[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 17 of about 17
1. Yoshioka N, Wang L, Kishimoto K, Tsuji T, Hu GF: A therapeutic target for prostate cancer based on angiogenin-stimulated angiogenesis and cancer cell proliferation. Proc Natl Acad Sci U S A; 2006 Sep 26;103(39):14519-24
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A therapeutic target for prostate cancer based on angiogenin-stimulated angiogenesis and cancer cell proliferation.
  • Human angiogenin is progressively up-regulated in the prostate epithelial cells during the development of prostate cancer from prostate intraepithelial neoplasia (PIN) to invasive adenocarcinoma.
  • Mouse angiogenin is the most up-regulated gene in AKT-induced PIN in prostate-restricted AKT transgenic mice.
  • These results suggest that angiogenin has a dual effect, angiogenesis and cancer cell proliferation, in prostate cancer and may serve as a molecular target for drug development.
  • Blocking nuclear translocation of angiogenin could have a combined benefit of antiangiogenesis and chemotherapy in treating prostate cancer.

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. NEOMYCIN .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Cell Biochem. 2000 Jan;76(3):452-62 [10649442.001]
  • [Cites] Clin Cancer Res. 1997 Sep;3(9):1579-86 [9815846.001]
  • [Cites] Cancer Res. 1999 Apr 1;59(7):1578-83 [10197632.001]
  • [Cites] Anticancer Res. 1999 Mar-Apr;19(2C):1537-40 [10365140.001]
  • [Cites] Cancer. 1999 Jul 15;86(2):316-24 [10421268.001]
  • [Cites] Br J Haematol. 1999 Aug;106(2):504-9 [10460612.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):445-56 [15558023.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1352-60 [15735021.001]
  • [Cites] J Pathol. 2005 Apr;205(5):585-91 [15776477.001]
  • [Cites] Clin Cancer Res. 2005 Dec 1;11(23):8358-63 [16322296.001]
  • [Cites] Clin Cancer Res. 2005 Dec 15;11(24 Pt 1):8745-52 [16361562.001]
  • [Cites] J Cancer Res Clin Oncol. 2000 Aug;126(8):468-74 [10961390.001]
  • [Cites] Bull Exp Biol Med. 2000 Jul;130(7):691-3 [11140588.001]
  • [Cites] J Urol. 2001 Jun;165(6 Pt 2):2274-9 [11371962.001]
  • [Cites] Br J Haematol. 2001 Aug;114(2):290-5 [11529846.001]
  • [Cites] Clin Cancer Res. 2001 Nov;7(11):3598-605 [11705882.001]
  • [Cites] J Hematother Stem Cell Res. 2002 Feb;11(1):119-25 [11847008.001]
  • [Cites] Int J Cancer. 2002 Apr 20;98(6):923-9 [11948474.001]
  • [Cites] Anticancer Res. 2002 Mar-Apr;22(2B):1045-52 [12168899.001]
  • [Cites] Biochemistry. 2003 Jan 14;42(1):121-8 [12515546.001]
  • [Cites] Nat Immunol. 2003 Mar;4(3):269-73 [12548285.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7841-6 [12799464.001]
  • [Cites] Clin Cancer Res. 2003 Oct 15;9(13):4852-9 [14581357.001]
  • [Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]
  • [Cites] Biochemistry. 1985 Sep 24;24(20):5480-6 [4074709.001]
  • [Cites] Biochemistry. 1985 Sep 24;24(20):5494-9 [2866795.001]
  • [Cites] Science. 1987 Jul 17;237(4812):280-2 [2440105.001]
  • [Cites] J Pathol. 1994 Feb;172(2):171-5 [7513352.001]
  • [Cites] Biochemistry. 1994 May 10;33(18):5421-7 [7514035.001]
  • [Cites] Cancer Res. 1996 Jun 15;56(12):2703-6 [8665497.001]
  • [Cites] J Cancer Res Clin Oncol. 1997;123(3):167-72 [9119882.001]
  • [Cites] Cancer Invest. 1998;16(3):152-9 [9541628.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9791-5 [9707554.001]
  • [Cites] Clin Cancer Res. 1998 Sep;4(9):2161-8 [9748135.001]
  • [Cites] Anticancer Res. 2000 May-Jun;20(3A):1679-84 [10928091.001]
  • (PMID = 16971483.001).
  • [ISSN] 0027-8424
  • [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 / NCI NIH HHS / CA / R01 CA105241; United States / NCI NIH HHS / CA / CA 105241
  • [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 / RNA, Ribosomal; 1404-04-2 / Neomycin; EC 3.1.27.- / angiogenin; EC 3.1.27.5 / Ribonuclease, Pancreatic
  • [Other-IDs] NLM/ PMC1599992
  •  go-up   go-down


