[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 31 of about 31
1. Kang TY, Nichols P, Skinner E, Groshen S, Valin G, Ye W, Raghavan D: Functional heterogeneity of prostatic intraepithelial neoplasia: the duration of hormonal therapy influences the response. BJU Int; 2007 May;99(5):1024-7
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Functional heterogeneity of prostatic intraepithelial neoplasia: the duration of hormonal therapy influences the response.
  • OBJECTIVES: To use a clinical model of androgen-deprivation therapy (ADT) followed by radical prostatectomy (RP) to test the hypothesis that prostatic intraepithelial neoplasia (PIN, a premalignant lesion of the prostate causally linked to prostate cancer) is heterogeneous for hormone responsiveness, which might explain aspects of the heterogeneity of the natural history of prostate cancer, for although ADT has been used to reduce prostate cancer, there are controversial data on the effect of ADT on PIN.
  • Patients were sequentially selected from the database and their pathology slides were reviewed by a pathologist unaware of the initial presence of PIN (assessed by an independent observer).
  • Fisher's exact test was used to compare the proportions of patients who had residual PIN in the study and control groups.
  • Exact logistic regression was used to evaluate the duration of ADT on PIN regression.
  • RESULTS: Eighteen patients initially diagnosed with PIN who had no ADT were identified, and 28 with PIN who had ADT were also assessed.
  • All patients who had had no ADT had residual PIN, whereas seven of 28 receiving ADT had no residual PIN (P=0.043).
  • The evaluation of ADT between responders and nonresponders showed a statistically significant association between PIN regression and the duration of ADT (P<0.001).
  • However, the response of PIN to ADT was not uniform, as 16% of patients on ADT for >6 months had residual PIN, suggesting variable sensitivity of PIN to ADT.
  • CONCLUSION: These results show that ADT causes PIN to regress, and that there is heterogeneity in this effect with the duration of ADT.
  • We propose future prospective, multicentre, randomized trials in which the effect of ADT on PIN is characterized further.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Antineoplastic Agents, Hormonal / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Cohort Studies. Combined Modality Therapy. Humans. Male. Middle Aged. Prostatectomy. Regression Analysis. Retrospective Studies. Sensitivity and Specificity. Treatment Outcome

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17244277.001).
  • [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 / Androgen Antagonists; 0 / Antineoplastic Agents, Hormonal
  •  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
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 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

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. TAMOXIFEN .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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
  • [Cites] Cancer Cell. 2003 Sep;4(3):209-21 [14522255.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7841-6 [12799464.001]
  • [Cites] PLoS Biol. 2003 Dec;1(3):E59 [14691534.001]
  • [Cites] Mol Endocrinol. 1994 Feb;8(2):230-9 [8170479.001]
  • [Cites] J Biol Chem. 1994 Dec 16;269(50):31763-9 [7989349.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3439-43 [7724580.001]
  • [Cites] Prostate. 1997 Jul 1;32(2):129-39 [9215401.001]
  • [Cites] J Androl. 1999 Mar-Apr;20(2):251-8 [10232660.001]
  • [Cites] J Mol Endocrinol. 1999 Jun;22(3):313-25 [10343290.001]
  • [Cites] Development. 1999 Aug;126(16):3693-701 [10409514.001]
  • [Cites] J Cell Biochem. 2005 Feb 1;94(2):279-97 [15565647.001]
  • [Cites] J Clin Pathol. 2005 Jul;58(7):673-84 [15976331.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5730-9 [15994948.001]
  • [Cites] Nature. 2005 Aug 4;436(7051):725-30 [16079851.001]
  • [Cites] Nat Rev Drug Discov. 2006 Aug;5(8):671-88 [16883305.001]
  • [Cites] Cancer Lett. 2006 Sep 28;241(2):184-96 [16412571.001]
  • [Cites] Clin Cancer Res. 2006 Sep 15;12(18):5305-11 [17000663.001]
  • [Cites] Biochem Soc Trans. 2006 Nov;34(Pt 5):647-62 [17052169.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Annu Rev Pathol. 2006;1:243-71 [18039115.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):572-85 [18068633.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2521-6 [18268330.001]
  • [Cites] Genesis. 2008 Apr;46(4):229-34 [18395839.001]
  • [Cites] Cell. 2008 May 2;133(3):403-14 [18455982.001]
  • [Cites] Biochem J. 2000 Mar 15;346 Pt 3:561-76 [10698680.001]
  • [Cites] Genesis. 2000 Feb;26(2):154-6 [10686616.001]
  • [Cites] Endocrinology. 2000 Dec;141(12):4698-710 [11108285.001]
  • [Cites] Mech Dev. 2001 Mar;101(1-2):61-9 [11231059.001]
  • [Cites] Trends Genet. 2002 May;18(5):S1-5 [12047956.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Feb 10;101(6):1725-30 [14747659.001]
  • (PMID = 19081794.001).
  • [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 / Androgen-Binding Protein; 0 / Arrestins; 0 / Ribosomal Protein S6; 0 / beta-arrestin; 094ZI81Y45 / Tamoxifen; 17197F0KYM / afimoxifene; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.7.- / Cre recombinase; EC 2.7.7.- / Integrases; EC 3.1.3.48 / Pten protein, mouse; EC 3.1.3.67 / PTEN Phosphohydrolase
  • [Other-IDs] NLM/ PMC2597775
  •  go-up   go-down


