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1. 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
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  • [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.
  • However, and unlike humans where prostate tumorigenesis likely evolves over decades, disease progression in the constitutively Pten deficient mouse prostate is relatively rapid, culminating in invasive cancer within several weeks post-puberty.
  • 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.
  • [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

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  • [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
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2. 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
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  • [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;.
  • 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.
  • [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

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  • (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
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3. Wislez M, Spencer ML, Izzo JG, Juroske DM, Balhara K, Cody DD, Price RE, Hittelman WN, Wistuba II, Kurie JM: Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras. Cancer Res; 2005 Apr 15;65(8):3226-35
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  • [Title] Inhibition of mammalian target of rapamycin reverses alveolar epithelial neoplasia induced by oncogenic K-ras.
  • mTOR inhibition in K-ras(LA1) mice by treatment with the rapamycin analogue CCI-779 reduced the size and number of early epithelial neoplastic lesions (atypical alveolar hyperplasia and adenomas) and induced apoptosis of intraepithelial macrophages.
  • LKR-13, a lung adenocarcinoma cell line derived from K-ras(LA1) mice, was resistant to treatment with CCI-779 in vitro.
  • However, LKR-13 cells grown as syngeneic tumors recruited macrophages, and those tumors regressed in response to treatment with CCI-779.
  • [MeSH-minor] Adenoma / drug therapy. Adenoma / enzymology. Adenoma / genetics. Adenoma / pathology. Animals. Cell Line, Tumor. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / metabolism. Disease Progression. Enzyme Activation. Hyperplasia. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / enzymology. Macrophages, Alveolar / pathology. Mice. Mutation. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. Ribosomal Protein S6 Kinases / biosynthesis. TOR Serine-Threonine Kinases

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  • (PMID = 15833854.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / R01 CA105155
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Proto-Oncogene Proteins; 624KN6GM2T / temsirolimus; EC 2.7.- / Protein Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; W36ZG6FT64 / Sirolimus
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4. 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
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  • [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.
  • 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.
  • 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.
  • The drug was well tolerated.
  • [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

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  • [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
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5. 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
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  • [Title] Dietary feeding of silibinin inhibits prostate tumor growth and progression in transgenic adenocarcinoma of the mouse prostate model.
  • 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.
  • [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

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  • (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
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6. Huh JI, Calvo A, Charles R, Green JE: Distinct tumor stage-specific inhibitory effects of 2-methoxyestradiol in a breast cancer mouse model associated with Id-1 expression. Cancer Res; 2006 Apr 1;66(7):3495-503
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  • [Title] Distinct tumor stage-specific inhibitory effects of 2-methoxyestradiol in a breast cancer mouse model associated with Id-1 expression.
  • We have analyzed the tumor stage-specific effects of 2ME(2) in the C3(1)/Tag transgenic mouse model for breast cancer, which spontaneously develops estrogen receptor-negative mammary tumors following a predictable progression of lesion formation.
  • When given either as a therapeutic agent in established tumors (late intervention study) or in mice with pre-invasive mammary lesions (early intervention study), tumor growth was reduced by 60% compared with untreated controls and was associated with an induction of apoptosis.
  • In a prevention study, a significant reduction in mammary intraepithelial neoplasia (MIN) lesions was observed in animals beginning treatment at 6 weeks of age, before the appearance of histopathologic abnormalities.
  • [MeSH-major] Estradiol / analogs & derivatives. Inhibitor of Differentiation Protein 1 / biosynthesis. Mammary Neoplasms, Experimental / drug therapy. Mammary Neoplasms, Experimental / metabolism
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Growth Processes / drug effects. Disease Models, Animal. Dose-Response Relationship, Drug. Down-Regulation / drug effects. Endothelial Cells / drug effects. Female. Mice. Mice, Transgenic. Neoplasm Staging

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  • (PMID = 16585173.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Idb1 protein, mouse; 0 / Inhibitor of Differentiation Protein 1; 4TI98Z838E / Estradiol; 6I2QW73SR5 / 2-methoxyestradiol
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7. Khor TO, Yu S, Barve A, Hao X, Hong JL, Lin W, Foster B, Huang MT, Newmark HL, Kong AN: Dietary feeding of dibenzoylmethane inhibits prostate cancer in transgenic adenocarcinoma of the mouse prostate model. Cancer Res; 2009 Sep 1;69(17):7096-102
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  • [Title] Dietary feeding of dibenzoylmethane inhibits prostate cancer in transgenic adenocarcinoma of the mouse prostate model.
  • Our results show that DBM-fed groups had a lower incidence of palpable tumor and high-grade prostatic intraepithelial neoplasia.


8. Ahmad I, Sansom OJ, Leung HY: Advances in mouse models of prostate cancer. Expert Rev Mol Med; 2008 Jun 09;10:e16
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  • [Title] Advances in mouse models of prostate cancer.
  • Advances in science and technology have allowed us to manipulate the mouse genome and analyse the effect of specific genetic alterations on the development of prostate cancer in vivo.
  • The current mouse models utilise knockout, knock-in or conditional regulation of expression using Cre-loxP technology.
  • 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.
  • Currently the PB-Cre4 x PTEN(loxP/loxP) mouse is the only model that spans the entire continuum from initiation to local invasion and metastasis.
  • Such mouse models increase our understanding of the disease process and provide targets for novel therapeutic approaches.
  • [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

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  • (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
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9. 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
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  • [Title] Adenocarcina of the mouse prostate growth inhibition by celecoxib: downregulation of transcription factors involved in COX-2 inhibition.
  • 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).
  • In this study, we examined a dose-dependent effect of a cyclooxygenase-2 (COX-2) inhibitor, celecoxib against transgenic adenocarcinoma of the mouse prostate.
  • METHODS: Efficacy of four different doses in parts per million of celecoxib, such as 200 ppm, 400 ppm, 600 ppm, and 1,000 ppm representing very low, moderate, and high doses, respectively were tested against adenocarcinoma of the mouse prostate using a transgenic adenocarcinoma of the mouse prostate (TRAMP) model assay.
  • 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

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  • [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
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10. Ghosh R, Graham H, Rivas P, Tan XJ, Crosby K, Bhaskaran S, Schoolfield J, Banu J, Fernandes G, Yeh IT, Kumar AP: Phellodendron amurense bark extract prevents progression of prostate tumors in transgenic adenocarcinoma of mouse prostate: potential for prostate cancer management. Anticancer Res; 2010 Mar;30(3):857-65
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  • [Title] Phellodendron amurense bark extract prevents progression of prostate tumors in transgenic adenocarcinoma of mouse prostate: potential for prostate cancer management.
  • Previous studies from our laboratory show that Nexrutine (bark extract from Phellodendron amurense) prevents prostate tumor development when given prior to the development of high-grade prostatic intraepithelial neoplasia in the transgenic adenocarcinoma of mouse prostate (TRAMP) model.
  • Our data indicate that Nexrutine inhibited progression of prostate tumors that was correlated with tissue levels of transcription factors nuclear factor kappa B, cyclic-AMP response element-binding protein and phosphorylated CREB.
  • Nexrutine treatment also significantly (p=0.005) inhibited invasion of androgen-independent prostate cancer cells.
  • [MeSH-major] Adenocarcinoma / drug therapy. Plant Extracts / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Bone Resorption / pathology. Cell Growth Processes / drug effects. Disease Progression. Male. Matrix Metalloproteinase 2 / biosynthesis. Matrix Metalloproteinase 3 / biosynthesis. Mice. Mice, Transgenic. Neoplasm Invasiveness. Neoplasm Metastasis. Phellodendron / chemistry. Plant Bark / chemistry. Proto-Oncogene Proteins c-bcl-2 / metabolism. bcl-2-Associated X Protein / metabolism

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  • (PMID = 20393007.001).
  • [ISSN] 1791-7530
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 98744; United States / NCI NIH HHS / CA / P30 CA54174
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Bax protein, mouse; 0 / Nexrutine; 0 / Plant Extracts; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.24 / Matrix Metalloproteinase 2
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11. 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
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  • [Title] OSU-HDAC42, a histone deacetylase inhibitor, blocks prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate model.
  • Here, we examined the effect of dietary administration of OSU-HDAC42, a novel HDAC inhibitor, on prostate tumor progression in the transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • 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

