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Article: Endogenous CD28 drives CAR T cell responses in multiple myeloma.

Lieberman, Mackenzie M / Tong, Jason H / Odukwe, Nkechi U / Chavel, Colin A / Purdon, Terence J / Burchett, Rebecca / Gillard, Bryan M / Brackett, Craig M / McGray, A J Robert / Bramson, Jonathan L / Brentjens, Renier J / Lee, Kelvin P / Olejniczak, Scott H

bioRxiv : the preprint server for biology

2024

Abstract: Recent FDA approvals of chimeric antigen receptor (CAR) T cell therapy for multiple myeloma (MM) have reshaped the therapeutic landscape for this incurable cancer. In pivotal clinical trials B cell maturation antigen (BCMA) targeted, 4-1BB co-stimulated ( ...

Abstract	Recent FDA approvals of chimeric antigen receptor (CAR) T cell therapy for multiple myeloma (MM) have reshaped the therapeutic landscape for this incurable cancer. In pivotal clinical trials B cell maturation antigen (BCMA) targeted, 4-1BB co-stimulated (BBζ) CAR T cells dramatically outperformed standard-of-care chemotherapy, yet most patients experienced MM relapse within two years of therapy, underscoring the need to improve CAR T cell efficacy in MM. We set out to determine if inhibition of MM bone marrow microenvironment (BME) survival signaling could increase sensitivity to CAR T cells. In contrast to expectations, blocking the CD28 MM survival signal with abatacept (CTLA4-Ig) accelerated disease relapse following CAR T therapy in preclinical models, potentially due to blocking CD28 signaling in CAR T cells. Knockout studies confirmed that endogenous CD28 expressed on BBζ CAR T cells drove
Language	English
Publishing date	2024-04-09
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.21.586084
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Article: Syngeneic model of carcinogen-induced tumor mimics basal/squamous, stromal-rich, and neuroendocrine molecular and immunological features of muscle-invasive bladder cancer.

Shah, Shruti D / Gillard, Bryan M / Wrobel, Michelle M / Karasik, Ellen / Moser, Michael T / Mastri, Michalis / Long, Mark D / Sule, Norbert / Brackett, Craig M / Huss, Wendy J / Foster, Barbara A

Frontiers in oncology

2023 Volume 13, Page(s) 1120329

Abstract: Introduction: Bladder cancer is a heterogenous disease and the emerging knowledge on molecular classification of bladder tumors may impact treatment decisions based on molecular subtype. Pre-clinical models representing each subtype are needed to test ... ...

Abstract	Introduction: Bladder cancer is a heterogenous disease and the emerging knowledge on molecular classification of bladder tumors may impact treatment decisions based on molecular subtype. Pre-clinical models representing each subtype are needed to test novel therapies. Carcinogen-induced bladder cancer models represent heterogeneous, immune-competent, pre-clinical testing options with many features found in the human disease. Methods: Invasive bladder tumors were induced in C57BL/6 mice when continuously exposed to N-butyl-N-(4-hydroxybutyl)-nitrosamine (BBN) in the drinking water. Tumors were excised and serially passed by subcutaneous implantation into sex-matched syngeneic C57BL/6 hosts. Eight lines were named BBN-induced Urothelium Roswell Park (BURP) tumor lines. BURP lines were characterized by applying consensus molecular classification to RNA expression, histopathology, and immune profiles by CIBERSORT. Two lines were further characterized for cisplatin response. Results: Eight BURP tumor lines were established with 3 male and 3 female BURP tumor lines, having the basal/squamous (BaSq) molecular phenotype and morphology. BURP-16SR was established from a male mouse and has a stromal-rich (SR) molecular phenotype and a sarcomatoid carcinoma morphology. BURP-19NE was established from a male mouse and has a neuroendocrine (NE)-like molecular phenotype and poorly differentiated morphology. The established BURP tumor lines have unique immune profiles with fewer immune infiltrates compared to their originating BBN-induced tumors. The immune profiles of the BURP tumor lines capture some of the features observed in the molecular classifications of human bladder cancer. BURP-16SR growth was inhibited by cisplatin treatment, while BURP-24BaSq did not respond to cisplatin. Discussion: The BURP lines represent several molecular classifications, including basal/squamous, stroma-rich, and NE-like. The stroma-rich (BURP-16SR) and NE-like (BURP-19NE) represent unique immunocompetent models that can be used to test novel treatments in these less common bladder cancer subtypes. Six basal/squamous tumor lines were established from both male and female mice. Overall, the BURP tumor lines have less heterogeneity than the carcinogen-induced tumors and can be used to evaluate treatment response without the confounding mixed response often observed in heterogeneous tumors. Additionally, basal/squamous tumor lines were established and maintained in both male and female mice, thereby allowing these tumor lines to be used to compare differential treatment responses between sexes.
Language	English
Publishing date	2023-02-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2023.1120329
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Article ; Online: Aryl hydrocarbon receptor is a tumor promoter in