2. Luchman HA, Benediktsson H, Villemaire ML, Peterson AC, Jirik FR: The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision. PLoS One; 2008;3(12):e3940
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision.
  • In keeping with its role as a pivotal upstream regulator of the phosphatidylinositol 3-kinase signaling pathway, experimentally-induced deletion of Pten in the murine prostate invariably results in neoplasia.
  • Given that the prostate undergoes rapid androgen-dependent growth at puberty, and that Pten excisions during this time might be especially tumorigenic, we hypothesized that delaying prostate-specific Pten deletions until immediately after puberty might alter the pace of tumorigenesis.
  • Despite evidence of increased Akt/mTOR/S6K axis activity at early time points in Pten-deficient epithelial cells, excisions induced in the post-pubertal (6 wk-old) prostate yielded gradual acquisition of a range of lesions.
  • These progressed from pre-malignant changes (nuclear atypia, focal hyperplasia) and low grade prostatic intraepithelial neoplasia (PIN) at 16-20 wks post-tamoxifen exposure, to overtly malignant lesions by approximately 1 yr of age, characterized by high-grade PIN and microinvasive carcinoma.
  • In contrast, when Pten excisions were triggered in the pre-pubertal (2 week-old) prostate, neoplasia evolved over a more abbreviated time-frame, with a spectrum of premalignant lesions, as well as overt PIN and microinvasive carcinoma by 10-12 wks post-tamoxifen exposure.
  • These results indicate that the developmental stage at which Pten deletions are induced dictates the pace of PIN development.
  • [MeSH-major] Gene Deletion. Genes, Tumor Suppressor. PTEN Phosphohydrolase / genetics. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgen-Binding Protein / genetics. Animals. Apoptosis. Arrestins / metabolism. Cell Proliferation. Crosses, Genetic. Disease Progression. Epithelium / enzymology. Epithelium / pathology. Female. Humans. Integrases / metabolism. Male. Mice. Neoplasm Invasiveness. Phosphatidylinositol 3-Kinases / metabolism. Precancerous Conditions / drug therapy. Precancerous Conditions / enzymology. Precancerous Conditions / genetics. Precancerous Conditions / pathology. Rats. Ribosomal Protein S6 / metabolism. Tamoxifen / analogs & derivatives. Tamoxifen / therapeutic use. Time Factors. Up-Regulation


3. Rubin MA, Mucci NR, Figurski J, Fecko A, Pienta KJ, Day ML: E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology. Hum Pathol; 2001 Jul;32(7):690-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] E-cadherin expression in prostate cancer: a broad survey using high-density tissue microarray technology.
  • To address these variations, we undertook a study to systematically evaluate E-cadherin expression in a broad range of prostate tissue.
  • Benign prostate, clinically localized prostate cancer, and hormone-refractory metastatic prostate cancer were analyzed under uniform conditions using high-density tissue microarrays (TMA).
  • Benign and atrophic prostate tissue and high-grade prostatic intraepithelial neoplasia (PIN) were also included from the clinically localized cases.
  • High (normal) E-cadherin expression was seen in 87% of 757 benign, 80% of 41 high-grade PIN, 82% of 325 prostate carcinoma and 90% of 97 hormone-refractory prostate carcinoma TMA samples.
  • [MeSH-major] Adenocarcinoma / metabolism. Cadherins / metabolism. Prostatic Neoplasms / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents, Hormonal / therapeutic use. Drug Resistance, Neoplasm. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology


Advertisement
4. Barve A, Khor TO, Hao X, Keum YS, Yang CS, Reddy B, Kong AN: Murine prostate cancer inhibition by dietary phytochemicals--curcumin and phenyethylisothiocyanate. Pharm Res; 2008 Sep;25(9):2181-9
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • PURPOSE: Prior studies from our laboratory have demonstrated the efficacy of a combined treatment of low doses of dietary agents curcumin and phenylethylisothiocyanate in effectively suppressing prostate cancer in vitro in human prostate cancer PC3 cells as well as in vivo in immunodeficient mice implanted with PC3 cells.
  • Immunohistochemistry revealed a significant inhibition of high-grade PIN (P = 0.0006, 0.000069, 0.00029 for a treatment period of 10 weeks and P = 0.02582, 0.022179, 0.0317 for a treatment period of 16 weeks) along with decreased proliferation and increased apoptotic index in the curcumin, PEITC or curcumin and PEITC treated animals, respectively.