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  • (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
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12. Namba R, Young LJ, Maglione JE, McGoldrick ET, Liu S, Wurz GT, DeGregorio MW, Borowsky AD, MacLeod CL, Cardiff RD, Gregg JP: Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ. Breast Cancer Res; 2005;7(6):R881-9
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  • [Title] Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ.
  • DCIS accounts for nearly 20% of newly diagnosed breast cancer, but the lack of experimentally amenable in vivo DCIS models hinders the development of treatment strategies.
  • Here, we demonstrate the utility of a mouse transplantation model of DCIS for chemoprevention studies using selective estrogen receptor modulators (SERMs).
  • This model consists of a set of serially transplanted lines of genetically engineered mouse mammary intraepithelial neoplasia (MIN) outgrowth (MIN-O) tissue that have stable characteristics.
  • METHODS: The estrogen receptor (ER) status and ovarian-hormone-dependence of the mouse MIN outgrowth tissue were determined by immunohistochemistry and ovarian ablation.
  • Likewise, tamoxifen and ospemifene treatments decreased the MIN growth and tumor incidence in comparison with the control (P < 0.01).
  • Between the two SERM treatment groups, there were no statistically significant differences in MIN-O size, tumor latency, or proliferation rate.
  • In contrast, the ospemifene treatment significantly increased ER levels while tamoxifen significantly decreased them.
  • CONCLUSION: Tamoxifen and ospemifene inhibit the growth of premalignant mammary lesions and the progression to invasive carcinoma in a transplantable mouse model of DCIS.
  • These data demonstrate the value of this model system for preclinical testing of antiestrogen or other therapies designed to prevent or delay the malignant transformation of premalignant mammary lesions in chemoprevention.

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  • [Cites] Endocrinology. 2000 Feb;141(2):809-20 [10650964.001]
  • [Cites] J Clin Oncol. 1999 May;17(5):1474-81 [10334533.001]
  • [Cites] Oncogene. 2000 Feb 21;19(8):968-88 [10713680.001]
  • [Cites] J Steroid Biochem Mol Biol. 2001 Jun;77(4-5):271-9 [11457665.001]
  • [Cites] Arch Toxicol. 2001 Aug;75(6):375-80 [11570696.001]
  • [Cites] Cancer Res. 2001 Nov 15;61(22):8298-305 [11719463.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6967-72 [12011455.001]
  • [Cites] Cancer Res. 2002 May 15;62(10):2798-805 [12019156.001]
  • [Cites] Lancet. 2005 Jan 1-7;365(9453):60-2 [15639680.001]
  • [Cites] Clin Cancer Res. 2005 Jan 15;11(2 Pt 2):951s-8s [15701892.001]
  • [Cites] J Clin Oncol. 2005 Apr 10;23(11):2469-76 [15753463.001]
  • [Cites] Cancer Res. 2005 Apr 15;65(8):3493-6 [15833886.001]
  • [Cites] Clin Breast Cancer. 2005 Apr;6(1):27-37 [15899070.001]
  • [Cites] Oncogene. 2005 Jun 16;24(26):4220-31 [15824740.001]
  • [Cites] Breast Cancer Res Treat. 2003 Mar;78(1):1-6 [12611451.001]
  • [Cites] Int J Cancer. 2003 Jun 20;105(3):384-9 [12704673.001]
  • [Cites] Cancer Res. 2003 May 15;63(10):2425-33 [12750262.001]
  • [Cites] Menopause. 2003 Sep-Oct;10(5):433-9 [14501605.001]
  • [Cites] Crit Rev Oncol Hematol. 2002 Jul;43(1):63-76 [12098608.001]
  • [Cites] Am J Pathol. 2002 Sep;161(3):1087-97 [12213737.001]
  • [Cites] Maturitas. 2002 Nov 20;43(3):207-14 [12443837.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):951-6 [12459733.001]
  • [Cites] Am J Pathol. 2003 Nov;163(5):2113-26 [14578209.001]
  • [Cites] Surg Oncol. 2003 Dec;12(4):213-9 [14998562.001]
  • [Cites] Mol Cancer Ther. 2004 Aug;3(8):941-53 [15299077.001]
  • [Cites] Mol Cancer Res. 2004 Aug;2(8):453-63 [15328372.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1558-68 [15466970.001]
  • [Cites] J Natl Cancer Inst. 1976 Aug;57(2):331-7 [826649.001]
  • [Cites] J Clin Oncol. 1986 Sep;4(9):1326-30 [3528402.001]
  • [Cites] Science. 1987 Jan 9;235(4785):177-82 [3798106.001]
  • [Cites] Breast Cancer Res Treat. 1997 Jul;44(3):201-10 [9266099.001]
  • [Cites] Lancet. 1998 May 16;351(9114):1451-67 [9605801.001]
  • [Cites] J Chromatogr B Biomed Sci Appl. 1999 Mar 5;724(1):163-71 [10202969.001]
  • [Cites] Cancer Res. 2000 Jan 15;60(2):273-5 [10667575.001]
  • (PMID = 16280035.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA89140-01; United States / NCI NIH HHS / CA / R01 CA089140; United States / NCRR NIH HHS / RR / U42 RR014905; United States / NCRR NIH HHS / RR / U42RR14905; United States / NCI NIH HHS / CA / R01CA81376
  • [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] England
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; B0P231ILBK / Ospemifene
  • [Other-IDs] NLM/ PMC1410776
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13. Singh RP, Raina K, Sharma G, Agarwal R: Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice. Clin Cancer Res; 2008 Dec 1;14(23):7773-80
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  • [Title] Silibinin inhibits established prostate tumor growth, progression, invasion, and metastasis and suppresses tumor angiogenesis and epithelial-mesenchymal transition in transgenic adenocarcinoma of the mouse prostate model mice.
  • Herein, for the first time, we investigated the effect and associated mechanisms of silibinin phosphatidylcholine (silybin-phytosome) on established prostate tumors in transgenic adenocarcinoma of the mouse prostate (TRAMP) model.
  • RESULTS: Dietary silibinin inhibited the growth of prostate tumors (up to 60%, P < 0.001) and suppressed tumor progression from prostatic intraepithelial neoplasia to differentiated adenocarcinoma and poorly differentiated adenocarcinoma, with a complete absence of poorly differentiated adenocarcinoma at higher doses.
  • CONCLUSIONS: Overall, silibinin treatment of TRAMP mice bearing prostate tumor inhibited tumor growth, progression, local invasion, and distant metastasis involving suppression of tumor angiogenesis and epithelial-mesenchymal transition.