Chaudhry, Kanita A / Jacobi, Justine J / Gillard, Bryan M / Karasik, Ellen / Martin, Jeffrey C / da Silva Fernandes, Tatiane / Hurley, Edward / Feltri, Maria Laura / Attwood, Kristopher M / Twist, Clare J / Smiraglia, Dominic J / Long, Mark D / Bianchi-Smiraglia, Anna

iScience

2023 Volume 26, Issue 11, Page(s) 108303

Abstract: Neuroblastoma is the most common extracranial solid tumor in children. ...

Abstract	Neuroblastoma is the most common extracranial solid tumor in children.
Language	English
Publishing date	2023-10-21
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108303
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Article: Patient derived models of bladder cancer enrich the signal of the tumor cell transcriptome facilitating the analysis of the tumor cell compartment.

Mastri, Michalis / Ramakrishnan, Swathi / Shah, Shruti D / Karasik, Ellen / Gillard, Bryan M / Moser, Michael T / Farmer, Bailey K / Azabdaftari, Gissou / Chatta, Gurkamal S / Woloszynska, Anna / Eng, Kevin H / Foster, Barbara A / Huss, Wendy J

American journal of clinical and experimental urology

2021 Volume 9, Issue 6, Page(s) 416–434

Abstract: The evolving paradigm of the molecular classification of bladder cancer requires models that represent the classifications with less heterogeneity. Robust transcriptome based molecular classifications are essential to address tumor heterogeneity. Patient ...

Abstract	The evolving paradigm of the molecular classification of bladder cancer requires models that represent the classifications with less heterogeneity. Robust transcriptome based molecular classifications are essential to address tumor heterogeneity. Patient derived models (PDMs) are a powerful preclinical tool to study specific tumor compartments. We tested if the consensus molecular subtype analysis was applicable to PDMs and evaluated the tumor compartment each model represents. PDMs derived from surgical specimens were established as xenografts (PDX), organoids (PDO), and spheroids (PDS). The surgical specimens and PDMs were molecularly characterized by RNA sequencing. PDMs that were established in immune deficient mice or
Language	English
Publishing date	2021-12-15
Publishing country	United States
Document type	Journal Article
ISSN	2330-1910
ISSN	2330-1910
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Article ; Online: Metastatic phenotype in CWR22 prostate cancer xenograft following castration.

Seedhouse, Steven J / Affronti, Hayley C / Karasik, Ellen / Gillard, Bryan M / Azabdaftari, Gissou / Smiraglia, Dominic J / Foster, Barbara A

The Prostate

2015 Volume 76, Issue 4, Page(s) 359–368

Abstract: Background: CWR22 is a human xenograft model of primary prostate cancer (PCa) that is often utilized to study castration recurrent (CR) PCa. CWR22 recapitulates clinical response to androgen deprivation therapy (ADT), in that tumors regress in response ... ...