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CURCUMIN .
  • 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] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10350-5 [11504910.001]
  • [Cites] Prostate Cancer Prostatic Dis. 2006;9(2):147-52 [16389264.001]
  • [Cites] Cancer Res. 2002 Jul 1;62(13):3615-9 [12097262.001]
  • [Cites] Am J Pathol. 2002 Aug;161(2):727-35 [12163397.001]
  • [Cites] J Biol Chem. 2002 Oct 18;277(42):39334-42 [12171915.001]
  • [Cites] Mol Cancer Ther. 2004 Jul;3(7):803-12 [15252141.001]
  • [Cites] Biochem Pharmacol. 1976 Aug 1;25(15):1811-2 [942483.001]
  • [Cites] Carcinogenesis. 1992 Nov;13(11):2183-6 [1423891.001]
  • [Cites] Mol Endocrinol. 1994 Feb;8(2):230-9 [8170479.001]
  • [Cites] Cancer Res. 1994 Nov 15;54(22):5841-7 [7954412.001]
  • [Cites] Cancer Res. 1996 Sep 15;56(18):4096-102 [8797572.001]
  • [Cites] Cancer Res. 1998 Sep 15;58(18):4102-6 [9751619.001]
  • [Cites] Eur Urol. 1999;35(5-6):377-87 [10325492.001]
  • [Cites] Ann Pharm Fr. 2005 Jan;63(1):69-75 [15803103.001]
  • [Cites] Clin Cancer Res. 2005 Apr 1;11(7):2670-9 [15814648.001]
  • [Cites] Prostate. 2005 Aug 1;64(3):224-39 [15712212.001]
  • [Cites] Mini Rev Med Chem. 2005 Dec;5(12):1125-32 [16375758.001]
  • [Cites] Cancer Res. 2006 Jan 15;66(2):613-21 [16423986.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):437-45 [16272172.001]
  • [Cites] Carcinogenesis. 2006 Mar;27(3):475-82 [16299382.001]
  • [Cites] Mol Cancer Ther. 2006 May;5(5):1335-41 [16731767.001]
  • [Cites] Trends Genet. 2002 May;18(5):S1-5 [12047956.001]
  • (PMID = 18437538.001).
  • [ISSN] 0724-8741
  • [Journal-full-title] Pharmaceutical research
  • [ISO-abbreviation] Pharm. Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA094828; United States / NCI NIH HHS / CA / R01-CA118947; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NCI NIH HHS / CA / R01 CA094828-07; United States / NCI NIH HHS / CA / R01 CA118947-03; United States / NCI NIH HHS / CA / CA118947-03; United States / NCI NIH HHS / CA / R01-CA094828; United States / NCI NIH HHS / CA / R01 CA118947; United States / NCI NIH HHS / CA / CA094828-07
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Bad protein, mouse; 0 / Forkhead Transcription Factors; 0 / Foxo1 protein, mouse; 0 / Isothiocyanates; 0 / bcl-Associated Death Protein; 6U7TFK75KV / phenethyl isothiocyanate; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.2 / pyruvate dehydrogenase (acetyl-transferring) kinase; EC 3.4.22.- / Casp3 protein, mouse; EC 3.4.22.- / Caspase 3; IT942ZTH98 / Curcumin
  • [Other-IDs] NLM/ NIHMS221201; NLM/ PMC3465714
  •  go-up   go-down


