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1. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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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2. 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
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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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  • (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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3. 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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  • (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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4. 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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  • (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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5. 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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6. 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


7. 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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  • (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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8. 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
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  • [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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9. 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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10. 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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  • (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
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11. 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
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  • [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


12. 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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13. 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
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  • 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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  • (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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14. 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


15. 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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  • (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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