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Items 1 to 63 of about 63
1. Desai D, Sinha I, Null K, Wolter W, Suckow MA, King T, Amin S, Sinha R: Synthesis and antitumor properties of selenocoxib-1 against rat prostate adenocarcinoma cells. Int J Cancer; 2010 Jul 1;127(1):230-8
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  • [Title] Synthesis and antitumor properties of selenocoxib-1 against rat prostate adenocarcinoma cells.
  • Hormone refractory prostate cancer poses a huge problem and standard of care chemotherapy has not been very successful.
  • We used a novel strategy to combine properties of 2 well-studied class of compounds (selenium and COX-2 inhibitor) and examined the resulting effectiveness against prostate cancer.
  • The PAIII cells derived from a metastatic prostate tumor that arose spontaneously in a Lobund-Wistar (LW) rat were used to examine the efficacy of Selenocoxib-1 in vitro.
  • In addition, human metastatic prostate cancer cells, PC-3M, were tested for antitumor effect of Selenocoxib-1 in vitro.
  • This study demonstrates that Selenocoxib-1 is more effective against prostate cancer than Celecoxib.
  • [MeSH-major] Adenocarcinoma / pathology. Antineoplastic Agents / pharmacology. Organoselenium Compounds / pharmacology. Prostatic Neoplasms / pathology. Sulfonamides / pharmacology

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  • (PMID = 19918950.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CB / N02-CB-56603
  • [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 / Antineoplastic Agents; 0 / Organoselenium Compounds; 0 / Sulfonamides; 0 / selenocoxib-1; EC 1.14.99.1 / Cyclooxygenase 1; EC 1.14.99.1 / Cyclooxygenase 2; H6241UJ22B / Selenium
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2. Mossine VV, Chopra P, Mawhinney TP: Interaction of tomato lycopene and ketosamine against rat prostate tumorigenesis. Cancer Res; 2008 Jun 1;68(11):4384-91
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  • [Title] Interaction of tomato lycopene and ketosamine against rat prostate tumorigenesis.
  • Prior investigations on the beneficial effect of dietary processed tomato products and lycopene on prostate cancer risk suggested that lycopene may require the presence of other constituents to exert its chemopreventive potential.
  • We investigated whether ketosamines, a group of carbohydrate derivatives present in dehydrated tomato products, may interact with lycopene against prostate tumorigenesis.
  • One ketosamine, FruHis, strongly synergized with lycopene against proliferation of the highly metastatic rat prostate adenocarcinoma MAT-LyLu cell line in vitro.
  • Energy-balanced diets, supplemented with tomato paste, tomato powder, or tomato paste plus FruHis, were fed to Wistar-Unilever rats (n = 20 per group) treated with N-nitroso-N-methylurea and testosterone to induce prostate carcinogenesis.
  • The proportions of dying rats with macroscopic prostate tumors in the control, tomato paste, tomato powder, and tomato paste/FruHis groups were 63% (12 of 19), 39% (5 of 13), 43% (6 of 14), and 18% (2 of 11), respectively.
  • [MeSH-minor] Animals. Carcinogens / toxicity. Cell Transformation, Neoplastic. Male. Prostate / drug effects. Prostate / pathology. Rats. Rats, Wistar

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  • (PMID = 18519700.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acids; 0 / Antioxidants; 0 / Carcinogens; 30237-26-4 / Fructose; 36-88-4 / Carotenoids; SB0N2N0WV6 / lycopene
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3. Hokaiwado N, Takeshita F, Naiki-Ito A, Asamoto M, Ochiya T, Shirai T: Glutathione S-transferase Pi mediates proliferation of androgen-independent prostate cancer cells. Carcinogenesis; 2008 Jun;29(6):1134-8
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  • [Title] Glutathione S-transferase Pi mediates proliferation of androgen-independent prostate cancer cells.
  • Prostate cancers generally acquire an androgen-independent growth capacity with progression, resulting in resistance to antiandrogen therapy.
  • Therefore, identification of the genes regulated through this process may be important for understanding the mechanisms of prostate carcinogenesis.
  • We here utilized androgen-dependent/independent transplantable tumors, newly established with the 'transgenic rat adenocarcinoma in prostate' (TRAP) model, to analyze their gene expression using microarrays.
  • Among the overexpressed genes in androgen-independent prostate cancers compared with the androgen-dependent tumors, glutathione S-transferase pi (GST-pi) was included.
  • In line with this, human prostate cancer cell lines PC3 and DU145 (androgen independent) had higher expression of GST-pi compared with LNCaP (androgen dependent) as determined by semiquantitative reverse transcription-polymerase chain reaction analysis.
  • To investigate the roles of GST-pi expression in androgen-independent human prostate cancers, GST-pi was knocked down by a small interfering RNA (siRNA), resulting in significant decrease of the proliferation rate in the androgen-independent PC3 cell line.
  • These findings suggest that GST-pi might play important roles in proliferation of androgen-independent human prostate cancer cells.

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  • (PMID = 18413363.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgens; 0 / RNA, Small Interfering; EC 2.5.1.18 / Glutathione S-Transferase pi
  • [Other-IDs] NLM/ PMC2443274
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4. Ozten N, Horton L, Lasano S, Bosland MC: Selenomethionine and alpha-tocopherol do not inhibit prostate carcinogenesis in the testosterone plus estradiol-treated NBL rat model. Cancer Prev Res (Phila); 2010 Mar;3(3):371-80
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  • [Title] Selenomethionine and alpha-tocopherol do not inhibit prostate carcinogenesis in the testosterone plus estradiol-treated NBL rat model.
  • Previous studies with selenium and/or vitamin E in prostate carcinogenesis animal models have been negative, but these models may not involve oxidative stress mechanisms.
  • In this study, we examined the potential of selenomethionine and alpha-tocopherol to modulate prostate cancer development in the testosterone plus estradiol-treated NBL rat, a model that does involve sex hormone-induced oxidative stress mechanisms and prostatic inflammation.
  • The development of prostate carcinomas was not affected by dietary treatment with either agent.
  • The high dose of selenomethionine reduced the severity of epithelial dysplasia in the lateral prostate that was not associated with inflammation, and alpha-tocopherol reduced in a dose-related fashion the incidence of marked inflammation and marked epithelial dysplasia in the lateral prostate, regardless of whether these lesions were associated with inflammation. alpha-Tocopherol significantly increased the incidence of adenocarcinomas of the mammary glands at both dietary concentrations.
  • Collectively, our findings suggest that selenomethionine and alpha-tocopherol supplementation does not prevent prostate cancer in rats fed diets with nutritionally adequate levels of selenium and vitamin E.

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  • (PMID = 20179302.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016087; United States / NIEHS NIH HHS / ES / P30 ES000260-429017; United States / NIEHS NIH HHS / ES / ES000260-469017; United States / NIEHS NIH HHS / ES / P30 ES000260; United States / NCI NIH HHS / CA / P30 CA16087; United States / NCI NIH HHS / CA / CA016087-239016; United States / NIEHS NIH HHS / ES / P30 ES00260; United States / NIEHS NIH HHS / ES / ES000260-429017; United States / NIEHS NIH HHS / ES / P30 ES000260-469017; United States / NCI NIH HHS / CA / P30 CA016087-239016; United States / NCI NIH HHS / CA / R01 CA104334; United States / NCI NIH HHS / CA / R01 CA104334-05
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Antioxidants; 0 / Estrogens; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 964MRK2PEL / Selenomethionine; H4N855PNZ1 / alpha-Tocopherol
  • [Other-IDs] NLM/ NIHMS161244; NLM/ PMC2833232
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5. Oltean S, Febbo PG, Garcia-Blanco MA: Dunning rat prostate adenocarcinomas and alternative splicing reporters: powerful tools to study epithelial plasticity in prostate tumors in vivo. Clin Exp Metastasis; 2008;25(6):611-9
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  • [Title] Dunning rat prostate adenocarcinomas and alternative splicing reporters: powerful tools to study epithelial plasticity in prostate tumors in vivo.
  • Using alternative splicing reporters we have previously observed mesenchymal epithelial transitions in Dunning AT3 rat prostate tumors.
  • We demonstrate here that the Dunning DT and AT3 cells, which express epithelial and mesenchymal markers, respectively, represent an excellent model to study epithelial transitions since these cells recapitulate gene expression profiles observed during human prostate cancer progression.

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  • (PMID = 18523850.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] ENG
  • [Grant] United States / NIGMS NIH HHS / GM / R01 GM063090; United States / NCI NIH HHS / CA / R33 CA097502; United States / NCI NIH HHS / CA / R33 CA97502
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Luminescent Proteins; EC 2.7.10.1 / Fgfr2 protein, rat; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2
  • [Other-IDs] NLM/ PMC2471395
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6. Wang Z, Luque RM, Kineman RD, Ray VH, Christov KT, Lantvit DD, Shirai T, Hedayat S, Unterman TG, Bosland MC, Prins GS, Swanson SM: Disruption of growth hormone signaling retards prostate carcinogenesis in the Probasin/TAg rat. Endocrinology; 2008 Mar;149(3):1366-76
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  • [Title] Disruption of growth hormone signaling retards prostate carcinogenesis in the Probasin/TAg rat.
  • We asked whether down-regulation of GH signaling could block carcinogenesis in the Probasin/TAg rat, a model of aggressive prostate cancer.
  • The Spontaneous Dwarf rat, which lacks GH due to a mutation (dr) in its GH gene, was crossed with the Probasin/TAg rat, which develops prostate carcinomas at 100% incidence by 15 wk of age.
  • Prostate tumor incidence and burden were significantly reduced, and tumor latency was delayed in TAg/Gh(dr/dr) rats relative to TAg/Gh(+/+) controls.
  • By 52 wk of age, invasive prostate adenocarcinomas were observed in all TAg/Gh(+/+) rats, whereas the majority of TAg/Gh(dr/dr) did not develop invasive tumors.
  • Suppression of carcinogenesis could not be attributed to alterations in prostate expression of TAg or androgen receptor or changes in serum testosterone levels.
  • As carcinogenesis progressed in TAg/Gh(+/+) rats, prostate GHR mRNA and protein expression increased significantly, but prostate IGF-I receptor mRNA and protein levels dropped.
  • Furthermore, serum IGF-I and prostate IGF-I levels did not change significantly over the course of carcinogenesis.
  • These findings suggest that GH plays a dominant role in progression from latent to malignant prostate cancer driven by the powerful probasin/TAg fusion gene in rats and suggest that GH antagonists may be effective at treating human prostate cancer.

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  • (PMID = 18079205.001).
  • [ISSN] 0013-7227
  • [Journal-full-title] Endocrinology
  • [ISO-abbreviation] Endocrinology
  • [Language] ENG
  • [Grant] United States / NIDDK NIH HHS / DK / R01 DK040890; United States / NIA NIH HHS / AG / R03 AG020820
  • [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 / Androgen-Binding Protein; 0 / Antigens, Viral, Tumor; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / Receptors, Somatotropin; 0 / probasin; 3XMK78S47O / Testosterone; 67763-96-6 / Insulin-Like Growth Factor I; 9002-72-6 / Growth Hormone; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Other-IDs] NLM/ PMC2275369
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7. Seeni A, Takahashi S, Takeshita K, Tang M, Sugiura S, Sato SY, Shirai T: Suppression of prostate cancer growth by resveratrol in the transgenic rat for adenocarcinoma of prostate (TRAP) model. Asian Pac J Cancer Prev; 2008 Jan-Mar;9(1):7-14
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  • [Title] Suppression of prostate cancer growth by resveratrol in the transgenic rat for adenocarcinoma of prostate (TRAP) model.
  • Since it was recently proposed as a potential prostate cancer chemopreventive agent, we here performed an in vivo experiment to explore its effect in the Transgenic Rat for Adenocarcinoma of Prostate (TRAP) model, featuring the rat probasin promoter/SV 40 T antigen.
  • Resveratrol suppressed prostate cancer growth and induction of apoptosis through androgen receptor (AR) down-regulation, without any sign of toxicity.
  • Resveratrol not only downregulated androgen receptor (AR) expression but also suppressed the androgen responsive glandular kallikrein 11 (Gk11), known to be an ortholog of the human prostate specific antigen (PSA), at the mRNA level.
  • The data provide a mechanistic basis for resveratrol chemopreventive efficacy against prostate cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Anticarcinogenic Agents / therapeutic use. Disease Models, Animal. Prostatic Neoplasms / drug therapy. Stilbenes / therapeutic use