5. Willman JH, Holden JA: Immunohistochemical staining for DNA topoisomerase II-alpha in benign, premalignant, and malignant lesions of the prostate. Prostate; 2000 Mar 1;42(4):280-6
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The DNA topoisomerase II-alpha (topo II-alpha)-targeting drug etoposide was recently shown to be an active agent in the combined chemotherapy of hormone-insensitive prostatic carcinoma.
  • Much experimental data indicate that cells sensitive to topo II-targeting chemotherapeutic drugs are rapidly proliferating and show elevated topo II expression.
  • METHODS: Paraffin blocks from cases of invasive prostatic carcinoma, prostatic intraepithelial neoplasia, and prostatic nodular hyperplasia were retrieved from the surgical pathology files at the University of Utah Health Sciences Center.
  • Using a new immunohistochemical stain, specific for the alpha isoform of DNA topo II, enzyme expression was evaluated in 54 prostatic adenocarcinomas, 22 lesions of high-grade prostatic intraepithelial neoplasia (PIN), and 10 cases of benign prostatic nodular hyperplasia.
  • RESULTS: The average topo II-alpha index for well-differentiated prostatic adenocarcinomas (Gleason scores 2-4) was 1.5 +/- 0.9; for moderately differentiated tumors (Gleason scores 5-7), 3.1 +/- 2.4; and for poorly differentiated tumors (Gleason scores 8-10), 6.7 +/- 5.5.
  • The average topo II-alpha index for all invasive prostatic adenocarcinomas was 4.0 (range, 0-19.0).
  • Benign prostatic nodular hyperplasia had the lowest average topo II-alpha index, of 0.54 (range, 0.2-1.0).
  • The average topo II-alpha index of 2.3 (range, 0-8.6) for high-grade prostatic intraepithelial neoplasia was intermediate between the invasive tumors and benign prostate.
  • Prostatic nodular hyperplasia shows little expression of topo II-alpha.
  • Prostatic intraepithelial neoplasia has an average topo II-alpha index intermediate between nodular hyperplasia and carcinoma.
  • [MeSH-major] Adenocarcinoma / enzymology. DNA Topoisomerases, Type II / analysis. Isoenzymes / analysis. Prostate / enzymology. Prostatic Hyperplasia / enzymology. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Neoplasms / enzymology

  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2000 Wiley-Liss, Inc.
  • (PMID = 10679757.001).
  • [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 / Antigens, Neoplasm; 0 / DNA-Binding Proteins; 0 / Isoenzymes; EC 5.99.1.3 / DNA Topoisomerases, Type II; EC 5.99.1.3 / DNA topoisomerase II alpha
  •  go-up   go-down


6. TĂȘtu B: Morphological changes induced by androgen blockade in normal prostate and prostatic carcinoma. Best Pract Res Clin Endocrinol Metab; 2008 Apr;22(2):271-83
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Morphological changes induced by androgen blockade in normal prostate and prostatic carcinoma.
  • The tumor volume, density, capsular penetration, and surgical margin involvement are strongly reduced following such treatment.
  • On histology, normal prostate tissue and tumor undergo marked atrophy and shrinkage.
  • Such therapy-induced changes may be reversible, although occasional clones of cancer cells are apparently not affected and have probably developed resistance.
  • Finally, MAB leads to marked but reversible morphologic changes and reduction in prevalence and extent of prostatic intra-epithelial neoplasia (PIN).
  • [MeSH-major] Androgen Antagonists / pharmacology. Carcinoma / pathology. Prostate / cytology. Prostate / drug effects. Prostatic Neoplasms / pathology
  • [MeSH-minor] Antineoplastic Agents, Hormonal / pharmacology. Antineoplastic Agents, Hormonal / therapeutic use. Humans. Male. Neoplasms, Hormone-Dependent / drug therapy. Neoplasms, Hormone-Dependent / pathology. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / pathology

  • 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 = 18471785.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 61
  •  go-up   go-down