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  • [Cites] Cancer Res. 2007 Nov 15;67(22):11083-91 [18006855.001]
  • [Cites] Semin Cancer Biol. 2007 Oct;17(5):403-10 [17574861.001]
  • [Cites] Cancer Invest. 2008 Feb;26(1):104-8 [18181052.001]
  • [Cites] Cancer Res. 2008 Mar 15;68(6):2043-50 [18339887.001]
  • [Cites] Biochim Biophys Acta. 2008 Apr;1785(2):156-81 [18166163.001]
  • [Cites] Carcinogenesis. 2007 Dec;28(12):2567-74 [17916909.001]
  • [Cites] Nat Cell Biol. 2000 Feb;2(2):84-9 [10655587.001]
  • [Cites] Cancer Res. 2000 Oct 15;60(20):5617-20 [11059749.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2736-43 [11289156.001]
  • [Cites] BioDrugs. 2001;15(7):465-89 [11520257.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3063-9 [12036915.001]
  • [Cites] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386.001]
  • [Cites] Prostate. 2002 Sep 1;52(4):253-63 [12210485.001]
  • [Cites] Mol Cancer Ther. 2002 May;1(7):525-32 [12479270.001]
  • [Cites] Urol Res. 2003 Feb;30(6):347-55 [12599013.001]
  • [Cites] Prostate. 2003 May 15;55(3):219-37 [12692788.001]
  • [Cites] Cancer Res. 2004 Mar 15;64(6):2270-305 [15026373.001]
  • [Cites] J Cell Biol. 1991 Apr;113(1):173-85 [2007622.001]
  • [Cites] Mol Endocrinol. 1994 Feb;8(2):230-9 [8170479.001]
  • [Cites] Cancer Res. 1996 Sep 15;56(18):4096-102 [8797572.001]
  • [Cites] Toxicol Pathol. 1996 Jul-Aug;24(4):502-4 [8864193.001]
  • [Cites] J Cell Biochem Suppl. 1996;25:156-64 [9027613.001]
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4687-91 [9354422.001]
  • [Cites] Cancer Res. 1998 May 1;58(9):1920-9 [9581834.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7490-5 [10377442.001]
  • [Cites] Oncogene. 2005 Feb 10;24(7):1188-202 [15558015.001]
  • [Cites] Nat Rev Cancer. 2005 Jun;5(6):436-46 [15928674.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):1053-69 [16205633.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 Feb;7(2):131-42 [16493418.001]
  • [Cites] Nat Rev Cancer. 2006 Mar;6(3):227-39 [16498445.001]
  • [Cites] Nat Rev Mol Cell Biol. 2006 May;7(5):359-71 [16633338.001]
  • [Cites] Mol Carcinog. 2006 Jun;45(6):436-42 [16637061.001]
  • [Cites] Endothelium. 2006 Mar-Apr;13(2):63-9 [16728325.001]
  • [Cites] J Natl Cancer Inst. 2006 Jun 21;98(12):846-55 [16788158.001]
  • [Cites] Endocr Relat Cancer. 2006 Sep;13(3):751-78 [16954429.001]
  • [Cites] Invest New Drugs. 2007 Apr;25(2):139-46 [17077998.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Nat Rev Cancer. 2007 Jun;7(6):415-28 [17508028.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5789-97 [17575146.001]
  • [Cites] Urol Oncol. 2007 Sep-Oct;25(5):413-9 [17826663.001]
  • [CommentIn] Clin Cancer Res. 2008 Dec 1;14(23):7581-2 [19047081.001]
  • (PMID = 19047104.001).
  • [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 / CA102514-05; United States / NCI NIH HHS / CA / R01 CA102514; United States / NCI NIH HHS / CA / R01 CA102514-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Cadherins; 0 / Silymarin; 0 / Vimentin; 0 / silybin-phytosome; EC 3.4.24.- / Matrix Metalloproteinases
  • [Other-IDs] NLM/ NIHMS82719; NLM/ PMC2639624
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14. Morales PR, Dillehay DL, Moody SJ, Pallas DC, Pruett S, Allgood JC, Symolon H, Merrill AH Jr: Safingol toxicology after oral administration to TRAMP mice: demonstration of safingol uptake and metabolism by N-acylation and N-methylation. Drug Chem Toxicol; 2007;30(3):197-216
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  • To determine if safingol can be absorbed orally and if it affects prostate cancer in a mouse strain used in prostate cancer studies, safingol was fed to TRAMP (transgenic adenocarcinoma of mouse prostate) mice for 2 weeks at 0.0125% to 0.1% w/w of the diet.
  • Analysis of safingol and safingol metabolites in blood and tissues by liquid chromatography electrospray ionization tandem mass spectrometry revealed uptake in tissue and extensive conversion of safingol to N-acyl species (comparable to natural "ceramides") and mono-, di-, and tri-N-methyl metabolites that have not been observed previously.
  • Safingol did not inhibit the prostate pre-neoplastic lesion (prostate intraepithelial neoplasia) in TRAMP mice; however, additional studies at lower dosages for longer time were not pursued due to host toxicity.
  • Safingol and its N-methyl metabolites were cytotoxic to both a human prostate cell line (DU145) and mouse BALB 3T3 cells; therefore, the host and potential antitumor toxicity may be due to multiple molecular species of safingol.

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  • (PMID = 17613006.001).
  • [ISSN] 0148-0545
  • [Journal-full-title] Drug and chemical toxicology
  • [ISO-abbreviation] Drug Chem Toxicol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA057327; United States / NCI NIH HHS / CA / U19 CA087525; United States / NCI NIH HHS / CA / CA57327; United States / NCI NIH HHS / CA / CA87525
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; NGZ37HRE42 / Sphingosine; OWA98U788S / safingol
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15. van der Burg SH, Kwappenberg KM, O'Neill T, Brandt RM, Melief CJ, Hickling JK, Offringa R: Pre-clinical safety and efficacy of TA-CIN, a recombinant HPV16 L2E6E7 fusion protein vaccine, in homologous and heterologous prime-boost regimens. Vaccine; 2001 Jun 14;19(27):3652-60
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  • Human papillomavirus (HPV) E6 and E7 oncoproteins are attractive targets for T-cell-based immunotherapy of cervical intraepithelial neoplasia (CIN) and cancer.
  • A newly designed vaccine, comprising the HPV16 L2, E6 and E7 as a single fusion protein (TA-CIN), was shown to elicit HPV16-specific CTL, T-helper cells and antibodies in a pre-clinical mouse model.
  • [MeSH-minor] Animals. Antigens, Neoplasm / administration & dosage. Antigens, Neoplasm / immunology. Antigens, Neoplasm / therapeutic use. Antigens, Neoplasm / toxicity. Antigens, Viral / administration & dosage. Antigens, Viral / immunology. Antigens, Viral / therapeutic use. Antigens, Viral / toxicity. Cell Line. Cell Line, Transformed. Cervical Intraepithelial Neoplasia / prevention & control. Cervical Intraepithelial Neoplasia / therapy. Cervical Intraepithelial Neoplasia / virology. Drug Evaluation, Preclinical. Immunotherapy. Mice. Mice, Inbred C57BL. Papillomavirus E7 Proteins. Vaccines, Acellular / administration & dosage. Vaccines, Acellular / immunology. Vaccines, Acellular / therapeutic use. Vaccines, Acellular / toxicity

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  • (PMID = 11395199.001).
  • [ISSN] 0264-410X
  • [Journal-full-title] Vaccine
  • [ISO-abbreviation] Vaccine
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Antigens, Viral; 0 / Cancer Vaccines; 0 / Capsid Proteins; 0 / L2 protein, Human papillomavirus type 16; 0 / Oncogene Proteins, Viral; 0 / Papillomavirus E7 Proteins; 0 / Recombinant Fusion Proteins; 0 / Vaccines, Acellular; 0 / oncogene protein E7, Human papillomavirus type 16
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16. Kladney RD, Cardiff RD, Kwiatkowski DJ, Chiang GG, Weber JD, Arbeit JM, Lu ZH: Tuberous sclerosis complex 1: an epithelial tumor suppressor essential to prevent spontaneous prostate cancer in aged mice. Cancer Res; 2010 Nov 1;70(21):8937-47
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  • Epithelial inactivation was not immediately tumorigenic, but Tsc1-deficient mice developed prostatic intraepithelial neoplasia (mPIN) in lateral and anterior prostates by 6 months of age, with increasing disease penetrance over time.
  • Lateral prostate lesions in 16- to 22-month-old mutant mice progressed to two types of more advanced lesions, adenomatous gland forming lesion (Type 1) and atypical glands embedded in massively expanded reactive stroma (Type 2).
  • Both Type 1 and Type 2 lesions contained multiple foci of microinvasive carcinoma.
  • Epithelial neoplastic and atypical stromal lesions persisted despite 4 weeks of RAD001 chemotherapy.
  • Thus, TSC1 inactivation distal to PI3K and AKT activation is sufficient to activate a molecular signaling cascade producing prostatic neoplasia and focal carcinogenesis.