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  • (PMID = 18439064.001).
  • [ISSN] 2476-762X
  • [Journal-full-title] Asian Pacific journal of cancer prevention : APJCP
  • [ISO-abbreviation] Asian Pac. J. Cancer Prev.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Thailand
  • [Chemical-registry-number] 0 / AR protein, human; 0 / Androgen Receptor Antagonists; 0 / Angiogenesis Inhibitors; 0 / Anticarcinogenic Agents; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / Stilbenes; 0 / Ubiquitin; 0 / trypsin-like serine protease; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; EC 3.4.21.- / Serine Endopeptidases; Q369O8926L / resveratrol
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8. Cadieux PA, Mikolajczak SA, Reeves J, Strathdee C, Reid G, Panchal CJ, Clarke MW: Rat PSP94 inhibits the growth and viability of the rat adenocarcinoma cell line PAIII in vitro. Cancer Invest; 2006 Apr-May;24(3):246-55
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  • [Title] Rat PSP94 inhibits the growth and viability of the rat adenocarcinoma cell line PAIII in vitro.
  • Previous studies have shown that human PSP94 can inhibit the growth of prostate cancer cells both in vitro and in vivo.
  • To further validate this potential and investigate the protein within a homologous setting, we examined the effects of rat PSP94 on the growth of the rat prostate adenocarcinoma cell line PAIII in vitro.
  • To generate rat PSP94, we used both a plasmid-based expression system and a recombinant rat PSP molecule.
  • Rat PSP was shown to inhibit the growth and survival of PAIII cells in a dose-dependent manner with > 90 percent reductions in both observed.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Proliferation / drug effects. Prostatic Neoplasms / drug therapy. Prostatic Secretory Proteins / pharmacology

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  • (PMID = 16809150.001).
  • [ISSN] 0735-7907
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Prostatic Secretory Proteins; 0 / Recombinant Proteins; 0 / beta-microseminoprotein
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9. Tardy I, Pochon S, Theraulaz M, Emmel P, Passantino L, Tranquart F, Schneider M: Ultrasound molecular imaging of VEGFR2 in a rat prostate tumor model using BR55. Invest Radiol; 2010 Oct;45(10):573-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Ultrasound molecular imaging of VEGFR2 in a rat prostate tumor model using BR55.
  • OBJECTIVES: To evaluate BR55, a new VEGFR2-specific ultrasound contrast agent, for imaging prostate tumors in an orthotopic model in the rat.
  • MATERIALS AND METHODS: Rat prostate adenocarcinoma were established by injection of G Dunning R-3327 tumor cells in one lobe of the prostate of Copenhagen rats.
  • Contrast enhancement in the tumor and healthy prostate was followed over time by intermittent imaging at low acoustic power.
  • Immunohistochemistry was performed on the prostate and tumor specimen to determine the expression of VEGFR2.
  • Then, once unbound microbubbles had cleared from the circulation, a strong enhancement of the tumor was obtained with BR55, whereas no significant microbubble accumulation was detected in the healthy prostate tissue.
  • The tumor to prostate ratio calculated after signal quantification was about 20 for the 3 doses of BR55 tested.
  • CONCLUSIONS: This study showed that BR55 binding to prostate tumors resulted in a strong enhancement of the lesions as early as a few minutes after contrast injection, whereas minimal nonspecific accumulation occurred in the healthy part of the gland.
  • The late phase enhancement of the tumor should be particularly valuable for prostate cancer detection and for biopsy guidance.
  • [MeSH-major] Adenocarcinoma / radionuclide imaging. Molecular Imaging / methods. Prostate / radionuclide imaging. Prostatic Neoplasms / radionuclide imaging. Vascular Endothelial Growth Factor Receptor-2 / drug effects

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  • (PMID = 20808233.001).
  • [ISSN] 1536-0210
  • [Journal-full-title] Investigative radiology
  • [ISO-abbreviation] Invest Radiol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contrast Media; 0 / Phospholipids; 0 / contrast agent BR1; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-2; WS7LR3I1D6 / Sulfur Hexafluoride
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10. Shikanov S, Shikanov A, Gofrit O, Nyska A, Corn B, Domb AJ: Intratumoral delivery of paclitaxel for treatment of orthotopic prostate cancer. J Pharm Sci; 2009 Mar;98(3):1005-14
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  • [Title] Intratumoral delivery of paclitaxel for treatment of orthotopic prostate cancer.
  • Locally recurrent prostate cancer can lead to significant morbidity, metastasis, and even death.
  • The objective of this study was to evaluate the efficacy of an injectable polymeric paste formulation containing paclitaxel against orthotopic prostate tumor in rats.
  • The Dunning R-3327 rat prostate adenocarcinoma is experimental tumor model used to study tumor progression.
  • The polymer loaded with paclitaxel was injected into the tumor bearing prostate glands of the rats 3 days after tumor cell inoculation.
  • In control untreated rats, tumor volume reached 14 cm(3) after 25 days, while in rats treated with intratumoral injection of polymer/paclitaxel formulation the prostate volume with the tumor was only 0.9 cm(3), 35 days posttumor cells inoculation.
  • The results of this study indicated that a site-directed, injectable, controlled release formulation of paclitaxel is effective against localized prostate tumors and metastasis.

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  • [Copyright] (c) 2008 Wiley-Liss, Inc. and the American Pharmacists Association
  • (PMID = 18661540.001).
  • [ISSN] 1520-6017
  • [Journal-full-title] Journal of pharmaceutical sciences
  • [ISO-abbreviation] J Pharm Sci
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Ointments; P88XT4IS4D / Paclitaxel
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11. Yeh IT, Reddick RL, Kumar AP: Malignancy arising in seminal vesicles in the transgenic adenocarcinoma of mouse prostate (TRAMP) model. Prostate; 2009 May 15;69(7):755-60
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Malignancy arising in seminal vesicles in the transgenic adenocarcinoma of mouse prostate (TRAMP) model.
  • BACKGROUND: Transgenic adenocarcinoma of mouse prostate (TRAMP) mice, derived by prostate specific expression of SV40 large T antigen using the rat probasin promoter, all develop prostate tumors akin to human prostate cancers.
  • In some cases, the stromal cells become large mass lesions that overgrow the prostate.
  • (1) A definite adenocarcinoma pattern metastatic from the prostate;.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology. Seminal Vesicles / pathology

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  • [Copyright] 2009 Wiley-Liss, Inc.
  • (PMID = 19170049.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
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12. Tani Y, Suttie A, Flake GP, Nyska A, Maronpot RR: Epithelial-stromal tumor of the seminal vesicles in the transgenic adenocarcinoma mouse prostate model. Vet Pathol; 2005 May;42(3):306-14
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  • [Title] Epithelial-stromal tumor of the seminal vesicles in the transgenic adenocarcinoma mouse prostate model.
  • The transgenic adenocarcinoma mouse prostate (TRAMP) model, designed for researching human prostatic cancer, was genetically engineered to harbor a transgene composed of the simian virus 40 Large-T/small-t antigen promoted by the rat probasin gene.
  • Some of the larger papillary, polypoid lesions exhibited a phyllodes pattern resembling that seen in mixed epithelial-stromal tumors of the breast, prostate, and seminal vesicles of humans.

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  • (PMID = 15872376.001).
  • [ISSN] 0300-9858
  • [Journal-full-title] Veterinary pathology
  • [ISO-abbreviation] Vet. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Polyomavirus Transforming; 0 / Desmin; G34N38R2N1 / Bromodeoxyuridine
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13. Tieva A, Bergh A, Damber JE: Alteration of gonadotropin-releasing hormone receptor expression with the progression of prostate cancer in the Dunning rat adenocarcinoma sublines. Acta Oncol; 2005;44(3):299-303
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Alteration of gonadotropin-releasing hormone receptor expression with the progression of prostate cancer in the Dunning rat adenocarcinoma sublines.
  • However, the role of GnRH receptors (GnRH-R) in prostate tumour progression is largely unknown.
  • The aim was therefore to investigate the variation of GnRH-R expression with prostate tumour progression using Dunning rat adenocarcinoma sublines representing different prostate tumour grades.
  • GnRH-R levels were quantified in the rat dorsolateral (DLP) and Dunning sublines (PAP, AT-1, AT-2, AT-3, MatLyLu) using competitive RT-PCR and Western blot.
  • Our data demonstrate the expression of GnRH-R in normal rat DLP and in different Dunning sublines.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology. Receptors, LHRH / analysis
  • [MeSH-minor] Anaplasia. Animals. Blotting, Western. Cell Line, Tumor. Disease Models, Animal. Disease Progression. Gene Expression Regulation, Neoplastic. Male. Prostate / pathology. RNA, Messenger / analysis. Rats. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 16076703.001).
  • [ISSN] 0284-186X
  • [Journal-full-title] Acta oncologica (Stockholm, Sweden)
  • [ISO-abbreviation] Acta Oncol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Norway
  • [Chemical-registry-number] 0 / RNA, Messenger; 0 / Receptors, LHRH
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14. Bernoulli J, Yatkin E, Laakso A, Anttinen M, Bosland M, Vega K, Kallajoki M, Santti R, Pylkkänen L: Histopathological evidence for an association of inflammation with ductal pin-like lesions but not with ductal adenocarcinoma in the prostate of the noble rat. Prostate; 2008 May 15;68(7):728-39
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  • [Title] Histopathological evidence for an association of inflammation with ductal pin-like lesions but not with ductal adenocarcinoma in the prostate of the noble rat.
  • BACKGROUND: Chronic inflammation may contribute to the development of prostate cancer.
  • The goal of this study was to determine the possible association of prostatic inflammation, prostatic intraepithelial neoplasia (PIN)-like lesion, and prostate cancer, and to assess the androgen and estrogen dependency of the early steps of carcinogenesis.
  • RESULTS: After treatment for 13 weeks, acute and chronic inflammation was found in the dorsolateral prostate lobes and both inflammation and PIN-like lesions were present in the periurethal area of the prostate in all animals (n = 8).
  • Following hormone exposure for 18 and 26 weeks, inflammation in the prostate remained, and adenocarcinomas in the periurethal prostate area with no adjacent inflammation were observed in all 18 animals studied.
  • When both hormone implants were removed after 15 weeks, PIN-like lesions progressed further to adenocarcinoma only in two of seven animals.
  • CONCLUSIONS: Even though adenocarcinomas were not morphologically associated with inflammation, PIN-like lesions preceding adenocarcinoma were found in close association with inflammation, pointing towards a possible initiator role of inflammation in the early steps of prostatic carcinogenesis.
  • [MeSH-major] Carcinoma, Ductal / pathology. Precancerous Conditions / pathology. Prostate / pathology. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Neoplasms / pathology. Prostatitis / pathology

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18302197.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Drug Implants; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 9002-62-4 / Prolactin
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15. Powolny AA, Wang S, Carlton PS, Hoot DR, Clinton SK: Interrelationships between dietary restriction, the IGF-I axis, and expression of vascular endothelial growth factor by prostate adenocarcinoma in rats. Mol Carcinog; 2008 Jun;47(6):458-65
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interrelationships between dietary restriction, the IGF-I axis, and expression of vascular endothelial growth factor by prostate adenocarcinoma in rats.
  • Human studies suggest that excessive energy intake and obesity may influence prostate cancer progression.
  • The present study examines changes in the insulin-like growth factor I (IGF-I) axis caused by dietary restriction and their association with the expression of vascular endothelial growth factor (VEGF) in prostate cancer.
  • After 8 wk, rats were implanted with rat AT6.3 prostate adenocarcinoma cells.
  • Two weeks later, the animals were sacrificed and serum, normal prostate, liver, and prostate tumor samples were collected for analyses.
  • Dietary restriction also lowered mRNA expression of IGF-I (45%, P = 0.0242) and its receptor IGFIR (40%, P = 0.0083) in prostate tumors.
  • Similarly, reduced VEGF mRNA (30%, P = 0.0176) and secreted VEGF protein (33%, P = 0.0003) were observed in prostate cancer of restricted rats.
  • An in vitro study employing AT6.3 prostate cancer cells demonstrated dose- and time-dependent stimulation of VEGF expression by IGF-I.
  • These results suggest that dietary restriction reduces endocrine and prostate tumor autocrine/paracrine IGF-I expression, which contributes to reduced VEGF expression and signaling, to inhibit tumor angiogenesis associated with prostate tumorigenesis.
  • [MeSH-major] Adenocarcinoma / metabolism. Caloric Restriction. Diet. Insulin-Like Growth Factor I / physiology. Prostatic Neoplasms / metabolism. Vascular Endothelial Growth Factor A / metabolism

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 18058807.001).
  • [ISSN] 1098-2744
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 P30 CA016058
  • [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 / Insulin-Like Growth Factor Binding Protein 3; 0 / Vascular Endothelial Growth Factor A; 67763-96-6 / Insulin-Like Growth Factor I
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16. Takahashi S, Takeshita K, Seeni A, Sugiura S, Tang M, Sato SY, Kuriyama H, Nakadate M, Abe K, Maeno Y, Nagao M, Shirai T: Suppression of prostate cancer in a transgenic rat model via gamma-tocopherol activation of caspase signaling. Prostate; 2009 May 1;69(6):644-51
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of prostate cancer in a transgenic rat model via gamma-tocopherol activation of caspase signaling.
  • BACKGROUND: Epidemiological data indicate that intake of one form of vitamin E, gamma-tocopherol, may reduce prostate cancer risk, and several in vitro studies have demonstrated that gamma-tocopherol can inhibit prostate cancer cell growth.
  • The purpose of the present study was to confirm effects of gamma-tocopherol on prostate cancer in the transgenic rat for adenocarcinoma of prostate (TRAP) model established in our laboratory.
  • However, quantitative evaluation of prostatic lesions demonstrated significantly suppression of sequential progression from PIN to adenocarcinoma in a dose-dependent manner, along with clear activation of caspases 3 and 7 in the ventral lobe in both experiments.
  • CONCLUSIONS: The present study clearly demonstrated that gamma-tocopherol suppresses prostate tumor progression in an in vivo TRAP model, and could be a candidate chemopreventive agent for human prostate cancer.
  • [MeSH-major] Adenocarcinoma / prevention & control. Prostatic Neoplasms / prevention & control. gamma-Tocopherol / therapeutic use