3. Christov KT, Moon RC, Lantvit DD, Boone CW, Steele VE, Lubet RA, Kelloff GJ, Pezzuto JM: 9-cis-retinoic acid but not 4-(hydroxyphenyl)retinamide inhibits prostate intraepithelial neoplasia in Noble rats. Cancer Res; 2002 Sep 15;62(18):5178-82
Hazardous Substances Data Bank. TESTOSTERONE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] 9-cis-retinoic acid but not 4-(hydroxyphenyl)retinamide inhibits prostate intraepithelial neoplasia in Noble rats.
  • In this study, we used prostate intraepithelial neoplasia (PIN) in Noble rats as an intermediate end point to examine the chemopreventive efficacy of two retinoids, 9-cis-retinoic acid (9cRA) and 4-(hydroxyphenyl)retinamide, which in previous studies have shown promising inhibitory effects on various carcinogenesis models.
  • We found that 80-100% of Noble rats treated for 36 weeks with testosterone + 17beta-estradiol developed multiple PIN lesions predominantly in the dorso-lateral prostate, which appears relevant to the place of origin of PIN and carcinoma in the human prostate.
  • 9cRA at 50 or 100 mg/kg diet significantly decreased the multiplicity of PIN, whereas 4-(hydroxyphenyl) retinamide at 392 or 784 mg/kg diet, did not have an inhibitory effect on PIN.
  • Thus, we provide for the first time evidence that the testosterone + 17beta-estradiol-induced PIN in Noble rats could be used as a potential intermediate end point in assessing the efficacy of retinoids and possibly of other agents on prostate carcinogenesis, and that 9cRA alone or in combination with other agents may have clinical promise in preventing the development of prostate cancer in men.
  • [MeSH-major] Anticarcinogenic Agents / pharmacology. Fenretinide / pharmacology. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / prevention & control. Tretinoin / pharmacology
  • [MeSH-minor] Animals. Body Weight / drug effects. Estradiol / toxicity. Male. Rats. Testosterone / toxicity

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ALL-TRANS-RETINOIC ACID .
  • Hazardous Substances Data Bank. ESTRADIOL .
  • Hazardous Substances Data Bank. ALITRETINOIN .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 12234981.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01 CN 25492-04
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 187EJ7QEXL / Fenretinide; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 5300-03-8 / alitretinoin; 5688UTC01R / Tretinoin
  •  go-up   go-down


Advertisement
4. Bostwick DG, Qian J: Effect of androgen deprivation therapy on prostatic intraepithelial neoplasia. Urology; 2001 Aug;58(2 Suppl 1):91-3

  • [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


5. Bettuzzi S, Brausi M, Rizzi F, Castagnetti G, Peracchia G, Corti A: Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study. Cancer Res; 2006 Jan 15;66(2):1234-40
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] Chemoprevention of human prostate cancer by oral administration of green tea catechins in volunteers with high-grade prostate intraepithelial neoplasia: a preliminary report from a one-year proof-of-principle study.
  • Recent studies showed that 30% of men with high-grade prostate intraepithelial neoplasia (HG-PIN) would develop prostate cancer (CaP) within 1 year after repeated biopsy.
  • This prompted us to do a proof-of-principle clinical trial to assess the safety and efficacy of GTCs for the chemoprevention of CaP in HG-PIN volunteers.
  • Sixty volunteers with HG-PIN, who were made aware of the study details, agreed to sign an informed consent form and were enrolled in this double-blind, placebo-controlled study.
  • Daily treatment consisted of three GTCs capsules, 200 mg each (total 600 mg/d).
  • [MeSH-major] Catechin / therapeutic use. Prostatic Hyperplasia / drug therapy. Prostatic Neoplasms / prevention & control. Tea


6. Bono AV, Mazzucchelli R, Ferrari I, Lopez-Beltran A, Galosi AB, Cheng L, Montironi R: Bicalutamide 50 mg monotherapy in patients with isolated high-grade PIN: findings in repeat biopsies at 6 months. J Clin Pathol; 2007 Apr;60(4):443-6
Hazardous Substances Data Bank. BICALUTAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Bicalutamide 50 mg monotherapy in patients with isolated high-grade PIN: findings in repeat biopsies at 6 months.
  • OBJECTIVES: To evaluate morphological findings in repeat biopsies in patients with isolated high-grade prostatic intraepithelial neoplasia (HGPIN) after a 6-month course of bicalutamide (Casodex) 50 mg/day.
  • After treatment, the patients were resubmitted to prostate biopsy mapping.
  • The control group included 22 untreated consecutive patients with isolated high-grade PIN with repeat biopsies taken 6 months after the initial biopsies.
  • Treatment did not affect the incidence of cancer (treated vs control: 5% vs 4.5%).
  • [MeSH-major] Anilides / therapeutic use. Antineoplastic Agents / therapeutic use. Nitriles / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy. Tosyl Compounds / therapeutic use
  • [MeSH-minor] Aged. Biopsy. Follow-Up Studies. Humans. Male. Middle Aged. Treatment Outcome