7. Berruti A, Dogliotti L, Mosca A, Bellina M, Mari M, Torta M, Tarabuzzi R, Bollito E, Fontana D, Angeli A: Circulating neuroendocrine markers in patients with prostate carcinoma. Cancer; 2000 Jun 1;88(11):2590-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Circulating neuroendocrine markers were measured in patients with prostate carcinoma (PC), prostatic intraepithelial neoplasia (PIN), and benign prostatic hypertrophy (BPH) with the goal to:.
  • 3) compare values in patients with hormone-naive and hormone-refractory disease; and 4) assess changes after androgen deprivation or chemotherapy.
  • METHODS: Serum neuron specific enolase (NSE) (immunoradiometric assay) and plasma chromogranin A (CgA) (enzyme-linked immunoadsorbent assay) were evaluated in 141 patients with BPH, 54 patients with PIN, and 159 patients with PC; 119 patients were bearing hormone-naive disease and 40 were bearing hormone-refractory disease.
  • CgA was monitored in 31 patients submitted to androgen deprivation and in 24 patients receiving chemotherapy.
  • RESULTS: Supranormal CgA was observed more frequently in patients with American Urologic Association (AUA) Stage D2 disease (45.5%) compared with those with Stage D1 disease (33.3%), Stage C disease (16.7%), Stage A/B disease (18.8%), PIN (25.9%), and BPH (17.0%) (P < 0.02).
  • Elevated baseline CgA values decreased > 50% in 1 of 12 patients who received luteinizing hormone-releasing hormone analogs and in 2 of 12 patients who underwent chemotherapy.
  • Elevated CgA values correlate with poor prognosis and are scarcely influenced by either endocrine therapy or chemotherapy.
  • [MeSH-major] Biomarkers, Tumor / blood. Carcinoma / blood. Chromogranins / blood. Phosphopyruvate Hydratase / blood. Prostatic Hyperplasia / blood. Prostatic Intraepithelial Neoplasia / blood. Prostatic Neoplasms / blood

  • MedlinePlus Health Information. consumer health - Enlarged Prostate (BPH).
  • 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
  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 10861438.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Chromogranin A; 0 / Chromogranins; EC 4.2.1.11 / Phosphopyruvate Hydratase
  •  go-up   go-down


8. Hull D, Bostwick DG: Androgen deprivation therapy for precancerous lesions of the prostate. Best Pract Res Clin Endocrinol Metab; 2008 Apr;22(2):285-91
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Androgen deprivation therapy for precancerous lesions of the prostate.
  • Androgen deprivation therapy has become well-established in the treatment of prostate cancer.
  • Luteinizing-hormone-releasing hormone (LHRH) agonists, anti-androgens, orchiectomy, and combination hormonal therapy are treatment options offered to select patients.
  • The prospect of intervention prior to the development of adenocarcinoma is appealing, and high-grade prostate intra-epithelial neoplasia (PIN), the only known precursor, is the best possible target.
  • There is a decrease in the incidence of high-grade PIN in patients treated with combination androgen deprivation therapy (LHRH agonist and anti-androgen).
  • Treatment with the 5alpha-reductase inhibitor finasteride results in a significant decrease in the incidence of high-grade PIN.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Antineoplastic Agents, Hormonal / therapeutic use. Humans. Male. Models, Biological. Neoplasm Staging. Neoplasms, Hormone-Dependent / drug therapy. Precancerous Conditions / drug therapy. Prostate / drug effects. Prostate / pathology. Selective Estrogen Receptor Modulators / therapeutic use

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18471786.001).
  • [ISSN] 1521-690X
  • [Journal-full-title] Best practice & research. Clinical endocrinology & metabolism
  • [ISO-abbreviation] Best Pract. Res. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal; 0 / Selective Estrogen Receptor Modulators
  • [Number-of-references] 42
  •  go-up   go-down


9. Matsuyama M, Hayama T, Funao K, Kawahito Y, Sano H, Takemoto Y, Nakatani T, Yoshimura R: Overexpression of cysteinyl LT1 receptor in prostate cancer and CysLT1R antagonist inhibits prostate cancer cell growth through apoptosis. Oncol Rep; 2007 Jul;18(1):99-104
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • CysLT1R expression in PC patients, prostatic intraepithelial neoplasia (PIN), benign prostatic hyperplasia (BPH), and normal prostate (NP) tissues were examined.
  • Initially, only slight CysLT1R expression was detected in BPH and NP tissues and marked CysLT1R expression was detected in PIN and PC tissues.
  • Furthermore, CysLT1R antagonist caused marked inhibition of PC cells in a concentration- and time-dependent manner through early apoptosis.
  • Thus, the target of CysLT1R may become a new therapy in the treatment of PC.
  • [MeSH-major] Acetates / pharmacology. Apoptosis / drug effects. Cell Proliferation / drug effects. Leukotriene Antagonists / pharmacology. Membrane Proteins / metabolism. Prostatic Neoplasms / enzymology. Prostatic Neoplasms / pathology. Quinolines / pharmacology. Receptors, Leukotriene / metabolism
  • [MeSH-minor] Aged. Disease Progression. Flow Cytometry. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. Male. Middle Aged. Prostate / metabolism. Prostate / pathology. Prostatic Hyperplasia / metabolism. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / metabolism. Prostatic Intraepithelial Neoplasia / pathology. Tumor Cells, Cultured / drug effects