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19143023.001).
  • [ISSN] 1097-0045
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antioxidants; 0 / Ceramides; 0 / Isoenzymes; 1406-66-2 / Tocopherols; 8EF1Z1238F / gamma-Tocopherol; EC 3.1.3.- / tartrate-resistant acid phosphatase; EC 3.1.3.2 / Acid Phosphatase
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17. McCormick DL, Johnson WD, Kozub NM, Rao KV, Lubet RA, Steele VE, Bosland MC: Chemoprevention of rat prostate carcinogenesis by dietary 16alpha-fluoro-5-androsten-17-one (fluasterone), a minimally androgenic analog of dehydroepiandrosterone. Carcinogenesis; 2007 Feb;28(2):398-403
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  • [Title] Chemoprevention of rat prostate carcinogenesis by dietary 16alpha-fluoro-5-androsten-17-one (fluasterone), a minimally androgenic analog of dehydroepiandrosterone.
  • Dehydroepiandrosterone (DHEA) is a potent inhibitor of prostate carcinogenesis in rats.
  • However, concerns related to the possible androgenicity of DHEA may preclude its use for chemoprevention of human prostate cancer.
  • Studies were performed to compare the androgenicity of DHEA and a fluorinated DHEA analog, 16alpha-fluoro-5-androsten-17-one (fluasterone), and to determine the chemopreventive activity of fluasterone in the rat prostate.
  • Fluasterone conferred significant protection against prostate carcinogenesis induced in Wistar-Unilever rats by a sequential regimen of N-methyl-N-nitrosourea+testosterone.
  • Chronic administration of fluasterone at levels of 2000 and 1000 mg/kg diet reduced the incidence of adenocarcinoma in the dorsolateral/anterior prostate from 64% in dietary controls to 28 and 31%, respectively.
  • These data demonstrate that a minimally androgenic analog of DHEA protects against prostate carcinogenesis induced in rats by a chemical carcinogen + androgen.
  • On this basis, fluasterone merits consideration for evaluation in clinical trials for prostate cancer prevention.
  • The chemopreventive activity of a non-androgenic DHEA analog suggests that at least a portion of the chemopreventive activity of DHEA in the rat prostate is unrelated to hormonal effects.

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  • (PMID = 16952912.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA016087; United States / NIEHS NIH HHS / ES / ES000260; United States / NCI NIH HHS / CN / N01-CN-65120
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 156680-74-9 / 5-androstene-16-fluoro-17-one; 459AG36T1B / Dehydroepiandrosterone
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18. Delella FK, Justulin LA Jr, Felisbino SL: Tissue inhibitor of metalloproteinase-2 (TIMP-2) location in the ventral, lateral, dorsal and anterior lobes of rat prostate by immunohistochemistry. Cell Biol Int; 2007 Mar;31(3):229-34
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  • [Title] Tissue inhibitor of metalloproteinase-2 (TIMP-2) location in the ventral, lateral, dorsal and anterior lobes of rat prostate by immunohistochemistry.
  • MMPs have been found in rat prostate secretions and are nearly lobe specific in expression pattern.
  • The aim of this study was to evaluate whether TIMP-2, like other semen components, is expressed differently from different rat prostatic lobes.
  • Immunohistochemical staining was performed in both young and adult rat ventral (VP), lateral (LP), dorsal (DP), and anterior (AP) prostatic lobes and confirmed by western blotting.
  • However, TIMP-2 expression in LP was not induced by prostatitis, since younger rat LPs were also strongly TIMP-2 positive.
  • Further studies should address whether TIMP-2 expression is related to the highest incidence of rat LP prostatitis and adenocarcinoma.
  • [MeSH-major] Prostate / anatomy & histology. Prostate / enzymology. Prostatitis / enzymology. Tissue Inhibitor of Metalloproteinase-2 / analysis

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  • (PMID = 17123845.001).
  • [ISSN] 1065-6995
  • [Journal-full-title] Cell biology international
  • [ISO-abbreviation] Cell Biol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 127497-59-0 / Tissue Inhibitor of Metalloproteinase-2
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19. Ribeiro DL, Marques SF, Alberti S, Spadella CT, Manzato AJ, Taboga SR, Dizeyi N, Abrahamsson PA, Góes RM: Malignant lesions in the ventral prostate of alloxan-induced diabetic rats. Int J Exp Pathol; 2008 Aug;89(4):276-83
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  • [Title] Malignant lesions in the ventral prostate of alloxan-induced diabetic rats.
  • The aim of this study was to evaluate the changes caused by chronic diabetes in the rat ventral prostate and to establish a correlation between diabetes and the development of prostatic lesions.
  • Ninety days after diabetes diagnosis, animals were sacrificed and the ventral prostate was removed and prepared for general and immunohistochemical analyses.
  • The prostate morphology and stereology showed high variation in the diabetic group.
  • Some animals had light changes; the great majority had an intense epithelial atrophy; and other rats showed premalignant and malignant lesions in the prostate.
  • The diabetic group also presented high incidence of prostatitis, adenocarcinoma and prostatic intra-epithelial neoplasia (PIN).
  • Samples with adenocarcinoma had poorly differentiated acini with high levels of cellular proliferation and nuclear atypia.
  • An association of PIA, PIN and adenocarcinoma was detected in one sample.
  • Reduced androgen levels have a synergic effect to insulin dysfunction promoting negative effects in the rat prostate.
  • [MeSH-major] Adenocarcinoma / etiology. Diabetes Mellitus, Experimental / complications. Prostatic Neoplasms / etiology
  • [MeSH-minor] Animals. Biomarkers, Tumor / analysis. Immunohistochemistry. Male. Prostate / pathology. Prostatic Hyperplasia / blood. Prostatic Hyperplasia / pathology. Prostatic Intraepithelial Neoplasia / blood. Prostatic Intraepithelial Neoplasia / pathology. Prostatitis / blood. Prostatitis / pathology. Proto-Oncogene Proteins c-bcl-2 / analysis. Rats. Rats, Wistar. Tenascin / analysis. Testosterone / blood

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  • (PMID = 18715471.001).
  • [ISSN] 1365-2613
  • [Journal-full-title] International journal of experimental pathology
  • [ISO-abbreviation] Int J Exp Pathol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tenascin; 3XMK78S47O / Testosterone
  • [Other-IDs] NLM/ PMC2525783
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20. Yamashita S, Takahashi S, McDonell N, Watanabe N, Niwa T, Hosoya K, Tsujino Y, Shirai T, Ushijima T: Methylation silencing of transforming growth factor-beta receptor type II in rat prostate cancers. Cancer Res; 2008 Apr 1;68(7):2112-21
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  • [Title] Methylation silencing of transforming growth factor-beta receptor type II in rat prostate cancers.
  • To identify methylation-silenced genes in prostate cancers, a microarray analysis for genes up-regulated by treatment with a demethylating agent, 5-aza-2'-deoxycytidine, was performed using three rat prostate cancer cell lines.
  • From the eight genes, Tgfbr2, a key mediator of transforming growth factor-beta (TGF-beta) signaling that has been strongly implicated in human and rat prostate carcinogenesis, was selected, and its silencing in primary samples was analyzed further.
  • Tgfbr2 was methylated and markedly down-regulated in three of seven 3,2'-dimethyl-4-aminobiphenyl-induced invasive adenocarcinomas in the dorsolateral lobe of the rat prostate.
  • In humans, marked down-regulation of TGFBR2 protein was observed in 12 of 20 high-grade prostatic intraepithelial neoplasia and 36 of 60 prostate cancers.
  • DNA methylation of the human TGFBR2 promoter CpG islands repressed transcription, if present, but neither methylation nor mutation were detected in 27 human prostate cancers analyzed.
  • Methylation silencing of rat Tgfbr2 was associated with histone H3 lysine 9 trimethylation, whereas decreased expression of human TGFBR2 was mainly due to decreased transcription activity, sometimes in concert with histone deacetylation and H3 lysine 27 trimethylation.
  • The identification of methylation silencing of Tgfbr2 in rat prostate cancers, in accordance with TGFBR2 down-regulation in human prostate cancers, will enable us to analyze how aberrant methylation is induced in vivo and identify factors that promote and suppress the induction of aberrant methylation.
  • [MeSH-major] Adenocarcinoma / genetics. DNA Methylation. Gene Silencing. Prostatic Neoplasms / genetics. Protein-Serine-Threonine Kinases / genetics. Receptors, Transforming Growth Factor beta / genetics

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  • (PMID = 18381416.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Histones; 0 / Receptors, Transforming Growth Factor beta; 776B62CQ27 / decitabine; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.30 / transforming growth factor-beta type II receptor; M801H13NRU / Azacitidine
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21. Suckow MA, Wolter W, Pollard M: Susceptibility of Lobund-Wistar x Copenhagen hybrid rats to autochthonous prostate carcinogenesis. Prostate; 2005 Jul 1;64(2):203-8
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  • [Title] Susceptibility of Lobund-Wistar x Copenhagen hybrid rats to autochthonous prostate carcinogenesis.
  • BACKGROUND: Transplantation of the Dunning R-3327 prostate tumor cell line is a common model of prostate cancer, though the rat strain (Copenhagen) from which the cell line was derived is resistant to spontaneous and chemically induced prostate cancer.
  • METHODS: To determine if susceptibility to chemically induced prostate carcinogenesis can be transferred from the susceptible Lobund-Wistar (LW) rat strain to the resistant Copenhagen (COP) strain, male COP rats and LW x COP hybrids were administered an intravenous dose (30 mg/kg) of methylnitrosourea (MNU) and implanted three times with silastic capsules containing testosterone propionate (25 mg each) at a 2-month interval.
  • Prostate cancer did not develop in COP rats, but 36% of LW x COP hybrids developed prostate-seminal vesicle tumors which expanded into the dorsolateral lobes within 10 months of MNU administration; this compares to 90% of LW rats which develop such tumors following this same induction protocol.
  • CONCLUSIONS: COP rats lack inherent susceptibility to development of prostate cancer; susceptibility may be transferred from LW rats, or resistance from COP rats, to LW x COP hybrids and is present in the haploid state, consistent with the two-mutation event hypothesis of Knudson which holds that two mutations are required at a genetic locus for development of some cancers.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15712219.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Gonadal Steroid Hormones; 3XMK78S47O / Testosterone; 684-93-5 / Methylnitrosourea
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22. McCormick DL, Rao KV, Johnson WD, Bosland MC, Lubet RA, Steele VE: Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate. Cancer Prev Res (Phila); 2010 Mar;3(3):381-92
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Null activity of selenium and vitamin e as cancer chemopreventive agents in the rat prostate.
  • To evaluate the potential efficacy of selenium and vitamin E as inhibitors of prostate carcinogenesis, four chemoprevention studies using a common protocol were done in a rat model of androgen-dependent prostate cancer.
  • After stimulation of prostate epithelial cell proliferation by a sequential regimen of cyproterone acetate followed by testosterone propionate, male Wistar-Unilever rats received a single i.v. injection of N-methyl-N-nitrosourea (MNU) followed by chronic androgen stimulation via subcutaneous implantation of testosterone pellets.
  • Each chemoprevention study was terminated at 13 months post-MNU, and prostate cancer incidence was determined by histopathologic evaluation.
  • No statistically significant reductions in prostate cancer incidence were identified in any group receiving dietary supplementation with selenium and/or vitamin E.
  • These data do not support the hypotheses that selenium and vitamin E are potent cancer chemopreventive agents in the prostate, and when considered with the recent clinical data reported in the Selenium and Vitamin E Cancer Prevention Trial (SELECT), show the predictive nature of this animal model for human prostate cancer chemoprevention.