  • 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] Prostate. 2004 Nov 1;61(3):260-6 [15368469.001]
  • [Cites] J Clin Oncol. 2004 Jul 1;22(13):2546-53 [15226323.001]
  • [Cites] Urology. 1994 Jul;44(1):91-5 [8042266.001]
  • [Cites] J Urol. 1995 Nov;154(5):1791-4 [7563348.001]
  • [Cites] Am J Surg Pathol. 1996 Jan;20(1):86-93 [8540613.001]
  • [Cites] Pathol Res Pract. 1995 Sep;191(9):838-41 [8606862.001]
  • [Cites] Anal Quant Cytol Histol. 1996 Dec;18(6):461-70 [8978870.001]
  • [Cites] Stat Med. 1997 Dec 15;16(23):2701-11 [9421870.001]
  • [Cites] J Clin Pathol. 1998 Jan;51(1):5-12 [9577363.001]
  • [Cites] J Urol. 1999 Sep;162(3 Pt 1):753-7 [10458359.001]
  • [Cites] J Urol. 2004 Nov;172(5 Pt 1):1865-70 [15540740.001]
  • [Cites] Urology. 2005 Mar;65(3):538-42 [15780372.001]
  • [Cites] J Urol. 2005 Dec;174(6):2098-104 [16280736.001]
  • [Cites] BJU Int. 2006 Jul;98(1):54-8 [16831143.001]
  • [Cites] J Urol. 2000 Nov;164(5):1579-82 [11025708.001]
  • [Cites] Prostate. 2001 Mar 1;46(4):275-80 [11241549.001]
  • [Cites] Curr Urol Rep. 2000 May;1(1):65-70 [12084343.001]
  • [Cites] Urology. 2002 Sep;60(3 Suppl 1):64-71 [12231053.001]
  • [Cites] Am J Surg Pathol. 2002 Nov;26(11):1400-13 [12409716.001]
  • [Cites] Urology. 2003 Feb;61(2 Suppl 1):3-7 [12667881.001]
  • [Cites] Clin Oncol (R Coll Radiol). 2003 Sep;15(6):318-21 [14524484.001]
  • [Cites] Oncology (Williston Park). 2004 Mar;18(3):303-9; discussion 310, 315, 319-21 [15065701.001]
  • [Cites] Am J Surg Pathol. 2004 May;28(5):629-33 [15105651.001]
  • [Cites] Mod Pathol. 2004 Mar;17(3):360-79 [14739906.001]
  • [Cites] Urology. 2004 Jun;63(6):1105-10 [15183961.001]
  • [Cites] Cancer. 1991 Jun 15;67(12):2949-58 [1710531.001]
  • (PMID = 16822873.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase II; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anilides; 0 / Antineoplastic Agents; 0 / Nitriles; 0 / Tosyl Compounds; A0Z3NAU9DP / bicalutamide
  • [Other-IDs] NLM/ PMC2001123
  •  go-up   go-down


7. Narayanan BA, Narayanan NK, Pittman B, Reddy BS: Regression of mouse prostatic intraepithelial neoplasia by nonsteroidal anti-inflammatory drugs in the transgenic adenocarcinoma mouse prostate model. Clin Cancer Res; 2004 Nov 15;10(22):7727-37
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] Regression of mouse prostatic intraepithelial neoplasia by nonsteroidal anti-inflammatory drugs in the transgenic adenocarcinoma mouse prostate model.
  • PURPOSE: Epidemiologic studies have revealed a decreased risk of colon cancer among people who have regularly taken cyclooxygenase (COX)-2 inhibitors such as aspirin or other nonsteroidal anti-inflammatory drugs (NSAIDs).
  • EXPERIMENTAL DESIGN: We used the transgenic mouse prostate (TRAMP) model, which exhibits similarities with human prostate cancer, including epithelial origin, progression from the PIN stage to adenocarcinoma, and metastasis by a transgene that is hormonally regulated by androgens.
  • In addition to histologically analyzing the PIN lesions of the dorsolateral prostate from TRAMP mice, we delineated the molecular targets and mechanisms of celecoxib and exisulind against mouse PIN lesions.
  • We performed Western blot analysis of the total protein lysate from the tissues of mouse PIN lesions to measure the level of expression of androgen receptor, vascular endothelial growth factor, nuclear factor-kappaB p65, BclII, AKT (total and phosphorylated Ser473), p53, cyclin-dependent kinase inhibitor p21WAF1/CIP1, p27, BAX, and caspase-3 to demonstrate the COX-2-independent mechanism involved in the inhibition of PIN lesions of the dorsolateral prostate by both celecoxib and exisulind.
  • RESULTS: We found for the first time that (a) both celecoxib and exisulind as dietary supplements induce strong inhibitory effects against prostate cancer at doses of 800 and 500 ppm, respectively, after 16 weeks;.
  • (b) the histologic analysis of the dorsolateral prostate after 2 weeks of treatment indicated a reduction of PIN lesions from 75% to 19% with celecoxib and to 16% with exisulind;.
  • To understand the molecular mechanisms involved in the inhibition of PIN lesions, first, we examined the expression of molecular targets involved in angiogenesis and inflammatory processes.
  • It was clearly evident from Western blot analysis of the total protein lysate derived from the dorsolateral prostate tissues with PIN lesions that expression of androgen receptor, vascular endothelial growth factor, nuclear factor-kappaB p65, and BclII is down-regulated more effectively by celecoxib.
  • CONCLUSIONS: Overall, the findings from this study clearly show the effectiveness of celecoxib and exisulind in reducing the PIN lesions by modulating a cascade of molecular targets involved in COX-2-dependent and -independent mechanisms.
  • [MeSH-major] Adenocarcinoma / drug therapy. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / drug therapy. Sulindac / analogs & derivatives
  • [MeSH-minor] Animals. Apoptosis. Blotting, Western. Celecoxib. Dietary Supplements. Dinoprostone / biosynthesis. Disease Models, Animal. Immunohistochemistry. Male. Mice. Mice, Transgenic. Models, Biological. Phosphorylation. Pyrazoles / therapeutic use. Sulfonamides / therapeutic use. Time Factors. Transgenes

