortality
  • [MeSH-minor] Aged. Area Under Curve. Humans. Male. Middle Aged. Neoplasm Staging. Predictive Value of Tests. Probability. Proportional Hazards Models. Prostate-Specific Antigen / blood. ROC Curve. Retrospective Studies. Survival Analysis

  • 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 = 16423446.001).
  • [ISSN] 0302-2838
  • [Journal-full-title] European urology
  • [ISO-abbreviation] Eur. Urol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Androgen Antagonists; EC 3.4.21.77 / Prostate-Specific Antigen
  •  go-up   go-down


93. Thall PF, Logothetis C, Pagliaro LC, Wen S, Brown MA, Williams D, Millikan RE: Adaptive therapy for androgen-independent prostate cancer: a randomized selection trial of four regimens. J Natl Cancer Inst; 2007 Nov 7;99(21):1613-22
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] Adaptive therapy for androgen-independent prostate cancer: a randomized selection trial of four regimens.
  • With the goal of efficiently selecting promising regimens for more advanced trials, we conducted a randomized selection trial of four regimens to identify promising treatments for androgen-independent prostate cancer.
  • Response was assessed by considering tumor-specific symptoms, tumor regression, and prostate-specific antigen (PSA) changes.
  • [MeSH-minor] Aged. Algorithms. Androgens / metabolism. Carboplatin / administration & dosage. Confidence Intervals. Cyclophosphamide / administration & dosage. Dexamethasone / administration & dosage. Disease-Free Survival. Doxorubicin / administration & dosage. Drug Administration Schedule. Estramustine. Etoposide / administration & dosage. Humans. Ketoconazole / administration & dosage. Logistic Models. Male. Middle Aged. Paclitaxel / administration & dosage. Prospective Studies. Prostate-Specific Antigen / blood. Research Design. Survival Analysis. Treatment Outcome. Vinblastine / administration & dosage. Vincristine / administration & dosage

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOXORUBICIN .
  • Hazardous Substances Data Bank. TAXOL .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • Hazardous Substances Data Bank. CARBOPLATIN .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • Hazardous Substances Data Bank. CYCLOPHOSPHAMIDE .
  • Hazardous Substances Data Bank. VINCRISTINE .
  • Hazardous Substances Data Bank. KETOCONAZOLE .
  • Hazardous Substances Data Bank. VINBLASTINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] J Natl Cancer Inst. 2008 May 7;100(9):681-2; author reply 682-3 [18445824.001]
  • [CommentIn] J Natl Cancer Inst. 2007 Nov 7;99(21):1577-82 [17971533.001]
  • (PMID = 17971530.001).
  • [ISSN] 1460-2105
  • [Journal-full-title] Journal of the National Cancer Institute
  • [ISO-abbreviation] J. Natl. Cancer Inst.
  • [Language] eng
  • [Publication-type] Journal Article; Randomized Controlled Trial
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 35LT29625A / Estramustine; 5J49Q6B70F / Vincristine; 5V9KLZ54CY / Vinblastine; 6PLQ3CP4P3 / Etoposide; 7S5I7G3JQL / Dexamethasone; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; BG3F62OND5 / Carboplatin; EC 3.4.21.77 / Prostate-Specific Antigen; P88XT4IS4D / Paclitaxel; R9400W927I / Ketoconazole
  •  go-up   go-down


94. Patel PH, Kockler DR: Sipuleucel-T: a vaccine for metastatic, asymptomatic, androgen-independent prostate cancer. Ann Pharmacother; 2008 Jan;42(1):91-8
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] Sipuleucel-T: a vaccine for metastatic, asymptomatic, androgen-independent prostate cancer.
  • OBJECTIVE: To review the design, efficacy, safety, dosing, therapeutic, and pharmacoeconomic considerations of sipuleucel-T, an investigational, autologous, dendritic, cell-based prostate cancer vaccine.
  • DATA SOURCES: English-language literature searches of MEDLINE (1966-September 2007) and the Cochrane Database (2007, Issue 3) were performed using the terms sipuleucel-T, APC8015, and prostate cancer vaccine.
  • STUDY SELECTION AND DATA EXTRACTION: All published articles or abstracts on human studies of sipuleucel-T for androgen-independent prostate cancer (AIPC) were reviewed for inclusion.
  • [MeSH-major] Cancer Vaccines / pharmacology. Prostatic Neoplasms / drug therapy. Tissue Extracts / pharmacology

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic 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 = 18094343.001).
  • [ISSN] 1542-6270
  • [Journal-full-title] The Annals of pharmacotherapy
  • [ISO-abbreviation] Ann Pharmacother
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cancer Vaccines; 0 / Tissue Extracts; 0 / sipuleucel-T
  • [Number-of-references] 31
  •  go-up   go-down