10. Segev Y, Nativ O: [Nutrition and pharmacological treatment for prevention of prostate cancer]. Harefuah; 2006 Jan;145(1):47-51, 76-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Nutrition and pharmacological treatment for prevention of prostate cancer].
  • Since high grade prostatic intraepithelial neoplasia (PIN) is an early predictor of prostate cancer, preventive strategies focusing on men with high grade PIN are being explored.
  • Further study will hopefully help to establish a core set of nutritional and dietary factors that can positively or negatively affect prostate cancer development, as well as a set of pharmacologic agents that can reduce the risk of prostate cancer development and/or progression in selected patients.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Nutritional Physiological Phenomena. Prostatic Neoplasms / prevention & control


11. Montironi R, Mazzucchelli R: HER-2 expression and gene amplification in high-grade PIN and prostate cancer. Arch Ital Urol Androl; 2006 Dec;78(4):135-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] HER-2 expression and gene amplification in high-grade PIN and prostate cancer.
  • All the patients were under total androgen ablation therapy for three months before surgery.
  • None of the patients belonging to Groups 1, 2, and 5 had received chemotherapy, hormone therapy, or radiation therapy before surgery.
  • Weak to moderate HER-2 membrane immunoreactivity was observed in most of the basal cells but not in the secretory cells of normal prostatic ducts and acini both in the cystoprostatectomies and in the radicals of the untreated patients.
  • High-grade PIN.

  • 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
  • (PMID = 17269616.001).
  • [ISSN] 1124-3562
  • [Journal-full-title] Archivio italiano di urologia, andrologia : organo ufficiale [di] Societa italiana di ecografia urologica e nefrologica
  • [ISO-abbreviation] Arch Ital Urol Androl
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] Italy
  •  go-up   go-down


12. Bardia A, Platz EA, Yegnasubramanian S, De Marzo AM, Nelson WG: Anti-inflammatory drugs, antioxidants, and prostate cancer prevention. Curr Opin Pharmacol; 2009 Aug;9(4):419-26
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-inflammatory drugs, antioxidants, and prostate cancer prevention.
  • Prostate cancer may be the most common preventable cancer among men in the United States (US) and the rest of the developed world.
  • In this milieu, the damaged epithelium may generate proliferative inflammatory atrophy (PIA) lesions, which may progress to prostatic intraepithelial neoplasia (PIN) or to prostate cancer.
  • To attenuate prostatic carcinogenesis driven by chronic or recurrent prostate inflammation, rational chemoprevention has thus far featured anti-inflammatory drugs and antioxidants.
  • Results from clinical trials of these approaches have been mixed, emphasizing the need for mechanistic studies of the contribution of inflammation to prostatic carcinogenesis, more extensive analyses of the pharmacology, including distribution of drugs into target tissue, and, rational development of biomarkers to identify patients that are most likely to respond to anti-inflammatory drugs and antioxidants (targeted chemoprevention), alone, or in combination (combination chemoprevention).
  • [MeSH-major] Anti-Inflammatory Agents / therapeutic use. Antioxidants / therapeutic use. Inflammation Mediators / physiology. Inflammation Mediators / therapeutic use. Prostatic Neoplasms / pathology. Prostatic Neoplasms / prevention & control
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Drug Delivery Systems. Humans. Inflammation / complications. Inflammation / drug therapy. Inflammation / metabolism. Inflammation / pathology. Male

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Antioxidants.
  • 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 = 19574101.001).
  • [ISSN] 1471-4973
  • [Journal-full-title] Current opinion in pharmacology
  • [ISO-abbreviation] Curr Opin Pharmacol
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA006973
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Inflammation Mediators
  • [Number-of-references] 61
  • [Other-IDs] NLM/ NIHMS700749; NLM/ PMC4479123
  •  go-up   go-down