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CELECOXIB .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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 = 15570007.001).
  • [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 / CA-17613
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Pyrazoles; 0 / Sulfonamides; 184SNS8VUH / Sulindac; JCX84Q7J1L / Celecoxib; K619IIG2R9 / sulindac sulfone; K7Q1JQR04M / Dinoprostone
  •  go-up   go-down


8. Steiner MS, Pound CR: Phase IIA clinical trial to test the efficacy and safety of Toremifene in men with high-grade prostatic intraepithelial neoplasia. Clin Prostate Cancer; 2003 Jun;2(1):24-31
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 IIA clinical trial to test the efficacy and safety of Toremifene in men with high-grade prostatic intraepithelial neoplasia.
  • Men with high-grade prostatic intraepithelial neoplasia (PIN) evident on prostate biopsy are at high risk for the eventual development of prostate cancer.
  • The ability to reverse high-grade PIN may reduce the incidence or delay the development of prostate cancer.
  • Toremifene (GTx-006, Acapodene trade mark ) is a selective estrogen receptor modulator that has been shown in the transgenic mouse model of prostate cancer to eliminate high-grade PIN and reduce the incidence of prostate cancer.
  • This study was aimed at the evaluation of the safety and efficacy of toremifene in men diagnosed with high-grade PIN.
  • This was an open-label, phase IIA clinical trial that enrolled 21 men (mean age, 64.7 years) with evidence of high-grade PIN on biopsy within 6 months of entry into the study.
  • Eighteen of these men (86%) completed toremifene treatment (60 mg/day orally for 4 months) and then underwent follow-up prostate biopsy (8 cores) to determine high-grade PIN status.
  • The effect of the drug on serum prostate-specific antigen (PSA), percentage of free PSA, testosterone, estradiol, and quality of life was also measured.
  • After toremifene treatment, 72% of these 18 men (vs. 17.9% of historical controls) had no high-grade PIN on subsequent prostate biopsies.
  • Quality of life was not significantly affected by treatment.
  • Toremifene appeared to reduce high-grade PIN in this small, exploratory trial.
  • The drug was well tolerated.
  • A double-blind, dose-finding, randomized, placebo-controlled phase IIB/III study is currently open to further study toremifene's activity against high-grade PIN and prostate cancer incidence.
  • [MeSH-major] Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / pathology. Toremifene / administration & dosage
  • [MeSH-minor] Administration, Oral. Aged. Antineoplastic Agents, Hormonal / administration & dosage. Antineoplastic Agents, Hormonal / adverse effects. Biopsy, Needle. Disease-Free Survival. Dose-Response Relationship, Drug. Drug Administration Schedule. Humans. Male. Maximum Tolerated Dose. Middle Aged. Neoplasm Staging. Prognosis. Quality of Life. Risk Assessment. Survival Analysis. Treatment Outcome

  • 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 .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Clin Prostate Cancer. 2003 Jun;2(1):32-3 [15046681.001]
  • (PMID = 15046680.001).
  • [ISSN] 1540-0352
  • [Journal-full-title] Clinical prostate cancer
  • [ISO-abbreviation] Clin Prostate Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase II; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 7NFE54O27T / Toremifene
  •  go-up   go-down


9. 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
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] 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 .
  • [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