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  • (PMID = 20145190.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CN / N01-CN-95113; United States / NCI NIH HHS / CA / P30 CA016087; United States / NCI NIH HHS / CN / N01 CN095113; United States / NIEHS NIH HHS / ES / P30-ES-00260; United States / NCI NIH HHS / CN / N01 CN065120; United States / NIEHS NIH HHS / ES / P30 ES000260; United States / NCI NIH HHS / CA / P30-CA-16087; United States / NCI NIH HHS / CA / N01 CN35566; United States / NCI NIH HHS / CN / CN35566-02; United States / NCI NIH HHS / CN / N01-CN-65120; United States / NCI NIH HHS / CN / N01 CN35566-02; United States / NCI NIH HHS / CN / N01-CN-35566-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Androgens; 0 / Antioxidants; 0 / Selenium Compounds; 1406-18-4 / Vitamin E; 3XMK78S47O / Testosterone; 4KM2BN5JHF / Cyproterone Acetate; 684-93-5 / Methylnitrosourea; 964MRK2PEL / Selenomethionine; H4N855PNZ1 / alpha-Tocopherol
  • [Other-IDs] NLM/ NIHMS161245; NLM/ PMC2945242
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23. Prawettongsopon C, Asawakarn S, Suthiphongchai T: Suppression of prometastatic phenotype of highly metastatic androgen-independent rat prostate cancer MLL cell line by PI3K inhibitor LY294002. Oncol Res; 2009;17(7):301-9
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  • [Title] Suppression of prometastatic phenotype of highly metastatic androgen-independent rat prostate cancer MLL cell line by PI3K inhibitor LY294002.
  • Upregulation of the PI3K pathway has often been reported in androgen-independent prostate cancer and is implicated in cancer cell survival and proliferation in the absence of androgen.
  • Inhibition of PI3K by LY294002 suppressed cell invasion and motility of the highly metastatic androgen-independent Dunning rat prostate cancer MLL cell line with similar IC50 values and inhibition profile.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Animals. Cell Movement / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Matrix Metalloproteinase 2 / genetics. Matrix Metalloproteinase 2 / metabolism. Phosphorylation / drug effects. RNA, Messenger / genetics. RNA, Messenger / metabolism. Rats. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction. Tumor Cells, Cultured. Urokinase-Type Plasminogen Activator / genetics. Urokinase-Type Plasminogen Activator / metabolism

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  • (PMID = 19408575.001).
  • [ISSN] 0965-0407
  • [Journal-full-title] Oncology research
  • [ISO-abbreviation] Oncol. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Chromones; 0 / Enzyme Inhibitors; 0 / Morpholines; 0 / RNA, Messenger; 154447-36-6 / 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.24 / Matrix Metalloproteinase 2
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24. Johansson A, Jones J, Pietras K, Kilter S, Skytt A, Rudolfsson SH, Bergh A: A stroma targeted therapy enhances castration effects in a transplantable rat prostate cancer model. Prostate; 2007 Nov 1;67(15):1664-76
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  • [Title] A stroma targeted therapy enhances castration effects in a transplantable rat prostate cancer model.
  • BACKGROUND: Castration results in a major involution of the normal prostate gland.
  • This process is initiated by effects in the prostate stroma and vasculature.
  • Castration-induced regression of androgen sensitive prostate tumors is however less prominent and hypothetically this could be related to a limited stromal/vascular response.
  • RESULTS: In the normal ventral prostate (VP) nuclear androgen receptors (AR) were rapidly downregulated after castration.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Orchiectomy. Piperazines / pharmacology. Prostatic Neoplasms / drug therapy. Pyrimidines / pharmacology. Receptor, TIE-2 / metabolism. Stromal Cells / drug effects
  • [MeSH-minor] Androgen Receptor Antagonists. Angiopoietins / antagonists & inhibitors. Angiopoietins / metabolism. Animals. Benzamides. Disease Models, Animal. Down-Regulation. Drug Therapy, Combination. Imatinib Mesylate. Immunoglobulin Fc Fragments / pharmacology. Male. Neoplasm Transplantation. Neovascularization, Pathologic / pathology. Neovascularization, Pathologic / prevention & control. Prostate / blood supply. Prostate / drug effects. Prostate / metabolism. Prostate / pathology. Rats. Receptor, Platelet-Derived Growth Factor beta / antagonists & inhibitors. Receptor, Platelet-Derived Growth Factor beta / metabolism. Receptors, Androgen / metabolism. Recombinant Fusion Proteins / pharmacology. Xenograft Model Antitumor Assays

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  • (PMID = 17854058.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen Receptor Antagonists; 0 / Angiopoietins; 0 / Antineoplastic Agents; 0 / Benzamides; 0 / Immunoglobulin Fc Fragments; 0 / Piperazines; 0 / Pyrimidines; 0 / Receptors, Androgen; 0 / Recombinant Fusion Proteins; 8A1O1M485B / Imatinib Mesylate; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta; EC 2.7.10.1 / Receptor, TIE-2
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25. Wang Y, Kasper S, Yuan J, Jin RJ, Zhang J, Ishii K, Wills ML, Hayward SW, Matusik RJ: Androgen-dependent prostate epithelial cell selection by targeting ARR(2)PBneo to the LPB-Tag model of prostate cancer. Lab Invest; 2006 Oct;86(10):1074-88
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  • [Title] Androgen-dependent prostate epithelial cell selection by targeting ARR(2)PBneo to the LPB-Tag model of prostate cancer.
  • Development was normal and all six ARR(2)PBneo transgenic founder lines expressed the Neo gene in a prostate-specific manner.
  • Line C, which expressed high levels of neo, was crossbred to LPB-Tag 12T-7f transgenic mice (in which the SV40 large T antigen (Tag) was targeted to the prostate by the large probasin (LPB) promoter).
  • Prostatic lesions developed in these mice in a predictable and heritable manner, indicating that Neo did not alter Tag-induced prostate tumor development and progression.
  • To determine if these NeoTag cells maintained a similar in vivo phenotype to the 12T-7f transgenic line, tissue recombinations were made with rat urogenital sinus mesenchyme (rUGM) and grafted under the renal capsule of male nude mouse hosts.
  • In recombinants, the three NeoTag strains developed PIN lesions and/or more extensive adenocarcinoma than seen in the 12T-7f mouse.
  • NeoTag cells grafted without rUGM developed undifferentiated adenocarcinoma demonstrating that prostatic stroma dictates the glandular architecture seen in the well-differentiated adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / pathology. Androgens / physiology. Epithelial Cells / pathology. Hybridization, Genetic. Prostate / pathology. Prostatic Neoplasms / pathology

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  • (PMID = 16894353.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Grant] United States / NIA NIH HHS / AG / R01 AG23490; United States / NCI NIH HHS / CA / R01 CA76142; United States / NCI NIH HHS / CA / U01 CA96403
  • [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 / Androgen-Binding Protein; 0 / Androgens; 0 / Receptors, Androgen; 0 / probasin; EC 2.7.1.95 / Kanamycin Kinase
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26. Liao Z, Wang S, Boileau TW, Erdman JW Jr, Clinton SK: Increased phospho-AKT is associated with loss of the androgen receptor during the progression of N-methyl-N-nitrosourea-induced prostate carcinogenesis in rats. Prostate; 2005 Jul 1;64(2):186-99
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  • [Title] Increased phospho-AKT is associated with loss of the androgen receptor during the progression of N-methyl-N-nitrosourea-induced prostate carcinogenesis in rats.
  • BACKGROUND: Characterization of molecular events during N-methyl-N-nitrosourea (MNU)-induced rat prostate carcinogenesis enhances the utility of this model for the preclinical assessment of preventive strategies.
  • Androgen independence is typical of advanced human prostate cancer and may occur through multiple mechanisms including the loss of androgen receptor (AR) expression and the activation of alternative signaling pathways.
  • METHODS: We examined the interrelationships between AR and p-AKT expression by immunohistochemical staining during MNU-androgen-induced prostate carcinogenesis in male Wistar-Unilever rats.
  • RESULTS: The percentage of AR positive nuclei decreased (P < 0.01) as carcinogenesis progressed: hyperplasia (92%), atypical hyperplasia (92%), well-differentiated adenocarcinoma (57%), moderately-differentiated adenocarcinoma (19%), and poorly-differentiated adenocarcinoma (10%).
  • Sparse staining was observed in normal tissues (0.2% of epithelial area) and hyperplastic lesions (0.1%), while expression increased significantly (P < 0.001) in atypical hyperplasia (7.6%), well-differentiated adenocarcinoma (16.7%), moderately-differentiated adenocarcinoma (19.6%), and poorly-differentiated adenocarcinoma (17.4%).
  • CONCLUSIONS: In the MNU model, the progressive evolution of dominant tumor cell populations showing an increase in p-AKT in parallel with a decline in AR staining suggests that activation of AKT signaling may be one of several mechanisms contributing to androgen insensitivity during prostate cancer progression.

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  • [Copyright] (c) 2005 Wiley-Liss, Inc.
  • (PMID = 15682402.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30-CA16058; United States / NCI NIH HHS / CA / R01-CA72482
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Proto-Oncogene Proteins; 0 / Receptors, Androgen; 684-93-5 / Methylnitrosourea; EC 2.7.11.1 / Akt1 protein, rat; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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27. Kraaij R, van der Weel L, de Ridder CM, van der Korput HA, Zweistra JL, van Rijswijk AL, Bangma CH, Trapman J: A small chimeric promoter for high prostate-specific transgene expression from adenoviral vectors. Prostate; 2007 Jun 1;67(8):829-39
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A small chimeric promoter for high prostate-specific transgene expression from adenoviral vectors.
  • For prostate cancer, transcriptional targeting has been applied but was hampered by loss of specificity and low activity.
  • We constructed a small chimeric promoter for high and prostate-specific transgene expression from adenoviral vectors.
  • METHODS: A chimeric promoter, composed of the prostate-specific antigen (PSA) enhancer and the rat probasin promoter, was cloned into an adenoviral vector and its activity was compared to vectors containing conventional prostate-specific promoters and the constitutive Cytomegalovirus (CMV) promoter in in vitro and in vivo prostate cancer models.
  • RESULTS: The chimeric PSA-probasin promoter was the most active prostate-specific promoter reaching up to 20% of CMV promoter activity while maintaining prostate-specificity.
  • CONCLUSIONS: The chimeric PSA-probasin promoter is a small promoter that can be utilized in viral vectors for high prostate-specific transgene expression.
  • [MeSH-major] Adenocarcinoma / therapy. Genetic Therapy / methods. Promoter Regions, Genetic. Prostatic Neoplasms / therapy. Transgenes
  • [MeSH-minor] Adenoviridae / genetics. Androgen-Binding Protein / genetics. Animals. Cell Line, Tumor. Cytomegalovirus / genetics. Genetic Vectors / genetics. Humans. Male. Mice. Mice, Nude. Microscopy, Fluorescence. Plasmids / genetics. Prostate-Specific Antigen / genetics. Recombinant Fusion Proteins / genetics

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  • [Copyright] Copyright 2007 Wiley-Liss, Inc.
  • (PMID = 17394196.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / Recombinant Fusion Proteins; 0 / probasin; EC 3.4.21.77 / Prostate-Specific Antigen
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28. Singh RP, Agarwal R: Prostate cancer chemoprevention by silibinin: bench to bedside. Mol Carcinog; 2006 Jun;45(6):436-42
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  • [Title] Prostate cancer chemoprevention by silibinin: bench to bedside.
  • Prostate cancer (PCA) is the most invasive malignancy and second leading cause of cancer deaths in American males.
  • Silibinin inhibits growth of PCA cells from human, mouse, and rat origins, and also suppresses human prostate tumor xenograft growth in nude mice.
  • Silibinin also inhibits PCA growth in the transgenic adenocarcinoma of mouse prostate (TRAMP) mouse model.

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  • (PMID = 16637061.001).
  • [ISSN] 0899-1987
  • [Journal-full-title] Molecular carcinogenesis
  • [ISO-abbreviation] Mol. Carcinog.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA102514
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / NF-kappa B; 0 / Silymarin; 4RKY41TBTF / silybin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptor, IGF Type 1
  • [Number-of-references] 20
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29. Gutierrez LS, Noria F, Finol H, Sun L, Castellino F, Pollard M: Fas ligand expression and its correlation with apoptosis and proliferation in Lobund-Wistar prostate carcinomas. Pathobiology; 2005;72(5):260-8
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  • [Title] Fas ligand expression and its correlation with apoptosis and proliferation in Lobund-Wistar prostate carcinomas.
  • The L-W rat strain develops spontaneous and induced adenocarcinomas in the anterior prostate and seminal vesicles.
  • Although FasL expression has been observed in a subset of human prostate carcinomas, this multistage model allowed in vivo evaluation of subclones of malignant cells with a single genetic susceptibility.
  • Therefore, analysis of FasL may have clinical relevance in detecting the malignant potential of prostate cancers.
  • [MeSH-major] Adenocarcinoma / metabolism. Apoptosis. Cell Proliferation. Membrane Glycoproteins / metabolism. Prostatic Neoplasms / metabolism. Tumor Necrosis Factors / metabolism

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  • (PMID = 16374070.001).
  • [ISSN] 1015-2008
  • [Journal-full-title] Pathobiology : journal of immunopathology, molecular and cellular biology
  • [ISO-abbreviation] Pathobiology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Membrane Glycoproteins; 0 / Proliferating Cell Nuclear Antigen; 0 / Tnfsf6 protein, rat; 0 / Tumor Necrosis Factors
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30. Gu LZ, Hu WY, Antic N, Mehta R, Turner JR, de Lanerolle P: Inhibiting myosin light chain kinase retards the growth of mammary and prostate cancer cells. Eur J Cancer; 2006 May;42(7):948-57
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  • [Title] Inhibiting myosin light chain kinase retards the growth of mammary and prostate cancer cells.
  • We have extended these studies and found that ML-7 stimulates the ability of etoposide to induce apoptosis in Mm5MT mouse mammary adenocarcinoma cells and Mat-Ly-Lu rat prostate cancer cells in vitro.
  • In vivo experiments demonstrated that ML-7 retards the growth of mammary tumours in mice and prostate tumours in rats.
  • Moreover, ML-7 significantly stimulates the ability of etoposide to prevent the growth of established mammary tumours in mice and prostate tumours in rats.
  • [MeSH-major] Adenocarcinoma / pathology. Azepines / pharmacology. Mammary Neoplasms, Experimental / pathology. Myosin-Light-Chain Kinase / antagonists & inhibitors. Naphthalenes / pharmacology. Prostatic Neoplasms / pathology