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  • [Cites] Mol Cell Biol. 2002 Mar;22(5):1495-503 [11839815.001]
  • [Cites] Cancer Res. 2006 Nov 15;66(22):10683-90 [17108105.001]
  • [Cites] Toxicol Pathol. 2002 Mar-Apr;30(2):228-34 [11950166.001]
  • [Cites] Cancer Cell. 2007 Jun;11(6):555-69 [17560336.001]
  • [Cites] Am J Pathol. 2007 Aug;171(2):667-81 [17600126.001]
  • [Cites] Prostate. 2007 Dec 1;67(16):1740-50 [17929276.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Nov 6;104(45):17771-6 [17978178.001]
  • [Cites] Cancer Cell. 2007 Dec;12(6):559-71 [18068632.001]
  • [Cites] Cancer Res. 2008 Apr 1;68(7):2223-32 [18381428.001]
  • [Cites] Hum Mol Genet. 2008 Jul 1;17(13):2006-17 [18397877.001]
  • [Cites] BMC Cancer. 2008;8:163 [18538015.001]
  • [Cites] Genes Dev. 2008 Aug 15;22(16):2172-7 [18708577.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3065-74 [18725988.001]
  • [Cites] J Clin Invest. 2008 Sep;118(9):3051-64 [18725989.001]
  • [Cites] Br J Cancer. 2008 Oct 21;99(8):1296-301 [18854827.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Nov 11;105(45):17414-9 [18955708.001]
  • [Cites] Sci Signal. 2009;2(67):pe24 [19383975.001]
  • [Cites] J Pathol. 2009 Aug;218(4):505-13 [19402094.001]
  • [Cites] Clin Cancer Res. 2009 Oct 1;15(19):6008-17 [19789314.001]
  • [Cites] J Cell Sci. 2009 Oct 15;122(Pt 20):3589-94 [19812304.001]
  • [Cites] Semin Cell Dev Biol. 2010 Feb;21(1):33-9 [19896548.001]
  • [Cites] Cancer Res. 2010 Mar 15;70(6):2146-57 [20179189.001]
  • [Cites] Lymphat Res Biol. 2010 Mar;8(1):51-7 [20235887.001]
  • [Cites] Cancer Res. 2010 Apr 15;70(8):3287-98 [20388784.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):2999-3004 [12036903.001]
  • [Cites] Mol Cell. 2002 Jul;10(1):151-62 [12150915.001]
  • [Cites] Nat Cell Biol. 2002 Sep;4(9):648-57 [12172553.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Oct 15;99(21):13571-6 [12271141.001]
  • [Cites] Mol Cell. 2003 Jun;11(6):1457-66 [12820960.001]
  • [Cites] Genes Dev. 2003 Aug 1;17(15):1829-34 [12869586.001]
  • [Cites] Curr Biol. 2003 Aug 5;13(15):1259-68 [12906785.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):209-21 [14522255.001]
  • [Cites] J Clin Invest. 2003 Oct;112(8):1223-33 [14561707.001]
  • [Cites] Cell. 2003 Nov 26;115(5):577-90 [14651849.001]
  • [Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]
  • [Cites] J Urol. 1992 Dec;148(6):1932-6 [1433648.001]
  • [Cites] Cancer Res. 1999 Mar 15;59(6):1206-11 [10096549.001]
  • [Cites] J Clin Invest. 1999 Sep;104(6):687-95 [10491404.001]
  • [Cites] Cell. 2005 Apr 22;121(2):179-93 [15851026.001]
  • [Cites] Cancer Res. 2005 Jul 1;65(13):5730-9 [15994948.001]
  • [Cites] Genes Dev. 2005 Aug 1;19(15):1779-86 [16027168.001]
  • [Cites] Genes Dev. 2005 Aug 1;19(15):1773-8 [16027169.001]
  • [Cites] Cell. 2005 Dec 16;123(6):1001-11 [16360031.001]
  • [Cites] Mol Cancer. 2006;5:3 [16412252.001]
  • [Cites] J Biol Chem. 2006 Mar 31;281(13):8313-6 [16464865.001]
  • [Cites] Cancer Cell. 2006 May;9(5):367-78 [16697957.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Sep;169(2):128-37 [16938570.001]
  • [Cites] Int J Cancer. 2006 Oct 15;119(8):1858-62 [16721785.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14477-82 [16973750.001]
  • [Cites] Proc Natl Acad Sci U S A. 2002 Mar 5;99(5):2884-9 [11854455.001]
  • (PMID = 20940396.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA093373; United States / NCI NIH HHS / CA / P01 CA120964-01A1; United States / NCI NIH HHS / CA / R01 CA101012-01; United States / NCI NIH HHS / CA / CA120436-04; United States / NCI NIH HHS / CA / R01 CA120436; United States / NCI NIH HHS / CA / P01 CA120964; United States / NCI NIH HHS / CA / CA101012-01; United States / NCI NIH HHS / CA / CA120964-01A1; United States / NCI NIH HHS / CA / R01 CA120436-04; United States / NCI NIH HHS / CA / R01 CA101012; United States / NCI NIH HHS / CA / 1P01CA120964-01A1; United States / NCI NIH HHS / CA / R01 CA10101
  • [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 / Homeodomain Proteins; 0 / Multiprotein Complexes; 0 / Nkx3-1 protein, mouse; 0 / Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / mechanistic target of rapamycin complex 1; 0 / tuberous sclerosis complex 1 protein; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.137 / Phosphatidylinositol 3-Kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS277034; NLM/ PMC3064856
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17. Lee EC, Frolov A, Li R, Ayala G, Greenberg NM: Targeting Aurora kinases for the treatment of prostate cancer. Cancer Res; 2006 May 15;66(10):4996-5002
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  • [Title] Targeting Aurora kinases for the treatment of prostate cancer.
  • Here, we report that Aurora-A and Aurora-B are highly expressed in primary human and mouse prostate cancers and prostate cancer cell lines.
  • In clinical samples, levels of Aurora-A and Aurora-B were significantly elevated in prostatic intraepithelial neoplasia lesions and prostate tumors when compared with the non-neoplastic samples.
  • In addition, nuclear expression of Aurora-B in prostatic intraepithelial neoplasia lesions correlated with clinical staging of the tumor (rho = -0.4, P = 0.0474) whereas cytoplasmic expression in tumors correlated with seminal vesicle invasion (rho = 0.282, P = 0.0098).
  • When human PC3, LNCaP, and mouse C1A cells were treated with the potent Aurora kinase inhibitor VX680, which attenuates phosphorylation of histone H3, cancer cell survival was reduced.
  • VX680 could further reduce cell viability >2-fold when used in combination with the chemotherapy drug doxorubicin.
  • Our findings support a functional relationship between Aurora kinase expression and prostate cancer and the application of small-molecule inhibitors in therapeutic modalities.
  • [MeSH-major] Piperazines / pharmacology. Prostatic Neoplasms / drug therapy. Prostatic Neoplasms / enzymology. Protein Kinase Inhibitors / pharmacology. Protein-Serine-Threonine Kinases / antagonists & inhibitors

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  • (PMID = 16707419.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01-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 / Piperazines; 0 / Protein Kinase Inhibitors; 639089-54-6 / VX680; EC 2.7.11.1 / AURKB protein, human; EC 2.7.11.1 / Aurka protein, mouse; EC 2.7.11.1 / Aurkb protein, mouse; EC 2.7.11.1 / Aurora Kinase A; EC 2.7.11.1 / Aurora Kinase B; EC 2.7.11.1 / Aurora Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases
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18. Giraudo E, Inoue M, Hanahan D: An amino-bisphosphonate targets MMP-9-expressing macrophages and angiogenesis to impair cervical carcinogenesis. J Clin Invest; 2004 Sep;114(5):623-33
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  • A mouse model involving the human papillomavirus type-16 oncogenes develops cervical cancers by lesional stages analogous to those in humans.
  • In this study the angiogenic phenotype was characterized, revealing intense angiogenesis in high-grade cervical intraepithelial neoplasias (CIN-3) and carcinomas.
  • ZA therapy increased neoplastic epithelial and endothelial cell apoptosis without affecting hyperproliferation, indicating that ZA was not antimitotic.
  • Given its track record in clinical use with limited toxicity, ZA holds promise as an "unconventional" MMP-9 inhibitor for antiangiogenic therapy of cervical cancer and potentially for additional cancers and other diseases where MMP-9 expression by infiltrating macrophages is evident.
  • [MeSH-major] Cervical Intraepithelial Neoplasia / blood supply. Diphosphonates / pharmacology. Imidazoles / pharmacology. Macrophages / drug effects. Matrix Metalloproteinase Inhibitors. Neovascularization, Pathologic / drug therapy. Uterine Cervical Neoplasms / blood supply
  • [MeSH-minor] Angiogenesis Inhibitors / pharmacology. Animals. Cell Movement / drug effects. Enzyme Activation / drug effects. Female. Humans. Macrophage Activation / drug effects. Matrix Metalloproteinase 9 / metabolism. Mice. Mice, Transgenic. Vascular Endothelial Growth Factors / metabolism