13. Mazzucchelli R, Montironi R, Santinelli A, Lucarini G, Pugnaloni A, Biagini G: Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients. Prostate; 2000 Sep 15;45(1):72-9
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients.
  • The aim of the study was to investigate immunohistochemically the expression of VEGF and its correlation with the pattern of capillary architecture in prostate cancer and high-grade prostatic intraepithelial neoplasia (PIN), in untreated and androgen-ablated patients.
  • The study population included two groups: 35 patients who did not receive chemo-, hormone, or radiation therapy before surgery, and 10 patients who were under complete androgen blockade (CAB) for 3 months at time of surgery.
  • VEGF was examined by immunohistochemistry, and its tissue expression was compared with the pattern of capillary architecture evaluated by immunostaining the endothelial antigen CD34.
  • RESULTS: In normal tissue, the intensity of the VEGF immunoreactivity in the cytoplasm of secretory cells ranged from negative to low.
  • Two discrete immunostaining patterns were observed in high-grade PIN.
  • The capillary architecture in high-grade PIN with pattern A was similar to the orderly vascular network seen in normal prostates, whereas in the pattern B it had the characteristics of microvessels usually seen in PCa.
  • CONCLUSIONS: Our immunohistochemical results indicate that significant levels of VEGF are present in prostate cancer and in a population of PIN lesions, expression being highest in association with NE cells.
  • [MeSH-major] Adenocarcinoma / blood supply. Androgen Antagonists / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Endothelial Growth Factors / biosynthesis. Lymphokines / biosynthesis. Neovascularization, Pathologic / physiopathology. Prostatic Intraepithelial Neoplasia / blood supply. Prostatic Neoplasms / blood supply
  • [MeSH-minor] Aged. Anilides / administration & dosage. Capillaries / anatomy & histology. Capillaries / drug effects. Capillaries / physiopathology. Goserelin / administration & dosage. Humans. Immunohistochemistry. Male. Middle Aged. Nitriles. Prostatectomy. Tosyl Compounds. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. GOSERELIN .
  • Hazardous Substances Data Bank. BICALUTAMIDE .
  • 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 2000 Wiley-Liss, Inc.
  • (PMID = 10960845.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Anilides; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Nitriles; 0 / Tosyl Compounds; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0F65R8P09N / Goserelin; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


14. Bostwick DG, Qian J: Effect of androgen deprivation therapy on prostatic intraepithelial neoplasia. Urology; 2001 Aug;58(2 Suppl 1):91-3
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of androgen deprivation therapy on prostatic intraepithelial neoplasia.
  • There is a marked decrease in the prevalence and extent of high-grade prostatic intraepithelial neoplasia (PIN) in men with prostate cancer after androgen deprivation therapy (ADT) when compared with untreated cases.
  • These findings indicate that the benign and dysplastic prostatic epithelium is androgen dependent.
  • In the normal prostatic epithelium, luminal secretory cells are more sensitive to the absence of androgen than basal cells, and the proliferative cells of high-grade PIN share this androgen sensitivity.
  • Remarkably little is known about the comparative effect of different forms of chemical ADT on PIN and cancer, although there appears to be a limited and consistent repertoire of morphologic responses to all forms of this therapy.
  • Conversely, blockade of 5alpha-reductase with finasteride has little or no effect on PIN (or benign epithelium and cancer), unlike other forms of ADT.
  • A recent international consensus conference sponsored by the World Health Organization concluded that identification of high-grade PIN offered the possibility of chemoprevention with hormonal therapy to block the development of clinical cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy
  • [MeSH-minor] Chemoprevention / methods. Chemoprevention / trends. Drug Administration Schedule. Humans. Male. Precancerous Conditions / drug therapy. Precancerous Conditions / pathology. Prostate / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11502458.001).
  • [ISSN] 1527-9995
  • [Journal-full-title] Urology
  • [ISO-abbreviation] Urology
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
  • [Number-of-references] 30
  •  go-up   go-down