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  • (PMID = 16574402.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 61931; United States / NIDDK NIH HHS / DK / DK 68271; United States / NHLBI NIH HHS / HL / HL 59618; United States / NHLBI NIH HHS / HL / HL 64702
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Azepines; 0 / Naphthalenes; 109376-83-2 / ML 7; 6PLQ3CP4P3 / Etoposide; EC 2.7.11.18 / Myosin-Light-Chain Kinase
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31. Kawai N, Futakuchi M, Yoshida T, Ito A, Sato S, Naiki T, Honda H, Shirai T, Kohri K: Effect of heat therapy using magnetic nanoparticles conjugated with cationic liposomes on prostate tumor in bone. Prostate; 2008 May 15;68(7):784-92
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  • [Title] Effect of heat therapy using magnetic nanoparticles conjugated with cationic liposomes on prostate tumor in bone.
  • Here, we examine the effects of MCL + AMF heat therapy on prostate cancer tissue in a bone microenvironment and on bone destruction in a rat model.
  • MATERIALS AND METHODS: Rat prostate cancer nodules were transplanted onto the calvaria of 6-week-old F344 male rats.
  • The bone destruction index, which indicates the degree of osteolysis associated with prostate tumor growth in the bone microenvironment, was 34.8% in the MCL group and 67.2% in the control group with significant difference.
  • If MCL are specifically taken into the prostate cancer cells in the bone microenvironment, this method may be useful for the treatment of bone metastatic lesions of prostate cancer.
  • [MeSH-major] Adenocarcinoma / therapy. Bone Neoplasms / therapy. Ferrosoferric Oxide / therapeutic use. Hypothermia, Induced / methods. Nanoparticles / therapeutic use. Prostatic Neoplasms / therapy

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  • [Copyright] (c) 2008 Wiley-Liss, Inc.
  • (PMID = 18302228.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cations; 0 / Liposomes; XM0M87F357 / Ferrosoferric Oxide
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32. Huss WJ, Gray DR, Greenberg NM, Mohler JL, Smith GJ: Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells. Cancer Res; 2005 Aug 1;65(15):6640-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Breast cancer resistance protein-mediated efflux of androgen in putative benign and malignant prostate stem cells.
  • Putative prostate stem cells and prostate tumor stem cells in benign and malignant human prostate tissue, in primary human prostate xenografts, and in the transgenic adenocarcinoma of the mouse prostate (TRAMP) mouse model of prostate cancer, are defined by expression of breast cancer resistance protein (BCRP), a marker of pluripotent hematopoietic, muscle, and neural stem cells, and by an absence of androgen receptor (AR) protein.
  • Inhibition of BCRP-mediated efflux of dihydrotestosterone by novobiocin or fumitremorgin C in a rat prostate progenitor cell line that expresses BCRP and AR mRNAs, but minimal AR protein, results in stabilization and nuclear translocation of AR protein, providing a mechanism for lack of AR protein in BCRP-expressing stem cells.
  • In both benign and malignant human prostate tissue, the rare epithelial cells that express BCRP and lack AR protein are localized in the basal cell compartment, survive androgen deprivation, and maintain proliferative potential in the hypoxic, androgen-deprived prostate.
  • Putative prostate tumor stem cells that express BCRP but not AR protein in TRAMP are the source of a BCRP-negative and AR-negative, Foxa2- and SV40Tag-expressing, transit amplifying compartment that progresses to the poorly differentiated carcinomas that arise rapidly after castration.
  • Therefore, BCRP expression isolates prostate stem/tumor stem cells from the prostate tissue microenvironment through constitutive efflux of androgen, protecting the putative tumor stem cells from androgen deprivation, hypoxia, or adjuvant chemotherapy, and providing the nidus for recurrent prostate cancer.

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  • (PMID = 16061644.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA84296; United States / NCI NIH HHS / CA / P01 CA077739; United States / NCI NIH HHS / CA / CA77739; United States / NCI NIH HHS / CA / CA64851; United States / NIEHS NIH HHS / ES / ES07017; United States / NCI NIH HHS / CA / CA64865
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ABCG2 protein, human; 0 / Androgens; 0 / Indoles; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Receptors, Androgen; 17EC19951N / Novobiocin; CW5S8OP3VO / tryptoquivaline
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33. Zeng Y, Yokohira M, Takeuchi H, Saoo K, Yamakawa K, Matsuda Y, Hosokawa K, Li JQ, Ikeda M, Imaida K: Lack of significant modifying effect of arctiin on prostate carcinogenesis in probasin/SV40 T antigen transgenic rats. Cancer Lett; 2005 May 26;222(2):145-51
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  • [Title] Lack of significant modifying effect of arctiin on prostate carcinogenesis in probasin/SV40 T antigen transgenic rats.
  • Modifying effects of arctiin on prostate carcinogenesis in probasin/SV 40 T antigen (Tag) transgenic (TG) rats were examined.
  • Histopathological evaluation of prostate revealed that all the rats in any group developed adenocarcinoma in dorsolateral lobe of prostate, except two rats in 0.1% arctiin treated and one rat in 0.002% arctiin treated groups without prostate adenocarcinoma development.
  • However, there were no definite treatment-related changes with statistical significance in all parameters for prostate carcinomas measured in this experiment.
  • These results indicated that arctiin might not exert significant modifying effect on prostate carcinogenesis in SV 40 Tag TG rats at least under the present experiment.

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  • (PMID = 15863263.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / Antigens, Polyomavirus Transforming; 0 / Drugs, Chinese Herbal; 0 / Furans; 0 / Glucosides; 0 / probasin; TM5RQ949K7 / arctiin
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34. Kandori H, Suzuki S, Asamoto M, Murasaki T, Mingxi T, Ogawa K, Shirai T: Influence of atrazine administration and reduction of calorie intake on prostate carcinogenesis in probasin/SV40 T antigen transgenic rats. Cancer Sci; 2005 Apr;96(4):221-6
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  • [Title] Influence of atrazine administration and reduction of calorie intake on prostate carcinogenesis in probasin/SV40 T antigen transgenic rats.
  • In this study, modifying effects of dietary feeding of 500 and 1000 p.p.m. atrazine on the development of androgen-dependent prostate cancer were investigated using male probasin/SV40 T antigen transgenic (TG) rats.
  • As administration of atrazine has now been identified as causing a decrease in bodyweight, a dietary-restricted TG rat group was also included in order to elucidate the influence of reduction of calorie intake per se on the development of prostate cancer.
  • At week 13, almost the entire lobes of the prostate were occupied with tumor lesions, with no clear intergroup differences in the incidences and multiplicities.
  • Therefore, morphometrical assessment ratios of the prostate epithelial area to the whole prostate tissue area were evaluated.
  • Our results indicate that the observed atrazine-related suppression of prostate carcinogenesis was probably caused by the decrease in calorie intake, rather than by atrazine-related endocrine disruption.
  • [MeSH-major] Adenocarcinoma / pathology. Atrazine / pharmacology. Caloric Restriction. Herbicides / pharmacology. Prostatic Neoplasms / pathology
  • [MeSH-minor] Androgen-Binding Protein / genetics. Animals. Animals, Genetically Modified. Antigens, Polyomavirus Transforming / genetics. Body Weight / drug effects. Immunohistochemistry. Male. Prostate / drug effects. Prostate / metabolism. Prostate / pathology. Rats. Testosterone / blood

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  • (PMID = 15819720.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / Antigens, Polyomavirus Transforming; 0 / Herbicides; 0 / probasin; 3XMK78S47O / Testosterone; QJA9M5H4IM / Atrazine
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35. Suthiphongchai T, Phimsen S, Sakulkhu U, Tohtong R: PD98059-inhibited invasion of Dunning rat prostate cancer cells involves suppression of motility but not MMP-2 or uPA secretion. Oncol Rep; 2006 Jun;15(6):1605-10
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  • [Title] PD98059-inhibited invasion of Dunning rat prostate cancer cells involves suppression of motility but not MMP-2 or uPA secretion.
  • We have previously shown that ERK1/2 is necessary for invasiveness of Dunning rat prostatic adenocarcinoma cell lines in which levels of activated ERK1/2 correlate with the metastatic potential.
  • [MeSH-major] Adenocarcinoma / drug therapy. Cell Movement / drug effects. Flavonoids / pharmacology. Matrix Metalloproteinase 2 / secretion. Prostatic Neoplasms / drug therapy. Urokinase-Type Plasminogen Activator / secretion

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  • (PMID = 16685402.001).
  • [ISSN] 1021-335X
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one; 0 / Flavonoids; 0 / Matrix Metalloproteinase Inhibitors; 0 / Myosin Light Chains; EC 2.7.11.18 / Myosin-Light-Chain Kinase; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; EC 3.4.24.24 / Matrix Metalloproteinase 2
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36. Xin DQ, Zhu XH, Lai YQ, You R, Na YQ, Guo YL, Mao ZB: [Regulation of expression of pituitary tumor transforming gene 1 (PTTG1) by androgen in prostate cancer]. Beijing Da Xue Xue Bao; 2005 Dec 18;37(6):638-40
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  • [Title] [Regulation of expression of pituitary tumor transforming gene 1 (PTTG1) by androgen in prostate cancer].
  • OBJECTIVE: To identify the androgen-responsive genes in prostate and screen the molecular targets for further studying human prostate cancer.
  • METHODS: The potential androgen-responsive gene pituitary tumor transforming gene 1 (PTTG1) was selected which had been previously screened by cDNA microarray in rat prostate and its mRNA level was detected by Northern blot in the castrated rat prostate with and without replacement of Mibolerone.
  • Immunohistochemistry was performed to determine the expression and location of PTTG1 in human prostate tissues.
  • Then human androgen-dependent prostate cancer cells LNCaP were used as a model to study the regulation of PTTG1 by Mibolerone.
  • RESULTS: PTTG1 mRNA was hardly detectable in the prostate of 7-day castrated rats, while it was up-regulated dramatically in the prostate of 7-day castrated rats treated with Mibolerone for 2 days.
  • It was showed that high expression of PTTG1 was localized to the epithelial cells of human prostate cancer but not to the stromal cells with Immunohistochemistry.
  • The basic expression of PTTG1 in human androgen-independent prostate cancer cell lines PC3 or DU145 was even higher than that in the human androgen-dependent prostate cancer cells LNCaP treated with Mibolerone.
  • CONCLUSION: Androgen can up-regulate the PTTG1 expression in castrated rat prostate and human prostate cancer cell LNCaP.
  • It suggests that PTTG1 is potential to play an important role in human prostate cancer progression.
  • [MeSH-major] Gene Expression / drug effects. Nandrolone / analogs & derivatives. Neoplasm Proteins / genetics. Prostate / metabolism
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Blotting, Northern. Cell Line, Tumor. Humans. Immunohistochemistry. Male. Orchiectomy. Prostatic Neoplasms / genetics. Prostatic Neoplasms / metabolism. Prostatic Neoplasms / pathology. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley. Securin. Testosterone Congeners / pharmacology

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  • (PMID = 16378119.001).
  • [ISSN] 1671-167X
  • [Journal-full-title] Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences
  • [ISO-abbreviation] Beijing Da Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / Securin; 0 / Testosterone Congeners; 0 / pituitary tumor-transforming protein 1, human; 6PG9VR430D / Nandrolone; 9OGY4BOR8D / mibolerone
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37. Oka H, Chatani Y, Kohno M, Kawakita M, Ogawa O: Constitutive activation of the 41- and 43-kDa mitogen-activated protein (MAP) kinases in the progression of prostate cancer to an androgen-independent state. Int J Urol; 2005 Oct;12(10):899-905
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  • [Title] Constitutive activation of the 41- and 43-kDa mitogen-activated protein (MAP) kinases in the progression of prostate cancer to an androgen-independent state.
  • In this study, we examined whether constitutive activation of MAPK was related to the progression to androgen independence of prostate cancer.
  • METHODS: MAPK activation was examined by the appearance of phosphorylated forms and an in vitro kinase assay in four human (androgen-dependent and independent) prostate cancer cell lines and rat prostate cancer cell line Dunning (androgen-sensitive G line, and androgen-independent AT-3, AT-6 sublines).
  • CONCLUSIONS: The present fi ndings suggest that constitutive activation of MAPK may be associated with the acquisition of hormone independence in prostate cancer and that clonal selection after androgen removal and hormone-independent growth through the MAPK signal transduction pathway could begin at a relatively early period in the individual cells.
  • [MeSH-major] Adenocarcinoma / enzymology. Androgens / pharmacology. Biomarkers, Tumor / blood. Mitogen-Activated Protein Kinase Kinases / blood. Prostatic Neoplasms / enzymology. Testosterone / pharmacology