95. Trump DL, Potter DM, Muindi J, Brufsky A, Johnson CS: Phase II trial of high-dose, intermittent calcitriol (1,25 dihydroxyvitamin D3) and dexamethasone in androgen-independent prostate cancer. Cancer; 2006 May 15;106(10):2136-42
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] Phase II trial of high-dose, intermittent calcitriol (1,25 dihydroxyvitamin D3) and dexamethasone in androgen-independent prostate cancer.
  • BACKGROUND: Data suggest that vitamin D plays a role in the treatment and prevention of prostate cancer.
  • RESULTS: Forty-three men with androgen-independent prostate cancer were entered; 37 received at least 1 month of calcitriol given at a dose of 12 microg every day x 3 per week.
  • The majority of patients had bone metastases and rising prostate-specific antigen (PSA) levels.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 1,25-DIHYDROXYCHOLECALCIFEROL .
  • Hazardous Substances Data Bank. DEXAMETHASONE .
  • 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
  • [Copyright] Copyright 2006 American Cancer Society
  • (PMID = 16598750.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA67267; United States / NCI NIH HHS / CA / CA85142; United States / NCI NIH HHS / CA / CA95045
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 7S5I7G3JQL / Dexamethasone; FXC9231JVH / Calcitriol
  •  go-up   go-down


96. Zhang H, Lü JJ, Gao QZ, Zhang J: [Induction of apoptosis by mifepristone in androgen-independent prostate cancer cell lines in vitro]. Zhonghua Wai Ke Za Zhi; 2006 Mar 15;44(6):382-5
Hazardous Substances Data Bank. MIFEPRISTONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Induction of apoptosis by mifepristone in androgen-independent prostate cancer cell lines in vitro].
  • OBJECTIVE: To investigate the effects of mifepristone on cell proliferation of human androgen-independent prostate carcinoma cell lines DU-145, PC-3 in vitro and the possible mechanisms involved.
  • METHODS: The A values of the prostate cancer cells DU-145 and PC-3 in each group with various concentrations (1, 10, 50, 100 micromol/L) of mifepristone at various time intervals (24-120 h) were detected with the colorimetric 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl tetrazolium bromide assay.
  • RESULTS: The A values of the cancer cells treated with 1 micromol/L of mifepristone were similar to that of controls, while those of the cells treated with 10 micromol/L, 50 micromol/L and 100 micromol/L of mifepristone were significantly different from that of controls (P < 0.01).
  • Mifepristone markedly inhibited cell proliferation of prostate cancer cells DU-145 and PC-3 on a dose- and time-depending manner.
  • CONCLUSIONS: Mifepristone can induce apoptosis of androgen-independent prostate cancer cell lines DU-145 and PC-3 in vitro.

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16638347.001).
  • [ISSN] 0529-5815
  • [Journal-full-title] Zhonghua wai ke za zhi [Chinese journal of surgery]
  • [ISO-abbreviation] Zhonghua Wai Ke Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Androgens; 0 / Hormone Antagonists; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Vascular Endothelial Growth Factor A; 0 / bcl-2-Associated X Protein; 320T6RNW1F / Mifepristone
  •  go-up   go-down


97. Attia S, Eickhoff J, Wilding G, McNeel D, Blank J, Ahuja H, Jumonville A, Eastman M, Shevrin D, Glode M, Alberti D, Staab MJ, Horvath D, Straus J, Marnocha R, Liu G: Randomized, double-blinded phase II evaluation of docetaxel with or without doxercalciferol in patients with metastatic, androgen-independent prostate cancer. Clin Cancer Res; 2008 Apr 15;14(8):2437-43
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] Randomized, double-blinded phase II evaluation of docetaxel with or without doxercalciferol in patients with metastatic, androgen-independent prostate cancer.
  • PURPOSE: Docetaxel is standard of care for androgen-independent prostate cancer (AIPC).
  • The primary end point was prostate-specific antigen (PSA) response.

  • Genetic Alliance. consumer health - Prostate cancer.
  • Genetic Alliance. consumer health - Metastatic cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18413835.001).
  • [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
  • [Grant] United States / NCI NIH HHS / CA / T32 CA009614
  • [Publication-type] Clinical Trial, Phase II; Journal Article; Randomized Controlled Trial; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Ergocalciferols; 0 / Taxoids; 15H5577CQD / docetaxel; 3DIZ9LF5Y9 / 1 alpha-hydroxyergocalciferol; SY7Q814VUP / Calcium
  •  go-up   go-down