15. Goeman L, Joniau S, Ponette D, Van der Aa F, Roskams T, Oyen R, Van Poppel H: Is low-grade prostatic intraepithelial neoplasia a risk factor for cancer? Prostate Cancer Prostatic Dis; 2003;6(4):305-10
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Is low-grade prostatic intraepithelial neoplasia a risk factor for cancer?
  • INTRODUCTION: High-grade prostatic intraepithelial neoplasia (HGPIN) is generally accepted to be a precursor lesion of prostate cancer.
  • The likely outcome of isolated low-grade PIN (LGPIN) lesions in prostate biopsies remains unclear.
  • MATERIALS AND METHODS: In a 2-y period, 207 men were diagnosed with isolated PIN on standard systematic sextant biopsy of the prostate.
  • No patients had ever received androgen deprivation therapy, chemotherapy or radiation therapy.
  • [MeSH-major] Prostatic Intraepithelial Neoplasia / blood. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / blood. Prostatic Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • Hazardous Substances Data Bank. SELENIUM, ELEMENTAL .
  • 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 = 14663472.001).
  • [ISSN] 1365-7852
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Clinical Trial; Controlled Clinical Trial; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 1406-18-4 / Vitamin E; EC 3.4.21.77 / Prostate-Specific Antigen; H6241UJ22B / Selenium
  •  go-up   go-down


16. Matsuyama M, Yoshimura R, Mitsuhashi M, Hase T, Tsuchida K, Takemoto Y, Kawahito Y, Sano H, Nakatani T: Expression of lipoxygenase in human prostate cancer and growth reduction by its inhibitors. Int J Oncol; 2004 Apr;24(4):821-7
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Expressions of 5- and 12-LOX in prostate cancer (PC) patients, prostatic intraepithelial neoplasia (PIN), benign prostatic hyperplasia (BPH), and normal prostate (NP) tissues were examined, as well as effects of their inhibitors on cell proliferation in 2 PC cell lines (PC3, DU-145).
  • While 5- and 12-LOX expressions were slightly detected in BPH and NP tissues, marked expressions of 5- and 12-lipoxygenase were detected in PIN and PC tissues.
  • The LOX inhibitors caused marked reduction of prostate cancer cells in a concentration- and time-dependent manner.
  • Thus, LOX may become a new target in treatment of prostate cancer.
  • [MeSH-major] Arachidonate 12-Lipoxygenase / metabolism. Arachidonate 5-Lipoxygenase / metabolism. Gene Expression Regulation, Enzymologic / drug effects. Gene Expression Regulation, Neoplastic. Lipoxygenase Inhibitors / pharmacology. Prostatic Neoplasms / enzymology
  • [MeSH-minor] Aged. Apoptosis / drug effects. Case-Control Studies. Cell Division / drug effects. Humans. Male. Middle Aged. Prostatic Hyperplasia / drug therapy. Prostatic Hyperplasia / enzymology. Prostatic Hyperplasia / genetics. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Intraepithelial Neoplasia / genetics. Tumor Cells, Cultured


17. Ahmad I, Sansom OJ, Leung HY: Advances in mouse models of prostate cancer. Expert Rev Mol Med; 2008 Jun 09;10:e16
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Bigenic models indicate that that two 'hits' are required for progression from intra-epithelial neoplasia (PIN) to invasion carcinoma, and two to five hits are needed for metastasis.
  • Here, we discuss the numerous models that mimic various aspects of the disease process, such as PIN, locally invasive adenocarcinoma and metastatic disease.
  • Such mouse models increase our understanding of the disease process and provide targets for novel therapeutic approaches.
  • [MeSH-major] Adenocarcinoma / genetics. Disease Models, Animal. Mice. Prostatic Neoplasms / genetics
  • [MeSH-minor] Androgens. Animals. Cocarcinogenesis. Dogs. Drug Screening Assays, Antitumor. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Humans. Male. Mice, Knockout. Mice, Transgenic. Neoplasms, Hormone-Dependent / genetics. Neoplasms, Hormone-Dependent / physiopathology. Neoplasms, Hormone-Dependent / prevention & control. Neoplasms, Hormone-Dependent / therapy. Oncogenes. Promoter Regions, Genetic. Prostate / anatomy & histology. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Intraepithelial Neoplasia / physiopathology. Rats. Receptors, Androgen / genetics. Receptors, Androgen / physiology

  • 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 = 18538039.001).
  • [ISSN] 1462-3994
  • [Journal-full-title] Expert reviews in molecular medicine
  • [ISO-abbreviation] Expert Rev Mol Med
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0500966; United Kingdom / Medical Research Council / / G0802141
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / Receptors, Androgen
  • [Number-of-references] 157
  •  go-up   go-down






Advertisement