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  • [Cites] Cancer Res. 2000 Mar 1;60(5):1267-75 [10728686.001]
  • [Cites] Cancer Res. 2003 Oct 1;63(19):6537-42 [14559848.001]
  • [Cites] Cancer Res. 2000 Jun 1;60(11):2949-54 [10850442.001]
  • [Cites] Cancer. 2000 Jun 15;88(12 Suppl):2961-78 [10898340.001]
  • [Cites] Nat Cell Biol. 2000 Oct;2(10):737-44 [11025665.001]
  • [Cites] Cell. 2000 Oct 27;103(3):481-90 [11081634.001]
  • [Cites] Bone. 2001 May;28(5):465-73 [11344045.001]
  • [Cites] Int J Biochem Cell Biol. 2001 Oct;33(10):960-70 [11470230.001]
  • [Cites] J Biol Chem. 2003 Oct 31;278(44):43603-14 [12933798.001]
  • [Cites] Nat Rev Cancer. 2004 Jan;4(1):71-8 [14708027.001]
  • [Cites] Cancer Res. 2004 Feb 1;64(3):952-61 [14871825.001]
  • [Cites] Development. 1992 Feb;114(2):447-56 [1317291.001]
  • [Cites] Cancer Res. 1994 Feb 1;54(3):800-4 [7508337.001]
  • [Cites] J Virol. 1994 Jul;68(7):4358-68 [7515971.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12485-90 [11606713.001]
  • [Cites] Science. 2002 Mar 29;295(5564):2387-92 [11923519.001]
  • [Cites] Br J Cancer. 2002 May 6;86(9):1479-86 [11986784.001]
  • [Cites] Cell. 2002 May 31;109(5):625-37 [12062105.001]
  • [Cites] Cancer Cell. 2002 May;1(4):339-53 [12086849.001]
  • [Cites] J Natl Cancer Inst. 2002 Aug 7;94(15):1134-42 [12165638.001]
  • [Cites] J Pharmacol Exp Ther. 2002 Sep;302(3):1055-61 [12183663.001]
  • [Cites] Br J Cancer. 2002 Aug 27;87(5):537-44 [12189553.001]
  • [Cites] Cancer Cell. 2002 Oct;2(4):289-300 [12398893.001]
  • [Cites] Oncologist. 2002;7(5):393-400 [12401901.001]
  • [Cites] Cancer Res. 2002 Nov 15;62(22):6538-44 [12438248.001]
  • [Cites] Clin Cancer Res. 2003 Jan;9(1):295-306 [12538482.001]
  • [Cites] Cancer. 2003 Feb 1;97(3 Suppl):840-7 [12548584.001]
  • [Cites] Anticancer Res. 2002 Nov-Dec;22(6C):3925-31 [12553014.001]
  • [Cites] Br J Cancer. 2003 Jan 13;88(1):63-73 [12556961.001]
  • [Cites] J Bone Miner Res. 2003 Feb;18(2):204-12 [12568397.001]
  • [Cites] Curr Opin Hematol. 2003 Mar;10(2):136-41 [12579040.001]
  • [Cites] Trends Mol Med. 2003 Mar;9(3):109-17 [12657432.001]
  • [Cites] J Cancer Res Clin Oncol. 2003 Feb;129(2):123-31 [12669237.001]
  • [Cites] J Biol Chem. 2003 Apr 25;278(17):15056-64 [12586837.001]
  • [Cites] Circ Res. 2003 May 2;92(8):827-39 [12730128.001]
  • [Cites] Nature. 2003 May 15;423(6937):337-42 [12748652.001]
  • [Cites] Nat Rev Cancer. 2003 Jun;3(6):401-10 [12778130.001]
  • [Cites] J Urol. 2003 Jul;170(1):246-52 [12796698.001]
  • [Cites] J Immunol. 2003 Jul 1;171(1):142-51 [12816992.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):589-601 [12842087.001]
  • [Cites] Lancet. 2003 Jun 28;361(9376):2217-25 [12842378.001]
  • [Cites] Clin Cancer Res. 2003 Jul;9(7):2394-9 [12855610.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2930-5 [8610145.001]
  • [Cites] Am J Pathol. 1996 Dec;149(6):1899-917 [8952526.001]
  • [Cites] Cancer Res. 1997 Apr 1;57(7):1294-300 [9102216.001]
  • [Cites] Br J Cancer. 1997;76(11):1410-5 [9400935.001]
  • [Cites] Cancer Res. 1998 Mar 1;58(5):1048-51 [9500469.001]
  • [Cites] J Bone Miner Res. 1998 Apr;13(4):581-9 [9556058.001]
  • [Cites] Cancer Res. 1998 May 1;58(9):1952-9 [9581838.001]
  • [Cites] Cell. 1998 May 1;93(3):411-22 [9590175.001]
  • [Cites] Gynecol Oncol. 1999 Mar;72(3):380-6 [10053110.001]
  • [Cites] Science. 1999 Apr 30;284(5415):808-12 [10221914.001]
  • [Cites] Genes Dev. 1999 Jun 1;13(11):1382-97 [10364156.001]
  • [Cites] Ann N Y Acad Sci. 1999 Jun 30;878:372-87 [10415742.001]
  • [Cites] Ann N Y Acad Sci. 1999 Jun 30;878:453-65 [10415748.001]
  • [Cites] J Natl Cancer Inst. 1995 Aug 16;87(16):1237-45 [7563170.001]
  • [Cites] Cold Spring Harb Symp Quant Biol. 2002;67:293-300 [12858552.001]
  • [Cites] Semin Oncol. 2003 Aug;30(4 Suppl 9):80-94 [12908139.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4862-71 [12941807.001]
  • [Cites] Life Sci. 2003 Sep 26;73(19):2413-20 [12954450.001]
  • [Cites] Cancer Res. 2003 Sep 1;63(17):5224-9 [14500349.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Oct 24;310(3):816-23 [14550277.001]
  • [Cites] J Clin Invest. 2000 Apr;105(8):1045-7 [10772648.001]
  • (PMID = 15343380.001).
  • [ISSN] 0021-9738
  • [Journal-full-title] The Journal of clinical investigation
  • [ISO-abbreviation] J. Clin. Invest.
  • [Language] eng
  • [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 / Angiogenesis Inhibitors; 0 / Diphosphonates; 0 / Imidazoles; 0 / Matrix Metalloproteinase Inhibitors; 0 / Vascular Endothelial Growth Factors; 6XC1PAD3KF / zoledronic acid; EC 3.4.24.35 / Matrix Metalloproteinase 9
  • [Other-IDs] NLM/ PMC514591
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19. 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.
  • Hence, this study was undertaken to examine the potential chemopreventive properties of the two agents against transgenic adenocarcinoma of the mouse prostate.
  • MATERIALS AND METHODS: The efficacy of AIN-76A diet supplemented with 2% curcumin or 0.05% PEITC or a combination of 1% curcumin and 0.025% PEITC for periods of 10 and 16 weeks was tested against adenocarcinoma of the mouse prostate.
  • 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.