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  • (PMID = 16323984.001).
  • [ISSN] 0919-8172
  • [Journal-full-title] International journal of urology : official journal of the Japanese Urological Association
  • [ISO-abbreviation] Int. J. Urol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Androgens; 0 / Biomarkers, Tumor; 0 / Culture Media; 3XMK78S47O / Testosterone; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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38. Lui K, Huang Y, Choi HL, Yu S, Wong KB, Chen S, Chan FL: Molecular cloning and functional study of rat estrogen receptor-related receptor gamma in rat prostatic cells. Prostate; 2006 Nov 1;66(15):1600-19
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  • [Title] Molecular cloning and functional study of rat estrogen receptor-related receptor gamma in rat prostatic cells.
  • METHODS: We examined the ERRgamma expressions in rat prostates and Nb rat prostate cancer model, and its growth regulation in stable transfectants of prostatic cells.
  • RESULTS: We cloned the ERRgamma cDNA from rat prostate by RACE-PCR.
  • CONCLUSIONS: Our studies show that ERRgamma is functionally expressed in rat prostate and may play anti-proliferative actions in prostatic cells.
  • [MeSH-major] Adenocarcinoma / genetics. Cloning, Molecular. Gene Expression Regulation, Neoplastic. Prostate / metabolism. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Neoplasms / genetics. Receptors, Cytoplasmic and Nuclear / genetics. Receptors, Estrogen / genetics

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  • (PMID = 16927302.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NIEHS NIH HHS / ES / ES08258
  • [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 / DNA Primers; 0 / DNA, Complementary; 0 / Esrrg protein, rat; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Estrogen
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39. Heinrich JE, Pollard M, Wolter WA, Liang Z, Song H, Rosen ED, Suckow MA: Vaccination against prostate cancer using a live tissue factor deficient cell line in Lobund-Wistar rats. Cancer Immunol Immunother; 2007 May;56(5):725-30
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  • [Title] Vaccination against prostate cancer using a live tissue factor deficient cell line in Lobund-Wistar rats.
  • Reducing expression of the tissue factor gene in prostate adenocarcinoma cells (PAIII) results in a cell line that, in vivo, mimics the growth of wildtype (wt) PAIII.
  • Here, we provide support for this notion, and a strategy through which to implement it, by demonstrating that subcutaneous vaccinations with the TFD PAIII protect the Lobund-Wistar rat against subsequent wt PAIII cell challenge.
  • These results offer the intriguing possibility that the TFD PAIII vaccine is an effective system for the prevention and, possibly, the treatment of prostate cancer.
  • [MeSH-major] Adenocarcinoma / prevention & control. Cancer Vaccines / therapeutic use. Immunotherapy / methods. Prostatic Neoplasms / prevention & control. Thromboplastin / deficiency

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  • (PMID = 16953436.001).
  • [ISSN] 0340-7004
  • [Journal-full-title] Cancer immunology, immunotherapy : CII
  • [ISO-abbreviation] Cancer Immunol. Immunother.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / NIH/HL073750-01A1
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Cancer Vaccines; 9035-58-9 / Thromboplastin
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40. Chen H, Karam JA, Schultz R, Zhang Z, Duncan C, Hsieh JT: Cloning of mouse Dab2ip gene, a novel member of the RasGTPase-activating protein family and characterization of its regulatory region in prostate. DNA Cell Biol; 2006 Apr;25(4):232-45
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  • [Title] Cloning of mouse Dab2ip gene, a novel member of the RasGTPase-activating protein family and characterization of its regulatory region in prostate.
  • The downregulation of human DAB2IP mRNA levels was detected in prostate cancer cells due to the epigenetic regulation.
  • Here, we isolated a mouse Dab2ip gene with a highly homologous sequence to that of the human and rat gene and mapped it at chromosome 2B.
  • It appears that epigenetic regulation, particularly histone acetylation of the Dab2ip gene promoter, plays an important role in modulating its gene expression in the mouse prostate cancer cell.
  • [MeSH-major] Adaptor Proteins, Vesicular Transport / genetics. Adenocarcinoma / genetics. Cloning, Molecular. Prostate / metabolism. Prostatic Neoplasms / genetics. Regulatory Sequences, Nucleic Acid

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  • (PMID = 16629596.001).
  • [ISSN] 1044-5498
  • [Journal-full-title] DNA and cell biology
  • [ISO-abbreviation] DNA Cell Biol.
  • [Language] eng
  • [Databank-accession-numbers] GENBANK/ AY305656/ AY305657/ AY305658
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adaptor Proteins, Vesicular Transport; 0 / Dab2 protein, mouse; EC 1.13.12.- / Luciferases
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41. Said MM, Hokaiwado N, Tang M, Ogawa K, Suzuki S, Ghanem HM, Esmat AY, Asamoto M, Refaie FM, Shirai T: Inhibition of prostate carcinogenesis in probasin/SV40 T antigen transgenic rats by leuprorelin, a luteinizing hormone-releasing hormone agonist. Cancer Sci; 2006 Jun;97(6):459-67
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  • [Title] Inhibition of prostate carcinogenesis in probasin/SV40 T antigen transgenic rats by leuprorelin, a luteinizing hormone-releasing hormone agonist.
  • The effects of leuprorelin acetate, a luteinizing hormone-releasing hormone agonist (LHRH-A), on prostate carcinogenesis in probasin/SV40 Tag transgenic rat was investigated.
  • Fifteen weeks after administration of 0.28 and 2.8 mg/kg leuprorelin, prostate weights and serum testosterone levels were significantly decreased compared to values for transgenic controls.
  • Histopathological findings revealed that the incidence of prostatic adenocarcinomas was significantly reduced in ventral, dorsal and lateral lobes of the prostate, correlating with decreased expression of SV40 Tag oncoprotein as well as inhibition of DNA synthesis and proliferation of epithelial cells in neoplastic lesions of the ventral prostate.
  • Microarray analysis further showed leuprorelin acetate to significantly inhibit testicular steroidogenesis, suppressing the expression of SV40 Tag oncoprotein and altering the expression of a large number of genes which might be involved in the inhibition of prostate cancer progression in this rat model.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents, Hormonal / pharmacology. Leuprolide / pharmacology. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Androgen-Binding Protein / genetics. Animals. Animals, Genetically Modified. Antigens, Polyomavirus Transforming / genetics. Follicle Stimulating Hormone / blood. Gonadotropin-Releasing Hormone / agonists. Immunohistochemistry. Luteinizing Hormone / blood. Luteinizing Hormone / drug effects. Male. Oligonucleotide Array Sequence Analysis. Prostate / drug effects. RNA, Messenger / analysis. Rats. Receptors, Androgen / drug effects. Receptors, Androgen / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Seminal Vesicles / drug effects. Testosterone / blood

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  • (PMID = 16734723.001).
  • [ISSN] 1347-9032
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen-Binding Protein; 0 / Antigens, Polyomavirus Transforming; 0 / Antineoplastic Agents, Hormonal; 0 / RNA, Messenger; 0 / Receptors, Androgen; 0 / probasin; 33515-09-2 / Gonadotropin-Releasing Hormone; 3XMK78S47O / Testosterone; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; EFY6W0M8TG / Leuprolide
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42. Ghosh R, Schoolfield J, Yeh IT, Smith ML, Hursting SD, Chan DC, Lucia MS, Kumar AP: Loss of NADPH quinone oxidoreductase in the prostate and enhanced serum levels of cytokine-induced neutrophil chemoattractant 2alpha in hormone-stimulated noble rats: potential role in prostatic intraepithelial neoplasia development. Transl Oncol; 2009 May;2(2):65-72
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  • [Title] Loss of NADPH quinone oxidoreductase in the prostate and enhanced serum levels of cytokine-induced neutrophil chemoattractant 2alpha in hormone-stimulated noble rats: potential role in prostatic intraepithelial neoplasia development.
  • The Noble rat is an established model for studying hormone-induced development of prostatic intraepithelial neoplasia and prostatic adenocarcinoma.
  • It is known that for a period, hormones in the prostate generate reactive molecules that have the capacity to overwhelm intracellular defenses, damage macromolecules, and modulate redox-regulated signaling pathways leading to increased oxidative stress.
  • Such hormone-induced imbalance in the oxidative stress/antioxidant defense enzymes may lead to neoplastic transformation of the prostate.
  • We investigated alteration in the expression of critical antioxidant defense enzymes, a redox-regulated transcription factor nuclear factor kappaB (NFkappaB) and its downstream target inflammation-associated cyclooxygenase 2 (Cox-2) in the prostate from hormone-stimulated Noble rats using immunohistochemistry.
  • Further, the prostate from hormone-stimulated rats showed very strong expressions of p65, Cox-2, and NFkappaB DNA binding activity.

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  • (PMID = 19412421.001).
  • [ISSN] 1936-5233
  • [Journal-full-title] Translational oncology
  • [ISO-abbreviation] Transl Oncol
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA054174; United States / NCI NIH HHS / CA / R21 CA098744
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Other-IDs] NLM/ PMC2670573
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43. Tavassoli P, Snoek R, Ray M, Rao LG, Rennie PS: Rapid, non-destructive, cell-based screening assays for agents that modulate growth, death, and androgen receptor activation in prostate cancer cells. Prostate; 2007 Mar 1;67(4):416-26
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  • [Title] Rapid, non-destructive, cell-based screening assays for agents that modulate growth, death, and androgen receptor activation in prostate cancer cells.
  • BACKGROUND: We developed non-invasive, cell-based screening assays to rapidly and biologically assess factors that modulate prostate cancer growth and affect androgen receptor (AR) activity.
  • Using these assays, we found that osteoblast conditioned media (CM) enhanced prostate cancer cell growth, but not AR activity.
  • CONCLUSION: These non-destructive, cell-based assays enable rapid systematic monitoring of the effects of drugs or complex mixtures on prostate cancer cell growth and/or AR activity.
  • [MeSH-major] Adenocarcinoma / pathology. Androgens. Cell Culture Techniques. Prostatic Neoplasms / pathology

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  • (PMID = 17219378.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Androgens; 0 / Culture Media, Conditioned; 0 / Insecticides; 0 / Interleukin-6; 0 / Receptors, Androgen; 147336-22-9 / Green Fluorescent Proteins; 1F7A44V6OU / Colforsin; 7U370BPS14 / Dichlorvos; EC 1.14.- / Steroid Hydroxylases; EC 1.14.14.1 / Aryl Hydrocarbon Hydroxylases; EC 1.14.14.1 / CYP2C11 protein, rat; EC 1.14.14.1 / Steroid 16-alpha-Hydroxylase
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44. Malik G, Rojahn E, Ward MD, Gretzer MB, Partin AW, Semmes OJ, Veltri RW: SELDI protein profiling of dunning R-3327 derived cell lines: identification of molecular markers of prostate cancer progression. Prostate; 2007 Oct 1;67(14):1565-75
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  • [Title] SELDI protein profiling of dunning R-3327 derived cell lines: identification of molecular markers of prostate cancer progression.
  • BACKGROUND: We recently demonstrated the protein expression profiling of Dunning rat tumor cell lines of varying metastatic potential (G (0%), AT-1 ( approximately 20%), and MLL (100%)) using SELDI-TOF-MS.
  • As a parallel effort, we have been pursuing the identification of the protein(s) comprising the individual discriminatory "peaks" and evaluating their utility as potential biomarkers for prostate cancer progression.
  • CONCLUSIONS: SELDI-TOF MS analysis of the Dunning prostate cancer cell lines confirmed the consistent overexpression of a 17.5 K m/z peak in metastatic MLL subline.

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  • (PMID = 17705230.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / U01 CA085067; United States / NCI NIH HHS / CA / CA 85067; United States / NCI NIH HHS / CA / P50 CA58236
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Neoplasm Proteins
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45. Pham H, Vang K, Ziboh VA: Dietary gamma-linolenate attenuates tumor growth in a rodent model of prostatic adenocarcinoma via suppression of elevated generation of PGE(2) and 5S-HETE. Prostaglandins Leukot Essent Fatty Acids; 2006 Apr;74(4):271-82
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  • [Title] Dietary gamma-linolenate attenuates tumor growth in a rodent model of prostatic adenocarcinoma via suppression of elevated generation of PGE(2) and 5S-HETE.
  • Prostate cancer poses considerable threat to the aging male population as it has become a leading cause of cancer death to this group.
  • Due to the complexity of this age-related disease, the mechanism(s) and factors resulting in prostate cancer remain unclear.
  • Therefore, using the Lobund-Wistar (L-W) rat model of prostate cancer, we tested the hypothesis whether dietary supplementation of GLA could suppress tumor growth and development in vivo.
  • Our findings revealed a decrease in prostate growth in the NMU/TP/GLA-fed group as determined by weight, tissue size, DNA content and prostate-specific antigen (tumor marker of prostate cancer).
  • [MeSH-major] Adenocarcinoma / metabolism. Dietary Fats, Unsaturated / pharmacology. Dinoprostone / metabolism. Hydroxyeicosatetraenoic Acids / metabolism. Prostatic Neoplasms / metabolism. gamma-Linolenic Acid / pharmacology
  • [MeSH-minor] Animals. Cyclooxygenase 2 / metabolism. Lipoxygenase / metabolism. Male. Models, Biological. Neoplasms, Experimental. Plant Oils / administration & dosage. Plant Oils / metabolism. Plant Oils / pharmacology. Prostaglandin-Endoperoxide Synthases / metabolism. Prostate-Specific Antigen / metabolism. Rats. Rats, Wistar. Time Factors

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  • (PMID = 16567086.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Dietary Fats, Unsaturated; 0 / Hydroxyeicosatetraenoic Acids; 0 / Plant Oils; 0 / borage oil; 78YC2MAX4O / gamma-Linolenic Acid; EC 1.13.11.12 / Lipoxygenase; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases; EC 1.14.99.1 / Ptgs2 protein, rat; EC 3.4.21.77 / Prostate-Specific Antigen; K7Q1JQR04M / Dinoprostone
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46. Sarkar DK, Boyadjieva NI, Chen CP, Ortigüela M, Reuhl K, Clement EM, Kuhn P, Marano J: Cyclic adenosine monophosphate differentiated beta-endorphin neurons promote immune function and prevent prostate cancer growth. Proc Natl Acad Sci U S A; 2008 Jul 1;105(26):9105-10
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclic adenosine monophosphate differentiated beta-endorphin neurons promote immune function and prevent prostate cancer growth.
  • Activation of the cAMP system in rat hypothalamic NSCs differentiated these cells into beta-endorphin (BEP)-producing neurons in culture.
  • When these in vitro differentiated neurons were transplanted into the paraventricular nucleus (PVN) of the hypothalamus of an adult rat, they integrated well with the surrounding cells and produced BEP and its precursor gene product, proopiomelanocortin (POMC).
  • Animals with BEP cell transplants demonstrated remarkable protection against carcinogen induction of prostate cancer.
  • Unlike carcinogen-treated animals with control cell transplants, rats with BEP cell transplants showed rare development of glandular hyperplasia, prostatic intraepithelial neoplasia (PIN), or well differentiated adenocarcinoma with invasion after N-methyl-N-nitrosourea (MNU) and testosterone treatments.
  • These results identified a critical role for cAMP in the differentiation of BEP neurons and revealed a previously undescribed role of these neurons in combating the growth and progression of neoplastic conditions like prostate cancer, possibly by increasing the innate immune function and reducing the inflammatory milieu.