98. Rumohr JA, Chang SS: Current chemotherapeutic approaches for androgen-independent prostate cancer. Curr Opin Investig Drugs; 2006 Jun;7(6):529-33
Hazardous Substances Data Bank. NOVANTRONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Current chemotherapeutic approaches for androgen-independent prostate cancer.
  • This review describes the current state of chemotherapy for androgen-independent prostate cancer.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cancer Vaccines / therapeutic use. Prostatic Neoplasms / drug therapy. Taxoids / therapeutic use. Tubulin Modulators / therapeutic use

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. DOCETAXEL .
  • Hazardous Substances Data Bank. PREDNISONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16784023.001).
  • [ISSN] 1472-4472
  • [Journal-full-title] Current opinion in investigational drugs (London, England : 2000)
  • [ISO-abbreviation] Curr Opin Investig Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Cancer Vaccines; 0 / Endothelin-1; 0 / Pyrrolidines; 0 / Taxoids; 0 / Tubulin Modulators; 0 / Vascular Endothelial Growth Factor A; 15H5577CQD / docetaxel; 2S9ZZM9Q9V / Bevacizumab; 35LT29625A / Estramustine; BZ114NVM5P / Mitoxantrone; V6D7VK2215 / atrasentan; VB0R961HZT / Prednisone
  • [Number-of-references] 25
  •  go-up   go-down


99. Trendel JA, Ellis N, Sarver JG, Klis WA, Dhananjeyan M, Bykowski CA, Reese MD, Erhardt PW: Catalytically active peptidylglycine alpha-amidating monooxygenase in the media of androgen-independent prostate cancer cell lines. J Biomol Screen; 2008 Sep;13(8):804-9
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] Catalytically active peptidylglycine alpha-amidating monooxygenase in the media of androgen-independent prostate cancer cell lines.
  • PAM is thought to play a role in the development of antiandrogen drug resistance in prostate cancer (CaP) through PAMactivated autocrine growth.
  • On the basis of the previous finding that many lung cancer cell lines excrete PAM into their culture media, this study investigates PAM levels in media collected from human CaP cell line cultures.
  • Androgen-independent DU145 and PC-3 prostate cancer cell lines exhibited readily detectable levels of PAM activity in extracts and media, whereas the androgen-dependent LNCaP cell line showed little or no activity.
  • A simple, scalable method to obtain PAM from the culture media of androgen-independent human prostate cancer cell lines is described in this article.
  • This approach provides a much easier means of collecting CaP-derived PAM than previously described cell fractionation procedures and should facilitate the investigations of the role and targeting of PAM in hormone-independent CaP.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. DOPAMINE .
  • Hazardous Substances Data Bank. DISULFIRAM .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18832192.001).
  • [ISSN] 1087-0571
  • [Journal-full-title] Journal of biomolecular screening
  • [ISO-abbreviation] J Biomol Screen
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Culture Media; 0 / Enzyme Inhibitors; 0 / Multienzyme Complexes; EC 1.- / Mixed Function Oxygenases; EC 1.14.17.3 / peptidylglycine monooxygenase; TR3MLJ1UAI / Disulfiram; VTD58H1Z2X / Dopamine
  •  go-up   go-down


100. Tesan T, Gustavsson H, Welén K, Damber JE: Differential expression of angiopoietin-2 and vascular endothelial growth factor in androgen-independent prostate cancer models. BJU Int; 2008 Sep;102(8):1034-9
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] Differential expression of angiopoietin-2 and vascular endothelial growth factor in androgen-independent prostate cancer models.
  • OBJECTIVE: To investigate the relationship between microvessel density (MVD), blood vessel morphology and the expression of angiopoietin (Ang)-1, Ang-2, tyrosine kinase with immunoglobulin and epidermal growth factor homology domains (Tie)-2, and vascular endothelial growth factor (VEGF) in androgen-dependent (AD) and androgen-independent (AI) prostate cancer models, to gain insight into the regulation of angiogenesis at different stages of prostate cancer.
  • The mRNA and protein secretion of the Angs, Tie-2 and VEGF were measured by real-time polymerase chain reaction and enzyme-linked immunosorbent assays, respectively, in LNCaP (AD) and LNCaP-19, C4-2, C4-2B4 and PC-3 (AI) prostate cancer xenografts in mice.
  • CONCLUSION: The differences in MVD, blood vessel morphology and the expression of Ang-2 and VEGF show that prostate cancer cells display angiogenic heterogeneity, which indicates different roles of these factors in the regulation of angiogenesis in different stages of prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18489523.001).
  • [ISSN] 1464-410X
  • [Journal-full-title] BJU international
  • [ISO-abbreviation] BJU Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Angiopoietin-1; 0 / Angiopoietin-2; 0 / Biomarkers, Tumor; 0 / Vascular Endothelial Growth Factor A
  •  go-up   go-down






Advertisement