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  • [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
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20. Casati A, Zimmermann VS, Benigni F, Bertilaccio MT, Bellone M, Mondino A: The immunogenicity of dendritic cell-based vaccines is not hampered by doxorubicin and melphalan administration. J Immunol; 2005 Mar 15;174(6):3317-25
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.
  • In the attempt to develop new strategies able to control tumor recurrence while allowing the development of protective immunity, we have investigated the immunogenic potential of two distinct vaccine formulations when provided alone or upon single and repeated treatment with chemotherapeutics drugs.
  • Vaccine-induced T cell responses were first investigated by tracing Ag-specific T cell responses in mice bearing detectable frequencies of Ag-specific TCR transgenic CD4 and CD8 T cells.
  • These studies indicated that immunization with peptide-pulsed dendritic cells and soluble Ag plus adjuvant elicited a comparable expansion and differentiation of CD4 and CD8 effector cells in the peripheral lymphoid tissues when provided alone or shortly after Doxorubicin or Melphalan administration.
  • We also analyzed the potency of the combined vaccination in transgenic adenocarcinoma mouse prostate mice, which develop spontaneous prostate cancer.
  • Dendritic cell-based vaccination elicited potent tumor-specific cytotoxic responses in mice bearing prostate intraepithelial neoplasia both in the absence and in the presence of Doxorubicin.
  • Together our results indicate that Doxorubicin- or Melphalan-based chemotherapy and Ag-specific vaccination can be combined for adjuvant treatments of cancer patients.
  • [MeSH-minor] Animals. Antibiotics, Antineoplastic / administration & dosage. Antibiotics, Antineoplastic / toxicity. Antineoplastic Agents, Alkylating / administration & dosage. Antineoplastic Agents, Alkylating / toxicity. CD4-Positive T-Lymphocytes / cytology. CD4-Positive T-Lymphocytes / drug effects. CD4-Positive T-Lymphocytes / immunology. CD8-Positive T-Lymphocytes / drug effects. CD8-Positive T-Lymphocytes / immunology. Cell Differentiation / drug effects. Cell Division / drug effects. Humans. In Vitro Techniques. Lymphocyte Count. Mice. Mice, Inbred BALB C. Mice, Inbred C57BL. Mice, Transgenic. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / immunology. Neoplasms, Experimental / therapy. Receptors, Antigen, T-Cell, alpha-beta / genetics

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  • (PMID = 15749863.001).
  • [ISSN] 0022-1767
  • [Journal-full-title] Journal of immunology (Baltimore, Md. : 1950)
  • [ISO-abbreviation] J. Immunol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antineoplastic Agents, Alkylating; 0 / Cancer Vaccines; 0 / Receptors, Antigen, T-Cell, alpha-beta; 80168379AG / Doxorubicin; Q41OR9510P / Melphalan
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21. 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 .

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  • [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.

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  • [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
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22. Hibbitts S: TA-CIN, a vaccine incorporating a recombinant HPV fusion protein (HPV16 L2E6E7) for the potential treatment of HPV16-associated genital diseases. Curr Opin Mol Ther; 2010 Oct;12(5):598-606
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  • [Title] TA-CIN, a vaccine incorporating a recombinant HPV fusion protein (HPV16 L2E6E7) for the potential treatment of HPV16-associated genital diseases.
  • Therefore, a therapeutic HPV vaccine would benefit patients with HPV-associated genital diseases.
  • Being developed by Cancer Research Technology Ltd, under license from Xenova Group plc, TA-CIN (Tissue Antigen - Cervical Intraepithelial Neoplasia) is a fusion protein vaccine comprising the HPV16 viral proteins L2, E6 and E7 for the treatment of HPV16-associated genital diseases.
  • In mouse models, TA-CIN induced dose-dependent HPV16-specific CD4 and CD8 T-cell responses, which were enhanced when boosted with the vaccinia-based vector vaccine TA-HPV (Therapeutic Antigen - HPV).
  • Phase II trials in patients with anogenital and vulval intraepithelial neoplasia investigated heterologous prime/boost strategies with TA-CIN/TA-HPV and TA-HPV/TA-CIN, but neither of the regimens offered advantages over single-agent TA-HPV.
  • A recent phase II trial investigating imiquimod/TA-CIN in patients with vulval intraepithelial neoplasia demonstrated significant infiltration of CD4 and CD8 T-cells in lesion responders and complete lesion regression in 63% of patients.
  • More comprehensive case-controlled trials are needed to define responders to immunotherapy with TA-CIN and verify its prophylactic and therapeutic properties.
  • [MeSH-major] Genital Diseases, Female / drug therapy. Genital Diseases, Female / virology. Genital Diseases, Male / drug therapy. Genital Diseases, Male / virology. Papillomavirus Infections / drug therapy. Papillomavirus Vaccines / therapeutic use. Recombinant Fusion Proteins / therapeutic use

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  • (PMID = 20886392.001).
  • [ISSN] 2040-3445
  • [Journal-full-title] Current opinion in molecular therapeutics
  • [ISO-abbreviation] Curr. Opin. Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Papillomavirus Vaccines; 0 / Recombinant Fusion Proteins
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23. Leav I, Plescia J, Goel HL, Li J, Jiang Z, Cohen RJ, Languino LR, Altieri DC: Cytoprotective mitochondrial chaperone TRAP-1 as a novel molecular target in localized and metastatic prostate cancer. Am J Pathol; 2010 Jan;176(1):393-401
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  • Here, we show that a mitochondria-localized Hsp90 chaperone, tumor necrosis factor receptor-associated protein-1 (TRAP-1), is abundantly and ubiquitously expressed in human high-grade prostatic intraepithelial neoplasia, Gleason grades 3 through 5 prostatic adenocarcinomas, and metastatic prostate cancer, but largely undetectable in normal prostate or benign prostatic hyperplasia in vivo.
  • Prostate lesions formed in genetic models of the disease, including the transgenic adenocarcinoma of the mouse prostate and mice carrying prostate-specific deletion of the phosphatase tensin homolog tumor suppressor (Pten(pc-/-)), also exhibit high levels of TRAP-1.
  • Targeting this pathway with Gamitrinibs could be explored as novel molecular therapy in patients with advanced prostate cancer.

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  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):584-93 [12154351.001]
  • [Cites] Science. 2001 Apr 27;292(5517):727-30 [11326099.001]
  • [Cites] Prostate. 2003 May 15;55(3):219-37 [12692788.001]
  • [Cites] Nature. 2003 Sep 25;425(6956):407-10 [14508491.001]
  • [Cites] Cancer Cell. 2003 Sep;4(3):209-21 [14522255.001]
  • [Cites] Nat Med. 2004 Jun;10(6):594-601 [15156201.001]
  • [Cites] Science. 2004 Jul 30;305(5684):626-9 [15286356.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1488-90 [15470210.001]
  • [Cites] N Engl J Med. 2004 Oct 7;351(15):1513-20 [15470214.001]
  • [Cites] Cancer Res. 1994 May 15;54(10):2577-81 [8168083.001]
  • [Cites] Nature. 2005 Mar 31;434(7033):652-8 [15800626.001]
  • [Cites] Nature. 2005 Mar 31;434(7033):658-62 [15800627.001]
  • [Cites] Nat Rev Cancer. 2005 Oct;5(10):761-72 [16175177.001]
  • [Cites] Oncology. 2005;69(4):273-82 [16282706.001]
  • [Cites] J Natl Cancer Inst. 2006 Nov 1;98(21):1521-7 [17077354.001]
  • [Cites] Nat Rev Cancer. 2007 Apr;7(4):256-69 [17384581.001]
  • [Cites] Arch Pathol Lab Med. 2007 Jul;131(7):1103-9 [17616999.001]
  • [Cites] J Biol Chem. 2007 Jul 13;282(28):20553-60 [17513296.001]
  • [Cites] J Clin Invest. 2007 Sep;117(9):2351-61 [17786228.001]
  • [Cites] J Urol. 2007 Nov;178(5):1846-54 [17868738.001]
  • [Cites] Cell. 2007 Oct 19;131(2):257-70 [17956728.001]
  • [Cites] Stress. 2007 Nov;10(4):342-50 [17853063.001]
  • [Cites] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387.001]
  • [Cites] FASEB J. 2008 Sep;22(9):3264-75 [18524868.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20882-7 [19088204.001]
  • [Cites] J Clin Invest. 2009 Mar;119(3):454-64 [19229106.001]
  • [Cites] Mol Cell. 2009 Mar 13;33(5):627-38 [19285945.001]
  • [Cites] PLoS Biol. 2007 Jul;5(7):e172 [17579517.001]
  • [Cites] FEBS Lett. 2002 Feb 13;512(1-3):1-7 [11852041.001]
  • [Cites] J Biol Chem. 2000 Feb 4;275(5):3305-12 [10652318.001]
  • [Cites] Cancer Cell. 2003 Mar;3(3):213-7 [12676580.001]
  • (PMID = 19948822.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA078810; United States / NCI NIH HHS / CA / R01 CA089720; United States / NCI NIH HHS / CA / CA118005; United States / NCI NIH HHS / CA / R01 CA109874-05; United States / NCI NIH HHS / CA / CA78810; United States / NCI NIH HHS / CA / CA109874-05; United States / NCI NIH HHS / CA / R01 CA109874; United States / NCI NIH HHS / CA / R01 CA089720-05; United States / NCI NIH HHS / CA / CA90917; United States / NCI NIH HHS / CA / CA089720-05; United States / NCI NIH HHS / CA / CA109874; United States / NCI NIH HHS / CA / CA89720; United States / NCI NIH HHS / CA / R56 CA089720; United States / NCI NIH HHS / CA / R01 CA118005; United States / NCI NIH HHS / CA / R01 CA090917
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HSP90 Heat-Shock Proteins; 0 / Molecular Chaperones; 0 / TRAP-1 protein, mouse; 0 / TRAP1 protein, human
  • [Other-IDs] NLM/ PMC2797899
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24. Kasper S, Smith JA Jr: Genetically modified mice and their use in developing therapeutic strategies for prostate cancer. J Urol; 2004 Jul;172(1):12-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Genetically modified mice and their use in developing therapeutic strategies for prostate cancer.
  • PURPOSE: At the National Cancer Institute a comprehensive program has been developed for accelerating prostate cancer research, especially in the area of mouse models for human cancers.
  • This review focuses on transgenic mouse models for elucidating the molecular and cellular processes that lead to prostate cancer initiation, progression and metastasis, and on their suitability for therapeutic and chemopreventive trials.
  • RESULTS: Currently no 1 mouse model displays the entire continuum of human prostate cancer initiation, development and metastasis.
  • The loss or over expression of a single gene results primarily in epithelial hyperplasia, prostatic intraepithelial neoplasia or more aggressive localized adenocarcinoma.
  • A number of models have been used to investigate the efficacy of androgen deprivation, lovastatin, vitamin D, the anti-inflammatory drug E-7869, genistein and (-)-epigallocatechin-3-gallate as therapeutic or chemopreventive agents.
  • Noninvasive optical imaging technologies facilitate the detection of metastatic lesions and the effects of therapeutic agents on tumor regression.
  • CONCLUSIONS: Integrating mouse studies with human clinical trials would ensure that mechanisms that promote prostate cancer are identified and potential therapeutic targets are validated.
  • [MeSH-major] Adenocarcinoma / therapy. Carcinoma, Neuroendocrine / therapy. Disease Models, Animal. Prostatic Neoplasms / physiopathology. Prostatic Neoplasms / therapy