10. Rhoden EL, Morgentaler A: Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia. J Urol; 2003 Dec;170(6 Pt 1):2348-51
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] Testosterone replacement therapy in hypogonadal men at high risk for prostate cancer: results of 1 year of treatment in men with prostatic intraepithelial neoplasia.
  • PURPOSE: One of the greatest concerns among clinicians regarding testosterone replacement therapy (TRT) is the fear of causing or promoting prostate cancer.
  • We evaluated prostatic changes in hypogonadal men with and without high grade prostatic intraepithelial neoplasia (PIN), which is considered a prostatic precancerous lesion, after 1 year of TRT.
  • All underwent prostate biopsy prior to initiating treatment.
  • Of the men 55 had benign prostate biopsies (PIN-) and 20 had PIN without frank cancer (PIN+).
  • All men with PIN underwent repeat biopsy to exclude cancer prior to the initiation of testosterone treatment.
  • Prostate specific antigen (PSA), and total and free testosterone were determined prior to treatment and at 1 year.
  • RESULTS: PSA was similar at baseline in men with and without PIN (1.49 +/- 1.1 and 1.53 +/- 1.6 ng/dl, p >0.05) and after 12 months of TRT (1.82 +/- 1.1 and 1.78 +/- 1.6 ng/dl, respectively, p >0.05).
  • A slight, similar increase in mean PSA was noted in the PIN- and PIN+ groups (0.25 +/- 0.6 and 0.33 +/- 0.6 ng/dl, p >0.05).
  • One man in the PIN+ group had cancer after biopsy was performed due to abnormal digital rectal examination.
  • Four additional men in the PIN- group and 2 in the PIN+ group underwent re-biopsy for elevated PSA and none had cancer.
  • No differences were noted between the PIN- and PIN+ groups with regard to total and free testosterone at baseline and at 1 year (p = 0.267).
  • CONCLUSIONS: After 1 year of TRT men with PIN do not have a greater increase in PSA or a significantly increased risk of cancer than men without PIN.
  • These results indicate that TRT is not contraindicated in men with a history of PIN.
  • [MeSH-major] Hormone Replacement Therapy. Hypogonadism / drug therapy. Prostatic Intraepithelial Neoplasia / complications. Prostatic Neoplasms / chemically induced. Testosterone / therapeutic use


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
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] 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.
  • [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. Mazzucchelli R, Montironi R, Santinelli A, Lucarini G, Pugnaloni A, Biagini G: Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients. Prostate; 2000 Sep 15;45(1):72-9
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Vascular endothelial growth factor expression and capillary architecture in high-grade PIN and prostate cancer in untreated and androgen-ablated patients.
  • 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 .
  • [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


13. Yamauchi A, Kawai K, Tsukamoto S, Ideyama Y, Shirai T, Akaza H: Persistence of prostatic intraepithelial neoplasia after effective chemoprevention of microscopic prostate cancer with antiandrogen in a rat model. J Urol; 2006 Jan;175(1):348-52
Hazardous Substances Data Bank. BICALUTAMIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Persistence of prostatic intraepithelial neoplasia after effective chemoprevention of microscopic prostate cancer with antiandrogen in a rat model.
  • We have previously reported that rat prostate microscopic carcinogenesis in this model was paradoxically enhanced when continuous treatment with bicalutamide was begun 20 weeks after the initiation of DMAB.
  • MATERIALS AND METHODS: DMAB at a dose of 50 mg/kg was injected subcutaneously into all animals 10 times at 2-week intervals.
  • Treatment with bicalutamide began in the 60th week in group 3 rats and continued for 14 weeks.
  • Delayed bicalutamide treatment significantly suppressed the cancer lesion.
  • In contrast, bicalutamide did not affect the incidence of PIN.
  • The difference in the incidence of PIN in groups 2 and 3 (84% and 78%, respectively) was not significant.
  • Despite this suppressive effect on microscopic cancer bicalutamide permits the persistence of PIN.
  • The latter finding suggests that the sensitivity of PIN to antiandrogen might be more complicated than previously recognized.
  • [MeSH-major] Androgen Antagonists / therapeutic use. Anilides / therapeutic use. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / prevention & control. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Intraepithelial Neoplasia / prevention & control. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / prevention & control

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16406940.001).
  • [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 / Aminobiphenyl Compounds; 0 / Androgen Antagonists; 0 / Anilides; 0 / Carcinogens; 0 / Nitriles; 0 / Tosyl Compounds; 13394-86-0 / 2',3-dimethyl-4-aminobiphenyl; A0Z3NAU9DP / bicalutamide
  •  go-up   go-down


14. 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
COS Scholar Universe. author profiles.

  • [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.
  • [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


15. 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
The Lens. Cited by Patents in .

  • [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.
  • [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


16. 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
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.
  • 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.
  • [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


17. 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
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.
  • 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


18. 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
The Lens. Cited by Patents in .