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  • (PMID = 18562281.001).
  • [ISSN] 1091-6490
  • [Journal-full-title] Proceedings of the National Academy of Sciences of the United States of America
  • [ISO-abbreviation] Proc. Natl. Acad. Sci. U.S.A.
  • [Language] ENG
  • [Grant] United States / NIAAA NIH HHS / AA / AA15718; United States / NIAAA NIH HHS / AA / R37 AA008757; United States / NIEHS NIH HHS / ES / ES-05022; United States / NIEHS NIH HHS / ES / P30 ES005022; United States / NIAAA NIH HHS / AA / AA00220; United States / NIAAA NIH HHS / AA / R01 AA015718; United States / NIAAA NIH HHS / AA / R01 AA008757; United States / NIAAA NIH HHS / AA / AA08757
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Tumor Necrosis Factor-alpha; 3XMK78S47O / Testosterone; 60617-12-1 / beta-Endorphin; 684-93-5 / Methylnitrosourea; 82115-62-6 / Interferon-gamma; E0399OZS9N / Cyclic AMP
  • [Other-IDs] NLM/ PMC2449372
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47. Cho YM, Takahashi S, Asamoto M, Suzuki S, Tang M, Shirai T: Suppressive effects of antiandrogens, finasteride and flutamide on development of prostatic lesions in a transgenic rat model. Prostate Cancer Prostatic Dis; 2007;10(4):378-83
Hazardous Substances Data Bank. FINASTERIDE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppressive effects of antiandrogens, finasteride and flutamide on development of prostatic lesions in a transgenic rat model.
  • Transgenic (TG) rats bearing a probasin promoter/simian virus 40 T antigen (SV40 Tag) construct were treated with antiandrogens to examine their ability to suppress prostate carcinogenesis.
  • Furthermore, quantitative data for ventral prostate adenocarcinomas showed significant decrease with antiandrogen treatment.
  • Both finasteride and flutamide had the ability to suppress SV40 Tag-driven carcinogenesis through their different antiandrogenic mechanisms, suggesting that this TG model is suitable for exploring the potential of agents to inhibit prostate cancer development.
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenocarcinoma / prevention & control. Animals. Antigens, Viral, Tumor / genetics. Disease Progression. Drug Therapy, Combination. Male. Prostate / metabolism. Prostate / pathology. Prostatic Intraepithelial Neoplasia / genetics. Prostatic Intraepithelial Neoplasia / pathology. Prostatic Intraepithelial Neoplasia / prevention & control. Rats. Rats, Sprague-Dawley. Testosterone / blood

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  • (PMID = 17457304.001).
  • [ISSN] 1476-5608
  • [Journal-full-title] Prostate cancer and prostatic diseases
  • [ISO-abbreviation] Prostate Cancer Prostatic Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Androgen Antagonists; 0 / Antigens, Viral, Tumor; 0 / Enzyme Inhibitors; 3XMK78S47O / Testosterone; 57GNO57U7G / Finasteride; 76W6J0943E / Flutamide
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48. Princivalle M, Broqua P, White R, Meyer J, Mayer G, Elliott L, Bjarnason K, Haigh R, Yea C: Rapid suppression of plasma testosterone levels and tumor growth in the dunning rat model treated with degarelix, a new gonadotropin-releasing hormone antagonist. J Pharmacol Exp Ther; 2007 Mar;320(3):1113-8
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Rapid suppression of plasma testosterone levels and tumor growth in the dunning rat model treated with degarelix, a new gonadotropin-releasing hormone antagonist.
  • Degarelix (FE 200486) is a member of a new class of water-soluble (>50 mg/ml) gonadotropin-releasing hormone (GnRH) antagonists in clinical development for prostate cancer.
  • One of the few animal models of prostate adenocarcinoma is the Dunning R-3327H rat carcinoma transplanted into Copenhagen rats.
  • We report in this study that degarelix produces a fast and sustained suppression of the pituitary gonadal axis in rats and a similar inhibition of tumor growth compared with surgical castration in the Dunning R-3327H rat carcinoma model.
  • These data provide a convincing profile of degarelix as a potential candidate for the clinical management of sex steroid-dependent pathologies, such as prostate cancer, where long-term reversible chemical castration is required.

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  • (PMID = 17179469.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Oligopeptides; 0 / acetyl-2-naphthylalanyl-3-chlorophenylalanyl-1-oxohexadecyl-seryl-4-aminophenylalanyl(hydroorotyl)-4-aminophenylalanyl(carbamoyl)-leucyl-ILys-prolyl-alaninamide; 33515-09-2 / Gonadotropin-Releasing Hormone; 3XMK78S47O / Testosterone; EFY6W0M8TG / Leuprolide
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49. Liepe K, Geidel H, Haase M, Hakenberg OW, Runge R, Kotzerke J: New model for the induction of osteoblastic bone metastases in rat. Anticancer Res; 2005 Mar-Apr;25(2A):1067-73
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New model for the induction of osteoblastic bone metastases in rat.
  • MATERIALS AND METHODS: Thirty male Copenhagen rats (age 9+/-2 months, mean weight 323+/-21 g) were each injected with 200,000 R-3327 prostate cancer cells.
  • CONCLUSION: The intra-osseous administration of MatLyLu R-3327 prostate cancer cells represents a useful and effective model for osteoblastic bone lesion, and allows further autoradiographic evaluation of bone uptake using bone-seeking radiopharmaceuticals.
  • [MeSH-major] Adenocarcinoma / secondary. Bone Neoplasms / secondary. Prostatic Neoplasms / pathology. Technetium Tc 99m Medronate / analogs & derivatives

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  • (PMID = 15868947.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Radiopharmaceuticals; 72945-61-0 / technetium Tc 99m hydroxymethylene diphosphonate; X89XV46R07 / Technetium Tc 99m Medronate
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50. Rezaeipoor R, Chaney EJ, Oldenburg AL, Boppart SA: Expression order of alpha-v and beta-3 integrin subunits in the N-methyl-N-nitrosourea-induced rat mammary tumor model. Cancer Invest; 2009 Jun;27(5):496-503
Hazardous Substances Data Bank. N-NITROSO-N-METHYLUREA .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression order of alpha-v and beta-3 integrin subunits in the N-methyl-N-nitrosourea-induced rat mammary tumor model.
  • We investigated the developmental time course of molecular expression of alpha(v)beta(3) subunits in a carcinogen-induced rat mammary tumor model for human ductal carcinoma in situ (DCIS).

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  • (PMID = 19234941.001).
  • [ISSN] 1532-4192
  • [Journal-full-title] Cancer investigation
  • [ISO-abbreviation] Cancer Invest.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB005221; United States / NIBIB NIH HHS / EB / EB005321-04; United States / NIBIB NIH HHS / EB / 1 R21 EB005321; United States / NIBIB NIH HHS / EB / R21 EB005321-04; United States / NCI NIH HHS / CA / U54 CA119342; United States / NIBIB NIH HHS / EB / 1 R01 EB005221; United States / NIBIB NIH HHS / EB / R21 EB005321; United States / NCI NIH HHS / CA / U54-CA119342-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Integrin alphaVbeta3; 0 / Protein Subunits; 684-93-5 / Methylnitrosourea
  • [Other-IDs] NLM/ NIHMS200427; NLM/ PMC2883327
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51. Mitrofanova E, Unfer R, Vahanian N, Kane S, Carvour M, Link C: Effective growth arrest of human colon cancer in mice, using rat sodium iodide symporter and radioiodine therapy. Hum Gene Ther; 2005 Nov;16(11):1333-7
MedlinePlus Health Information. consumer health - Colorectal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effective growth arrest of human colon cancer in mice, using rat sodium iodide symporter and radioiodine therapy.
  • We have demonstrated that the rat sodium iodide symporter (rNIS) and 131I can effectively induce growth arrest of human prostate tumor xenografts [Mitrofanova, E., Unfer, R., Vahanian, N., Daniels, W., Roberson, E., Seregina, T., Seth, P., and Link, C. (2004).
  • Rat sodium iodide symporter (rNIS) for radioiodide therapy of cancer. Clin.
  • This is the first report demonstrating that rat NIS and 131I can effectively induce growth arrest of relatively large tumors in an animal model.
  • [MeSH-major] Adenocarcinoma / pathology. Cell Division. Colorectal Neoplasms / pathology. Iodine Radioisotopes / therapeutic use. Symporters / physiology

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  • (PMID = 16259567.001).
  • [ISSN] 1043-0342
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Iodine Radioisotopes; 0 / Symporters; 0 / sodium-iodide symporter
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52. Zhang RX, Li A, Liu B, Wang L, Xin J, Ren K, Qiao JT, Berman BM, Lao L: Electroacupuncture attenuates bone-cancer-induced hyperalgesia and inhibits spinal preprodynorphin expression in a rat model. Eur J Pain; 2008 Oct;12(7):870-8
MedlinePlus Health Information. consumer health - Bone Cancer.

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  • [Title] Electroacupuncture attenuates bone-cancer-induced hyperalgesia and inhibits spinal preprodynorphin expression in a rat model.
  • To examine its effects and underlying mechanisms on cancer pain, we injected AT-3.1 prostate cancer cells into the tibia to induce bone cancer in the male Copenhagen rat.

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  • (PMID = 18221900.001).
  • [ISSN] 1532-2149
  • [Journal-full-title] European journal of pain (London, England)
  • [ISO-abbreviation] Eur J Pain
  • [Language] ENG
  • [Grant] United States / NCCIH NIH HHS / AT / AT002605-02; United States / NCCIH NIH HHS / AT / P01 AT002605; United States / NCI NIH HHS / CA / CA102383-02; United States / NCI NIH HHS / CA / R21 CA102383; United States / NCCIH NIH HHS / AT / P01 AT002605-02; United States / NCI NIH HHS / CA / R21 CA102383-02
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Immune Sera; 0 / Protein Precursors; 0 / pre-prodynorphin; 74913-18-1 / Dynorphins
  • [Other-IDs] NLM/ NIHMS170491; NLM/ PMC3107701
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53. Williams K, Fernandez S, Stien X, Ishii K, Love HD, Lau YF, Roberts RL, Hayward SW: Unopposed c-MYC expression in benign prostatic epithelium causes a cancer phenotype. Prostate; 2005 Jun 1;63(4):369-84
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: We have sought to develop a new in vivo model of prostate carcinogenesis using human prostatic epithelial cell cultures.
  • Human prostate cancers frequently display DNA amplification in the 8q24 amplicon, which leads to an increase in the copy number of the c-MYC gene, a finding that suggests a role for c-MYC in human prostate carcinogenesis.
  • These cells were recombined with inductive rat urogenital sinus mesenchyme and grafted beneath the renal capsule of immunocompromised rodent hosts.
  • RESULTS: The resultant tissue displayed a phenotype consistent with a poorly differentiated human prostatic adenocarcinoma.
  • The neoplastic cells in the tumor expressed both androgen receptors (AR) and prostate-specific antigen (PSA), both characteristic markers of human prostate cancers.
  • CONCLUSIONS: By using a retroviral infection strategy followed by tissue recombination we have created a model of human prostate cancer that demonstrates that the c-MYC gene is sufficient to induce carcinogenesis.
  • [MeSH-major] Adenocarcinoma / genetics. Prostate / cytology. Prostate / physiology. Prostatic Neoplasms / genetics. Proto-Oncogene Proteins c-myc / genetics