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  • (PMID = 15201729.001).
  • [ISSN] 0022-5347
  • [Journal-full-title] The Journal of urology
  • [ISO-abbreviation] J. Urol.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / 1 R01 DK59142; United States / NIDDK NIH HHS / DK / 1 R01 DK60957; United States / NCI NIH HHS / CA / U01-CA84239
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming
  • [Number-of-references] 73
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25. Lee CW, Rickman B, Rogers AB, Ge Z, Wang TC, Fox JG: Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice. Cancer Res; 2008 May 1;68(9):3540-8
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  • In this study, we investigated the efficacy of H. pylori eradication in preventing the progression of gastritis to gastric cancer in H. pylori-infected transgenic INS-GAS mice. H. pylori infection induced severe dysplasia and gastric cancer classified as high-grade and low-grade gastrointestinal intraepithelial neoplasia (GIN) in INS-GAS mice at 28 weeks postinfection (WPI). H. pylori eradication therapy using omeprazole, metronidazole, and clarithromycin was administered p.o. at 8, 12, or 22 WPI.
  • Although not as effective as early antimicrobial treatment, prevention of progression to high-grade GIN was achieved by H. pylori eradication at 12 and 22 WPI (P < 0.05).
  • Consistent with reduced gastric pathology, H. pylori eradication at all time points significantly down-regulated gastric Interferon-gamma, tumor necrosis factor-alpha, inducible nitric oxide synthase, and Reg 1 mRNA levels (P < 0.05) and reduced epithelial proliferation in the corpus (P < 0.01) compared with untreated infected mice.
  • We concluded that H. pylori eradication prevented gastric cancer to the greatest extent when antibiotics are given at an early point of infection, but that eradication therapy given at a later time point delayed the development of severe dysplastic lesions.

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  • [Cites] J Natl Cancer Inst. 1995 Jan 4;87(1):28-33 [7666459.001]
  • [Cites] J Natl Cancer Inst. 2000 Dec 6;92(23):1881-8 [11106679.001]
  • [Cites] J Clin Invest. 1996 Oct 15;98(8):1918-29 [8878444.001]
  • [Cites] Gastroenterology. 1997 Apr;112(4):1386-97 [9098027.001]
  • [Cites] Gastroenterology. 1998 Dec;115(6):1483-93 [9834276.001]
  • [Cites] Am J Physiol. 1999 Oct;277(4 Pt 1):G773-84 [10516143.001]
  • [Cites] Cancer Sci. 2004 Nov;95(11):872-7 [15546504.001]
  • [Cites] Infect Immun. 2005 Mar;73(3):1664-70 [15731067.001]
  • [Cites] Lab Invest. 2005 May;85(5):702-15 [15765119.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):1937-52 [15940628.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):1965-83 [15940630.001]
  • [Cites] Gut. 2005 Nov;54(11):1536-40 [15985559.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10709-15 [16322215.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Jan;290(1):G175-82 [16109843.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):732-7 [16407106.001]
  • [Cites] J Natl Cancer Inst. 2006 Jul 19;98(14):974-83 [16849680.001]
  • [Cites] J Natl Cancer Inst. 2006 Oct 4;98(19):1426 [17018791.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):60-9 [17200707.001]
  • [Cites] Infect Immun. 2007 Jun;75(6):2699-707 [17353283.001]
  • [Cites] Gut. 2007 Jun;56(6):772-81 [17170018.001]
  • [Cites] Am J Pathol. 2007 Nov;171(5):1520-8 [17982128.001]
  • [Cites] Carcinogenesis. 2007 Dec;28(12):2597-604 [17724378.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1994;61:1-241 [7715068.001]
  • [Cites] J Antimicrob Chemother. 1999 Nov;44(5):629-40 [10552979.001]
  • [Cites] Gastroenterology. 2000 Jan;118(1):36-47 [10611152.001]
  • [Cites] Gastroenterology. 2000 Jul;119(1):7-14 [10889149.001]
  • [Cites] Cancer Res. 2000 Nov 15;60(22):6376-80 [11103800.001]
  • [Cites] N Engl J Med. 2001 Sep 13;345(11):829-32 [11556306.001]
  • [Cites] Infect Immun. 2002 May;70(5):2630-9 [11953405.001]
  • [Cites] Aliment Pharmacol Ther. 2002 Aug;16(8):1449-56 [12182744.001]
  • [Cites] Gastroenterology. 2003 Mar;124(3):762-77 [12612914.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):942-50 [12615707.001]
  • [Cites] Gastroenterology. 2003 Jun;124(7):1879-90 [12806621.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Jul;47(7):2249-55 [12821476.001]
  • [Cites] JAMA. 2004 Jan 14;291(2):187-94 [14722144.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):4-10 [14744726.001]
  • [Cites] Appl Environ Microbiol. 2004 May;70(5):2791-800 [15128534.001]
  • [Cites] Gut. 2004 Sep;53(9):1244-9 [15306578.001]
  • [Cites] Lancet. 1984 Jun 16;1(8390):1311-5 [6145023.001]
  • [Cites] Cancer Res. 1988 Jul 1;48(13):3554-60 [3288329.001]
  • [Cites] Ital J Gastroenterol. 1991 Jan;23(1):24-8 [1747497.001]
  • [Cites] J Cell Biochem Suppl. 1992;16G:73-8 [1469907.001]
  • [Cites] J Biol Chem. 1996 Feb 16;271(7):3671-6 [8631979.001]
  • (PMID = 18441088.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI037750-12; United States / NIEHS NIH HHS / ES / P30ES02109; United States / NIEHS NIH HHS / ES / ES002109-299010; United States / NIAID NIH HHS / AI / AI037750-12; United States / NCI NIH HHS / CA / R01 CA093405; United States / NIAID NIH HHS / AI / R01 AI037750-13; United States / NIAID NIH HHS / AI / AI037750-13; United States / NIAID NIH HHS / AI / R01AI37750; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NIAID NIH HHS / AI / R01 AI037750; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / P01 CA026731-299002; United States / NIEHS NIH HHS / ES / P30 ES002109-299010; United States / NCI NIH HHS / CA / P01 CA026731; United States / NCI NIH HHS / CA / P01CA26731; United States / NCI NIH HHS / CA / CA026731-299002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Anti-Ulcer Agents; 0 / Lithostathine; 0 / Reg1 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole
  • [Other-IDs] NLM/ NIHMS95242; NLM/ PMC2653414
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26. Lee CW, Rickman B, Rogers AB, Muthupalani S, Takaishi S, Yang P, Wang TC, Fox JG: Combination of sulindac and antimicrobial eradication of Helicobacter pylori prevents progression of gastric cancer in hypergastrinemic INS-GAS mice. Cancer Res; 2009 Oct 15;69(20):8166-74
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  • Helicobacter pylori infection causes severe dysplasia manifested as gastrointestinal intraepithelial neoplasia (GIN) after 28 weeks post-H. pylori infection (WPI) in cancer-prone, hypergastrinemic male INS-GAS mice.
  • We examined the efficacy of the nonsteroidal anti-inflammatory drug sulindac (400 ppm in drinking water) alone, the CCK2/gastrin receptor antagonist YM022 (45 mg/kg/wk) alone, and sulindac or YM022 combined with H. pylori eradication therapy to prevent H. pylori-associated gastric cancer in male INS-GAS mice.
  • Treatments started at 22 WPI, and mice were euthanized at 28 WPI.
  • In uninfected mice, all treatments significantly delayed development of spontaneous GIN (P < 0.05).
  • In infected mice, sulindac or YM022 treatment did not alter gastric expression of the proinflammatory cytokines Ifn-gamma and Tnf-alpha and mucosal cell proliferation.