  • [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


19. Narayanan BA, Narayanan NK, Pttman B, Reddy BS: Adenocarcina of the mouse prostate growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition. Prostate; 2006 Feb 15;66(3):257-65
Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: Epidemiological studies have shown a decreased risk of prostate cancer among men who regularly take aspirin or other non-steroidal anti-inflammatory drugs (NSAIDs).
  • RESULTS: Dietary supplement of celecoxib at doses of 400 ppm, 600 ppm, and 1,000 ppm are most effective against mPIN (mouse prostatic intraepithelial neoplasia) and adenocarcinoma of the prostate.
  • At 1,000 ppm, a complete inhibition of the PIN lesions was extended to limit the growth of adenocarcinoma (from 85% to 15%) and metastasis of the mouse prostate.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cyclooxygenase 2 / metabolism. Cyclooxygenase Inhibitors / pharmacology. Prostatic Intraepithelial Neoplasia / drug therapy. Prostatic Neoplasms / drug therapy. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Transcription Factor RelA / antagonists & inhibitors
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Celecoxib. Cell Growth Processes / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Down-Regulation. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. CELECOXIB .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2005 Wiley-Liss, Inc.
  • (PMID = 16175586.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA107813-01
  • [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 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Transcription Factor RelA; EC 1.14.99.1 / Cyclooxygenase 2; JCX84Q7J1L / Celecoxib
  •  go-up   go-down


20. 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
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] 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

  • [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


21. Ahmad I, Sansom OJ, Leung HY: Advances in mouse models of prostate cancer. Expert Rev Mol Med; 2008 Jun 09;10:e16
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.
  • 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.
  • [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


22. 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
COS Scholar Universe. author profiles.

  • [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.
  • [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


23. Segev Y, Nativ O: [Nutrition and pharmacological treatment for prevention of prostate cancer]. Harefuah; 2006 Jan;145(1):47-51, 76-7
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] [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

  • Genetic Alliance. consumer health - Prostate cancer.
  • MedlinePlus Health Information. consumer health - Nutrition.
  • 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 = 16450727.001).
  • [ISSN] 0017-7768
  • [Journal-full-title] Harefuah
  • [ISO-abbreviation] Harefuah
  • [Language] heb
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Israel
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents
  • [Number-of-references] 40
  •  go-up   go-down


24. Raina K, Blouin MJ, Singh RP, Majeed N, Deep G, Varghese L, Glodé LM, Greenberg NM, Hwang D, Cohen P, Pollak MN, Agarwal R: Dietary feeding of silibinin inhibits prostate tumor growth and progression in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2007 Nov 15;67(22):11083-91
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.
  • Herein, for the first time, we evaluated the chemopreventive efficacy of dietary silibinin against prostate cancer (PCa) growth and progression in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice from two different genetic backgrounds [C57BL/6 (TRAMP) x FVB; C57BL/6 (TRAMP) x C57BL/6].
  • Silibinin-fed groups had a lower tumor grade and higher incidence of prostatic intraepithelial neoplasia (PIN) at the expense of a strong decrease in adenocarcinoma incidence.
  • Prostate tissue showed a 47% (P < 0.001) decrease in proliferating cell nuclear antigen (PCNA)-positive cells and an approximately 7-fold (P < 0.001) increase in apoptotic cells at the highest silibinin dose.
  • As potential mechanisms of silibinin efficacy, an approximately 50% (P < 0.05) decrease in insulin-like growth factor (IGF) receptor type I beta and an approximately 13-fold (P < 0.001) increase in IGF-binding protein 3 (IGFBP-3) protein levels were also observed.
  • Together, these findings suggest that oral silibinin blocks PCa growth and progression at PIN stage in TRAMP mice via modulation of tumor IGF-IGFBP-3 axis and cell cycle regulation, and therefore it has practical and translational potential in suppressing growth and neoplastic conversion of PIN to PCa in humans.
  • [MeSH-major] Adenocarcinoma / prevention & control. Adenocarcinoma / therapy. Prostatic Neoplasms / prevention & control. Prostatic Neoplasms / therapy
  • [MeSH-minor] Animals. Anticarcinogenic Agents / therapeutic use. Antioxidants / therapeutic use. Disease Models, Animal. Disease Progression. Male. Mice. Mice, Inbred C57BL. Mice, Transgenic. Phosphorylation. Prostate / drug effects. Silymarin / therapeutic use. Species Specificity

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • 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 = 18006855.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA100938; United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R01 CA104286; United States / NCI NIH HHS / CA / R01 CA84296
  • [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 / Anticarcinogenic Agents; 0 / Antioxidants; 0 / Silymarin; 4RKY41TBTF / silybin
  •  go-up   go-down


25. Sargeant AM, Rengel RC, Kulp SK, Klein RD, Clinton SK, Wang YC, Chen CS: OSU-HDAC42, a histone deacetylase inhibitor, blocks prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2008 May 15;68(10):3999-4009
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Based on a series of pilot studies, an AIN-76A diet was formulated containing 208 ppm OSU-HDAC42, which was estimated to deliver approximately 25 mg/kg of drug per day to each mouse and found to cause a suppression of PC-3 xenograft tumor growth equivalent to that achieved by gavage administration of a similar dose.
  • At 6 weeks of age, TRAMP mice received this drug-containing or control diet for 4 or 18 weeks and were evaluated for prostatic intraepithelial neoplasia (PIN) and carcinoma development, respectively.
  • OSU-HDAC42 not only decreased the severity of PIN and completely prevented its progression to poorly differentiated carcinoma (74% incidence in controls versus none in drug-treated mice), but also shifted tumorigenesis to a more differentiated phenotype, suppressing absolute and relative urogenital tract weights by 86% and 85%, respectively, at 24 weeks of age.
  • With the exception of completely reversible hematologic alterations and testicular degeneration, no significant changes in body weight or other indicators of general health were observed in drug-treated mice.
  • [MeSH-major] Adenocarcinoma / drug therapy. Enzyme Inhibitors / pharmacology. Histone Deacetylase Inhibitors. Phenylbutyrates / pharmacology. Prostatic Neoplasms / drug therapy