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  • [Copyright] Copyright 2004 Wiley-Liss, Inc.
  • (PMID = 15937962.001).
  • [ISSN] 0270-4137
  • [Journal-full-title] The Prostate
  • [ISO-abbreviation] Prostate
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA96403; United States / NCI NIH HHS / CA / P30 CA68485; United States / NIDDK NIH HHS / DK / P60 DK20593
  • [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.; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Proto-Oncogene Proteins c-myc; 147336-22-9 / Green Fluorescent Proteins
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54. Tawadros T, Martin D, Abderrahmani A, Leisinger HJ, Waeber G, Haefliger JA: IB1/JIP-1 controls JNK activation and increased during prostatic LNCaP cells neuroendocrine differentiation. Cell Signal; 2005 Aug;17(8):929-39
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  • In this study, we described the presence of IB1/JIP-1 in epithelium of the rat prostate as well as in the human prostatic LNCaP cells.
  • In prostatic adenocarcinoma cells, the neuroendocrine (NE) phenotype acquisition is associated with tumor progression and androgen independence.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenoviridae / genetics. Animals. Apoptosis. Benzimidazoles / pharmacology. Blotting, Northern. Blotting, Western. Cell Differentiation. Cell Line, Tumor. Densitometry. Disease Progression. Enzyme Activation. Epithelial Cells / metabolism. Fenretinide / pharmacology. HeLa Cells. Humans. Luciferases / metabolism. MAP Kinase Kinase 4. Male. Microscopy, Fluorescence. Neoplasms / pathology. Neurons / metabolism. Phenotype. Plasmids / metabolism. Prostate / metabolism. RNA / metabolism. Rats. Repressor Proteins / physiology. Reverse Transcriptase Polymerase Chain Reaction. Synaptophysin / metabolism. Tetrazolium Salts / pharmacology. Thiazoles / pharmacology. Tissue Distribution. Transcription Factors / physiology. Transcription, Genetic. Up-Regulation

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  • (PMID = 15894166.001).
  • [ISSN] 0898-6568
  • [Journal-full-title] Cellular signalling
  • [ISO-abbreviation] Cell. Signal.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adaptor Proteins, Signal Transducing; 0 / Benzimidazoles; 0 / MAPK8IP1 protein, human; 0 / RE1-silencing transcription factor; 0 / Repressor Proteins; 0 / Synaptophysin; 0 / Tetrazolium Salts; 0 / Thiazoles; 0 / Transcription Factors; 187EJ7QEXL / Fenretinide; 23491-52-3 / HOE 33342; 298-93-1 / thiazolyl blue; 63231-63-0 / RNA; EC 1.13.12.- / Luciferases; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.12.2 / MAP Kinase Kinase 4; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases
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55. Sudo H, Maru Y: LAPSER1 is a putative cytokinetic tumor suppressor that shows the same centrosome and midbody subcellular localization pattern as p80 katanin. FASEB J; 2007 Jul;21(9):2086-100
Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .

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  • Prostate cancer is one of the most common cancers in men, with more than 500,000 new worldwide cases reported annually, resulting in 200,000 deaths of mainly older men in developed countries.
  • Existing treatments have not proved very effective in managing prostate cancer, and continuing efforts therefore are ongoing to explore novel targets and strategies for future therapies.
  • LAPSER1 has been identified as a candidate tumor suppressor gene in prostate cancer, but its true functions remain unknown.
  • [MeSH-minor] Adenocarcinoma / pathology. Amino Acid Chloromethyl Ketones / pharmacology. Animals. Apoptosis. Bone Neoplasms / pathology. CHO Cells. Cell Line. Cell Line, Transformed. Cell Line, Tumor / chemistry. Cell Line, Tumor / ultrastructure. Cell Transformation, Viral. Cricetinae. Cricetulus. Fusion Proteins, gag-onc / physiology. Humans. Leucine Zippers. Male. Microtubule-Associated Proteins / analysis. Oncogene Protein p21(ras) / physiology. Oncogene Proteins v-abl / physiology. Osteosarcoma / pathology. Polyploidy. Prostatic Neoplasms / pathology. Protein Subunits. Protein-Tyrosine Kinases / physiology. RNA Interference. RNA, Small Interfering / pharmacology. Rats. Recombinant Fusion Proteins / physiology. Spindle Apparatus / ultrastructure. Subcellular Fractions / chemistry. Tubulin / analysis

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  • (PMID = 17351128.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Fusion Proteins, gag-onc; 0 / KIF23 protein, human; 0 / LAPSER1 protein, rat; 0 / Membrane Proteins; 0 / Microtubule-Associated Proteins; 0 / Oncogene Proteins v-abl; 0 / Protein Subunits; 0 / RNA, Small Interfering; 0 / Recombinant Fusion Proteins; 0 / Tubulin; 0 / Tumor Suppressor Proteins; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.2 / v-fps oncogene protein, Fujinami sarcoma virus; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.1.- / katanin; EC 3.6.5.2 / Oncogene Protein p21(ras)
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56. Krupka TM, Dremann D, Exner AA: Time and dose dependence of pluronic bioactivity in hyperthermia-induced tumor cell death. Exp Biol Med (Maywood); 2009 Jan;234(1):95-104
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  • DHD/K12/TRb rat adenocarcinoma cells were exposed to low-grade hyperthermia at 43 degrees C with or without Pluronic P85 or Pluronic L61.

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  • (PMID = 18997100.001).
  • [ISSN] 1535-3702
  • [Journal-full-title] Experimental biology and medicine (Maywood, N.J.)
  • [ISO-abbreviation] Exp. Biol. Med. (Maywood)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA136857; United States / NCI NIH HHS / CA / R01 CA136857-01; United States / NCI NIH HHS / CA / R01CA1118399
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / pluronic L61; 106392-12-5 / Poloxamer; 8L70Q75FXE / Adenosine Triphosphate; 9003-11-6 / Poloxalene
  • [Other-IDs] NLM/ NIHMS359379; NLM/ PMC3293626
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57. Abakumova OIu, Podobed OV, Borisova AA, Sidoruk KV, Aleksandrova SS, Omel'ianiuk NM, Pokrovskaia MV, Kondakova LI, Sokolov NN: [Antitumor activity of L-asparaginase from Yersinia pseudotuberculosis]. Biomed Khim; 2008 Nov-Dec;54(6):712-9

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  • The cytotoxic activity of L-asparaginases from Yersinia pseudotuberculosis and from Erwinia carotovora were investigated in vitro using several tumor cells lines: Jurkat and Molt-4 (human T-lymphoblastic leukemia), MCF-7 (human breast adenocarcinoma), LnCap (human prostate carcinoma), NGUK1 (rat Gasser node neurinoma). E. coli L-asparaginase produced by "Medak" (Germany) was used as a reference.

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  • (PMID = 19205431.001).
  • [ISSN] 2310-6972
  • [Journal-full-title] Biomedit︠s︡inskai︠a︡ khimii︠a︡
  • [ISO-abbreviation] Biomed Khim
  • [Language] rus
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Russia (Federation)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; EC 3.5.1.1 / Asparaginase
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58. Cunningham CH, Chen AP, Lustig M, Hargreaves BA, Lupo J, Xu D, Kurhanewicz J, Hurd RE, Pauly JM, Nelson SJ, Vigneron DB: Pulse sequence for dynamic volumetric imaging of hyperpolarized metabolic products. J Magn Reson; 2008 Jul;193(1):139-46
The Lens. Cited by Patents in .

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  • This high frame rate was used to measure the different lactate dynamics in different tissues in a normal rat model and a mouse model of prostate cancer.

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  • (PMID = 18424203.001).
  • [ISSN] 1090-7807
  • [Journal-full-title] Journal of magnetic resonance (San Diego, Calif. : 1997)
  • [ISO-abbreviation] J. Magn. Reson.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB007588; United States / NIBIB NIH HHS / EB / R21 EB005363-04; United States / NIBIB NIH HHS / EB / EB005363-04; United States / NIBIB NIH HHS / EB / R21 EB005363; United States / NCI NIH HHS / CA / R01 CA111291
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Isotopes; 0 / Lactates; 0 / Pyruvates
  • [Other-IDs] NLM/ NIHMS55765; NLM/ PMC3051833
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59. Wang XP, Li ZJ, Magnusson J, Brunicardi FC: Tissue MicroArray analyses of pancreatic duodenal homeobox-1 in human cancers. World J Surg; 2005 Mar;29(3):334-8
The Lens. Cited by Patents in .

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  • In previous studies, we demonstrated that rat insulin promoter (RIP)-driven gene therapy successfully targeted human pancreatic tumor PANC-1 cells and mouse insulinoma NIT-1 cells, which are both pancreatic duodenal homeobox-1 (PDX-1)-positive.
  • The custom-designed Tissue MicroArray of human tumor specimens consists of human cancer specimens from different origins, such as the pancreas, breast, colon, prostate, kidney, liver, lung, and ovary.
  • PDX-1 expression intensity was elevated in both benign and malignant tissues from the same patient with pancreas, breast, colon, prostate, and kidney cancers, whereas normal human tissues from control subjects without cancer did not express PDX-1.
  • [MeSH-major] Adenocarcinoma / metabolism. Homeodomain Proteins / metabolism. Pancreatic Neoplasms / metabolism. Trans-Activators / metabolism

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  • (PMID = 15706433.001).
  • [ISSN] 0364-2313
  • [Journal-full-title] World journal of surgery
  • [ISO-abbreviation] World J Surg
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA95731
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / RNA, Messenger; 0 / Trans-Activators; 0 / pancreatic and duodenal homeobox 1 protein
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60. Wu H, Exner AA, Krupka TM, Weinberg BD, Haaga JR: Vasomodulation of tumor blood flow: effect on perfusion and thermal ablation size. Ann Biomed Eng; 2009 Mar;37(3):552-64
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  • To verify this hypothesis, we measured the tumor perfusion changes in response to phenylephrine (PE) and hydralazine (HYZ) using a CT perfusion method in a rat subcutaneous tumor model.

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  • (PMID = 19085107.001).
  • [ISSN] 1573-9686
  • [Journal-full-title] Annals of biomedical engineering
  • [ISO-abbreviation] Ann Biomed Eng
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA131014; United States / NCI NIH HHS / CA / R21 CA131014-02; United States / NIGMS NIH HHS / GM / T32 GM007250; United States / PHS HHS / / 5P30 043703-17S3
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Other-IDs] NLM/ NIHMS359380; NLM/ PMC3294296
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61. Pilli T, Prasad KV, Jayarama S, Pacini F, Prabhakar BS: Potential utility and limitations of thyroid cancer cell lines as models for studying thyroid cancer. Thyroid; 2009 Dec;19(12):1333-42
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.
  • Further, many cell lines have lost the expression of thyroid-specific genes and have altered karyotypes, while they exhibit activation of several oncogenes (BRAF, v-raf murine sarcoma viral oncogene homolog B1; RAS, rat sarcoma; and RET/PTC, rearranged in transformation/papillary thyroid carcinoma) and inactivation of tumor suppressor gene (TP53) which is known to be important for thyroid tumorigenesis.

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  • (PMID = 20001716.001).
  • [ISSN] 1557-9077
  • [Journal-full-title] Thyroid : official journal of the American Thyroid Association
  • [ISO-abbreviation] Thyroid
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA107506-01A2; United States / NCI NIH HHS / CA / R01 CA107506; United States / NCI NIH HHS / CA / 5R01CA107506; United States / NCI NIH HHS / CA / R01 CA107506-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / Transcription Factors; 0 / thyroid nuclear factor 1; 9002-71-5 / Thyrotropin; EC 2.7.11.1 / BRAF protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins B-raf; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases
  • [Number-of-references] 80
  • [Other-IDs] NLM/ PMC2833173
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62. Yoo J, Kim HR, Lee YJ: Hyperthermia enhances tumour necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in human cancer cells. Int J Hyperthermia; 2006 Dec;22(8):713-28

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • METHODS: Human prostate adenocarcinoma DU-145, human pancreatic carcinoma MIA PaCa-2 and BxPC-3, human colon fibroblast CCD-33Co and rat prostate endothelial YPEN-1 cells were treated with various concentrations of TRAIL (0-200 ngml(-1)) with hyperthermia (40-42 degrees C).

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  • (PMID = 17391000.001).
  • [ISSN] 0265-6736
  • [Journal-full-title] International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group
  • [ISO-abbreviation] Int J Hyperthermia
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA121395; United States / NCI NIH HHS / CA / CA95191; United States / NCI NIH HHS / CA / CA96989
  • [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, TNF-Related Apoptosis-Inducing Ligand; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.36 / Caspase 1
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63. Vegh I, de Salamanca RE: Prolactin, TNF alpha and nitric oxide expression in nitroso-N-methylurea-induced-mammary tumours. J Carcinog; 2007;6:18

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The N-Nitrosomethylurea breast cancer model induced in rats is used for the study of carcinogenesis in mammary cancer, prostate, pancreas, etc.
  • NMU was administered to female Wistar rats on 2 occasions (5 mg/100 g body w/rat).
  • RESULTS: The administration of metoclopramide made the induction time shorter and increased the incidence and average of tumours per rat.
  • The ploidy of adenocarcinoma was polyploid-aneuploid type (average S = 60%).

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  • (PMID = 18045456.001).
  • [ISSN] 1477-3163
  • [Journal-full-title] Journal of carcinogenesis
  • [ISO-abbreviation] J Carcinog
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Other-IDs] NLM/ PMC2219956
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