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  • [Cites] J Antimicrob Chemother. 1999 Nov;44(5):629-40 [10552979.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3540-8 [18441088.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1960-8 [10874065.001]
  • [Cites] Cancer Res. 2001 Mar 15;61(6):2399-403 [11289104.001]
  • [Cites] Infect Immun. 2001 Aug;69(8):5056-63 [11447186.001]
  • [Cites] Lancet Oncol. 2002 Mar;3(3):166-74 [11902503.001]
  • [Cites] J Clin Invest. 2002 Sep;110(6):761-9 [12235107.001]
  • [Cites] Gastroenterology. 2003 Mar;124(3):762-77 [12612914.001]
  • [Cites] Cancer Res. 2003 Mar 1;63(5):942-50 [12615707.001]
  • [Cites] Gastroenterology. 2003 Jun;124(7):1879-90 [12806621.001]
  • [Cites] Antimicrob Agents Chemother. 2003 Jul;47(7):2249-55 [12821476.001]
  • [Cites] Aliment Pharmacol Ther. 2003 Jun 15;17(12):1535-43 [12823157.001]
  • [Cites] J Immunol. 2003 Oct 15;171(8):3913-7 [14530307.001]
  • [Cites] J Natl Cancer Inst. 2003 Dec 3;95(23):1784-91 [14652240.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2004 Jan;286(1):G148-56 [12958020.001]
  • [Cites] EMBO J. 2004 Apr 7;23(7):1669-78 [15014433.001]
  • [Cites] Appl Environ Microbiol. 2004 May;70(5):2791-800 [15128534.001]
  • [Cites] Lancet. 1984 Jun 16;1(8390):1311-5 [6145023.001]
  • [Cites] Cancer Res. 1988 Jul 1;48(13):3554-60 [3288329.001]
  • [Cites] Cancer Res. 1988 Aug 1;48(15):4399-404 [3390835.001]
  • [Cites] J Pathol. 1988 Dec;156(4):341-7 [3225717.001]
  • [Cites] Gastroenterology. 1991 Sep;101(3):635-9 [1650315.001]
  • [Cites] Gut. 1993 Jun;34(6):757-61 [8314507.001]
  • [Cites] J Pharmacol Exp Ther. 1994 May;269(2):725-31 [7910212.001]
  • [Cites] IARC Monogr Eval Carcinog Risks Hum. 1994;61:1-241 [7715068.001]
  • [Cites] Am J Physiol. 1996 Mar;270(3 Pt 1):G393-400 [8638704.001]
  • [Cites] J Med Chem. 1997 Jan 31;40(3):331-41 [9022799.001]
  • [Cites] J Clin Invest. 1997 May 1;99(9):2254-9 [9151799.001]
  • [Cites] J Clin Gastroenterol. 1998;27 Suppl 1:S47-52 [9872498.001]
  • [Cites] J Biol Chem. 1999 Mar 19;274(12):8328-34 [10075740.001]
  • [Cites] Gastroenterology. 2005 Jun;128(7):1965-83 [15940630.001]
  • [Cites] J Immunol. 2005 Aug 1;175(3):1483-90 [16034085.001]
  • [Cites] Oncology. 2005;69 Suppl 1:28-32 [16210874.001]
  • [Cites] Gut. 2005 Nov;54(11):1536-40 [15985559.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10709-15 [16322215.001]
  • [Cites] Am J Physiol Gastrointest Liver Physiol. 2006 Jan;290(1):G175-82 [16109843.001]
  • [Cites] J Infect Dis. 2006 Apr 1;193(7):1037-46 [16518767.001]
  • [Cites] J Natl Cancer Inst. 2006 Jun 7;98(11):736-47 [16757698.001]
  • [Cites] Clin Cancer Res. 2006 Aug 1;12(15):4766-72 [16899628.001]
  • [Cites] J Natl Cancer Inst. 2006 Oct 4;98(19):1426 [17018791.001]
  • [Cites] J Clin Invest. 2007 Jan;117(1):60-9 [17200707.001]
  • [Cites] Aliment Pharmacol Ther. 2007 Feb 15;25(4):455-61 [17270001.001]
  • [Cites] Ann Intern Med. 2007 Mar 6;146(5):376-89 [17339623.001]
  • [Cites] Helicobacter. 2007 Jun;12(3):193-9 [17492998.001]
  • [Cites] Infect Immun. 2007 Jun;75(6):2699-707 [17353283.001]
  • [Cites] Gut. 2007 Jun;56(6):772-81 [17170018.001]
  • [Cites] ACS Chem Biol. 2007 Jul 20;2(7):479-83 [17602619.001]
  • [Cites] Gastroenterology. 2000 Jan;118(1):36-47 [10611152.001]
  • (PMID = 19826057.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI037750-10; United States / NIEHS NIH HHS / ES / P30ES02109; United States / NIEHS NIH HHS / ES / ES002109-309010; United States / NCI NIH HHS / CA / R01 CA093405; United States / NCI NIH HHS / CA / P01 CA026731-199002; United States / NIAID NIH HHS / AI / R01AI37750; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NIAID NIH HHS / AI / R01 AI037750; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / P01 CA026731; United States / NIAID NIH HHS / AI / R01 AI037750-10; United States / NCI NIH HHS / CA / P01CA26731; United States / NCI NIH HHS / CA / CA026731-199002; United States / NCI NIH HHS / CA / R01CA093405-07A1; United States / NIEHS NIH HHS / ES / P30 ES002109-309010
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Antineoplastic Agents; 0 / Hormone Antagonists; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 12794-10-4 / Benzodiazepines; 145084-28-2 / YM 022; 184SNS8VUH / Sulindac; 82115-62-6 / Interferon-gamma; EC 1.14.99.- / Ptgs2 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Ptgs1 protein, mouse; K7Q1JQR04M / Dinoprostone
  • [Other-IDs] NLM/ NIHMS142041; NLM/ PMC2766772
  •  go-up   go-down


27. 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.
  • Immunohistochemistry was performed using the immunoglobulin G1 mouse monoclonal antibody (HECD-1; Zymed, San Francisco, CA).
  • [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






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