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. Vorinostat .
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18483287.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA112250
  • [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 / Antineoplastic Agents; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / OSU-HDAC42 compound; 0 / Phenylbutyrates; 58IFB293JI / vorinostat
  •  go-up   go-down


26. Quader ST, Bello-DeOcampo D, Williams DE, Kleinman HK, Webber MM: Evaluation of the chemopreventive potential of retinoids using a novel in vitro human prostate carcinogenesis model. Mutat Res; 2001 Sep 20;496(1-2):153-61
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The prevalence of prostatic intraepithelial neoplasia (PIN) and latent prostatic carcinoma, representing multiple steps in carcinogenesis and progression to invasive carcinoma, makes them relevant targets for prevention.
  • Both RA and 4-HPR inhibited anchorage-dependent growth of all cell lines and anchorage-independent growth of WPE1-NB14 and WPE1-NB11 cells, in a dose-dependent manner, however, 10 times more RA than 4-HPR was required to produce the same effect.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Prostatic Neoplasms / drug therapy. Retinoids / therapeutic use
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Transformed / drug effects. Cell Transformation, Neoplastic. Chemoprevention. Dose-Response Relationship, Drug. Epithelial Cells / drug effects. Humans. Male. Methylnitrosourea / pharmacology. Mice. Mice, Nude. Mutagenicity Tests. Neoplasm Transplantation. Phenotype. Tumor Cells, Cultured / drug effects

  • MedlinePlus Health Information. consumer health - Prostate Cancer.
  • COS Scholar Universe. author profiles.
  • American Type Culture Collection. culture/stock collections - ATCC CRL-11609 (subscription/membership/fee required).
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 11551491.001).
  • [ISSN] 0027-5107
  • [Journal-full-title] Mutation research
  • [ISO-abbreviation] Mutat. Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / Retinoids; 684-93-5 / Methylnitrosourea
  •  go-up   go-down


27. 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
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] 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 .
  • [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


28. Chang SS, Reuter VE, Heston WD, Hutchinson B, Grauer LS, Gaudin PB: Short term neoadjuvant androgen deprivation therapy does not affect prostate specific membrane antigen expression in prostate tissues. Cancer; 2000 Jan 15;88(2):407-15
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] Short term neoadjuvant androgen deprivation therapy does not affect prostate specific membrane antigen expression in prostate tissues.
  • METHODS: The study included patients with clinically localized prostate carcinoma who were prospectively randomized into 1 of 2 treatment groups: 3 months of neoadjuvant androgen deprivation therapy followed by radical prostatectomy (ADT/RP), or radical prostatectomy (RP) alone.
  • The authors recorded the staining intensity and the percentage of positive cells stained in benign epithelium, high grade prostatic intraepithelial neoplasia (PIN), and prostate carcinoma.
  • They compared the results of 7E11 with those of PM2J004.5 in benign epithelium, high grade prostate, and carcinoma and also compared the results between the two treatment groups (ADT/RP vs. RP alone).
  • RESULTS: Both anti-PSMA mAbs stained benign secretory-acinar epithelium, high grade PIN, and prostate carcinoma.
  • In both treatment groups, PM2J004.5 reacted with a significantly greater percentage of cells (P < 0.001) and with significantly greater intensity (P < 0.001) compared with 7E11 in benign epithelium and prostate carcinoma.
  • With both anti-PSMA mAbs, the percentage of cells stained and the intensity of staining in high grade PIN was similar to that in prostate carcinoma.
  • In the group that received RP alone, the percentage of cells stained and the intensity of staining with 7E11 were significantly greater in high grade PIN and prostate carcinoma compared with benign epithelium (P < 0.001), and the intensity of staining with the PM2J004.5 was significantly greater in high grade PIN and prostate carcinoma compared with benign epithelium (P < 0.001).
  • PSMA staining did not correlate with either Gleason score (in the group that received RP alone) or pathologic stage (in both the RP-alone and ADT/RP groups) and did not differ between the two treatment groups.
  • CONCLUSIONS: Short term neoadjuvant ADT does not affect PSMA expression in benign prostate secretory-acinar epithelium, high grade PIN, or prostate carcinoma.
  • Prostate carcinoma and high grade PIN express significantly higher levels of PSMA than benign prostate secretory-acinar epithelium.
  • Compared with 7E11, the PM2J004.5 anti-PSMA mAb is a more sensitive immunohistochemical marker of prostate carcinoma in formalin fixed, paraffin embedded tissue.
  • [MeSH-major] Androgen Antagonists / pharmacology. Antigens, Surface. Carboxypeptidases / biosynthesis. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Aged. Antibodies, Monoclonal. Glutamate Carboxypeptidase II. Humans. Immunohistochemistry. Male. Middle Aged. Neoadjuvant Therapy. Prostatectomy. Sensitivity and Specificity

  • 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
  • [Copyright] Copyright 2000 American Cancer Society.
  • (PMID = 10640975.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 47650
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antibodies, Monoclonal; 0 / Antigens, Surface; EC 3.4.- / Carboxypeptidases; EC 3.4.17.21 / Glutamate Carboxypeptidase II; EC 3.4.17.21 / glutamate carboxypeptidase II, human
  •  go-up   go-down


29. 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
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.
  • 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 .
  • [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


30. Ibaragi S, Yoshioka N, Li S, Hu MG, Hirukawa S, Sadow PM, Hu GF: Neamine inhibits prostate cancer growth by suppressing angiogenin-mediated rRNA transcription. Clin Cancer Res; 2009 Mar 15;15(6):1981-8
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.
  • It was then examined in the murine prostate-restricted AKT transgenic mice that develop prostate intraepithelial neoplasia (PIN) owing to AKT transgene overexpression.
  • Neamine also prevents AKT-induced PIN formation as well as reverses fully developed PIN in murine prostate-restricted AKT mice, accompanied by a decrease in rRNA synthesis, cell proliferation, and angiogenesis and an increase in prostate epithelial cell apoptosis.
  • CONCLUSION: We confirmed that ANG is a molecular target for cancer drug development and that blocking nuclear translocation of ANG is an effective means to inhibit its activity.

  • 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
  • [Cites] Proc Natl Acad Sci U S A. 1995 Jan 17;92(2):442-6 [7831307.001]
  • [Cites] Science. 1949 Mar 25;109(2830):305-7 [17782716.001]
  • [Cites] J Cell Biochem. 2000 Jan;76(3):452-62 [10649442.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jan 27;267(3):719-25 [10673358.001]
  • [Cites] Cell. 2000 Feb 18;100(4):387-90 [10693755.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):136-41 [11134523.001]
  • [Cites] Am J Pathol. 2001 Aug;159(2):431-7 [11485901.001]
  • [Cites] Trends Mol Med. 2001 Nov;7(11):482-4 [11689313.001]
  • [Cites] Clin Cancer Res. 2001 Nov;7(11):3598-605 [11705882.001]
  • [Cites] Int J Cancer. 2002 Apr 20;98(6):923-9 [11948474.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Jun 7;294(2):287-92 [12051708.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):10066-71 [12118120.001]
  • [Cites] Biochemistry. 2003 Jan 14;42(1):121-8 [12515546.001]
  • [Cites] Nat Rev Cancer. 2003 Mar;3(3):179-92 [12612653.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Jun 24;100(13):7841-6 [12799464.001]
  • [Cites] Biochemistry. 1985 Sep 24;24(20):5494-9 [2866795.001]
  • [Cites] Antimicrob Agents Chemother. 1986 Sep;30(3):395-7 [3777905.001]
  • [Cites] Science. 1987 Jul 17;237(4812):280-2 [2440105.001]
  • [Cites] Antimicrob Agents Chemother. 1987 Apr;31(4):570-4 [3606061.001]
  • [Cites] Biochemistry. 1987 Aug 11;26(16):5141-6 [3663649.001]
  • [Cites] Exp Cell Res. 1989 Sep;184(1):131-7 [2477263.001]
  • [Cites] Pathol Res Pract. 1989 Dec;185(6):878-85 [2616372.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Mar 1;91(5):1677-81 [8127865.001]
  • [Cites] Cancer Res. 1994 Sep 1;54(17):4576-9 [8062244.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Nov 22;91(24):11477-81 [7972087.001]
  • [Cites] EMBO J. 1997 Jun 16;16(12):3693-704 [9218810.001]
  • [Cites] Biochem Biophys Res Commun. 1997 Sep 18;238(2):305-12 [9299500.001]
  • [Cites] Nat Genet. 1998 Aug;19(4):348-55 [9697695.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):9791-5 [9707554.001]
  • [Cites] Cancer. 1999 Jul 15;86(2):316-24 [10421268.001]
  • [Cites] Oncogene. 2005 Jan 13;24(3):445-56 [15558023.001]
  • [Cites] Cancer Res. 2005 Feb 15;65(4):1352-60 [15735021.001]
  • [Cites] 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] Dev Dyn. 2006 Jul;235(7):1984-93 [16673408.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14519-24 [16971483.001]
  • [Cites] Cancer Res. 1996 Jun 15;56(12):2703-6 [8665497.001]
  • (PMID = 19276260.001).
  • [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 / CA105241-04; United States / NCI NIH HHS / CA / R01 CA105241; United States / NCI NIH HHS / CA / R01 CA105241-04; United States / NCI NIH HHS / CA / R01CA105241
  • [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 / Angiogenesis Inhibitors; 0 / Antineoplastic Agents; 0 / RNA, Ribosomal; 4BOC774388 / Framycetin; 5981U00LY0 / neamine; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.1.27.- / angiogenin; EC 3.1.27.5 / Ribonuclease, Pancreatic
  • [Other-IDs] NLM/ NIHMS98288; NLM/ PMC2670466
  •  go-up   go-down


31. 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
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] 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