Abstract	Background: CWR22 is a human xenograft model of primary prostate cancer (PCa) that is often utilized to study castration recurrent (CR) PCa. CWR22 recapitulates clinical response to androgen deprivation therapy (ADT), in that tumors regress in response to castration, but can recur after a period of time. Methods: Two cohorts of mice, totaling 117 mice were implanted with CWR22, allowed to develop tumors, castrated by pellet removal and followed for a period of 32 and 50 weeks. Mice presenting with tumors >2.0 cm(3) at the primary site, moribund appearance, or palpable masses other than the primary tumor were sacrificed prior to the endpoint of the study. Tumor tissue, serum, and abnormal lesions were collected upon necropsy and analyzed by IHC, H&E, and PCR for presence of metastatic lesions arising from CWR22. Results: Herein, we report that CWR22 progresses after castration from a primary, hormonal therapy-naïve tumor to metastatic disease in 20% of castrated nude mice. Histological examination of CWR22 primary tumors revealed distinct pathologies that correlated with metastatic outcome after castration. Conclusion: This is the first report and characterization of spontaneous metastasis in the CWR22 model, thus, CWR22 is a bona-fide model of clinical PCa representing the full progression from androgen-sensitive, primary PCa to metastatic CR-PCa.
MeSH term(s)	Androgens ; Animals ; Biomarkers, Tumor/analysis ; Disease Models, Animal ; Heterografts ; Humans ; Immunohistochemistry ; Lymphatic Metastasis/pathology ; Male ; Mice ; Mice, Nude ; Neoplasm Metastasis/genetics ; Neoplasm Metastasis/pathology ; Neoplasm Recurrence, Local/pathology ; Neoplasm Transplantation ; Neoplasms, Hormone-Dependent ; Orchiectomy ; Phenotype ; Prostatic Neoplasms/pathology ; Prostatic Neoplasms/surgery ; Prostatic Neoplasms, Castration-Resistant/pathology ; Testosterone/blood
Chemical Substances	Androgens ; Biomarkers, Tumor ; Testosterone (3XMK78S47O)
Language	English
Publishing date	2015-12-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604707-5
ISSN	1097-0045 ; 0270-4137
ISSN (online)	1097-0045
ISSN	0270-4137
DOI	10.1002/pros.23127
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Zs.A 1608: Show issues

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Article ; Online: Pharmacological polyamine catabolism upregulation with methionine salvage pathway inhibition as an effective prostate cancer therapy.

Nature communications

2020 Volume 11, Issue 1, Page(s) 52

Abstract: Prostatic luminal epithelial cells secrete high levels of acetylated polyamines into the prostatic lumen, sensitizing them to perturbations of connected metabolic pathways. Enhanced flux is driven by spermidine/spermine N1-acetyltransferase (SSAT) ... ...

Abstract	Prostatic luminal epithelial cells secrete high levels of acetylated polyamines into the prostatic lumen, sensitizing them to perturbations of connected metabolic pathways. Enhanced flux is driven by spermidine/spermine N1-acetyltransferase (SSAT) activity, which acetylates polyamines leading to their secretion and drives biosynthetic demand. The methionine salvage pathway recycles one-carbon units lost to polyamine biosynthesis to the methionine cycle to overcome stress. Prostate cancer (CaP) relies on methylthioadenosine phosphorylase (MTAP), the rate-limiting enzyme, to relieve strain. Here, we show that inhibition of MTAP alongside SSAT upregulation is synergistic in androgen sensitive and castration recurrent CaP models in vitro and in vivo. The combination treatment increases apoptosis in radical prostatectomy ex vivo explant samples. This unique high metabolic flux through polyamine biosynthesis and connected one carbon metabolism in CaP creates a metabolic dependency. Enhancing this flux while simultaneously targeting this dependency in prostate cancer results in an effective therapeutic approach potentially translatable to the clinic.
MeSH term(s)	Acetyltransferases/genetics ; Acetyltransferases/metabolism ; Adenine/administration & dosage ; Adenine/analogs & derivatives ; Animals ; Apoptosis ; Cell Line, Tumor ; Drug Therapy, Combination ; Humans ; Male ; Methionine/metabolism ; Mice ; Mice, Inbred BALB C ; Polyamines/metabolism ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/enzymology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Purine-Nucleoside Phosphorylase/genetics ; Purine-Nucleoside Phosphorylase/metabolism ; Pyrrolidines/administration & dosage ; Salvage Therapy ; Spermine/administration & dosage ; Spermine/analogs & derivatives ; Spermine/metabolism
Chemical Substances	Polyamines ; Pyrrolidines ; methylthio-DADMe-immucillin-A ; N(1),N(11)-diethylnorspermine (121749-39-1) ; Spermine (2FZ7Y3VOQX) ; Methionine (AE28F7PNPL) ; Acetyltransferases (EC 2.3.1.-) ; diamine N-acetyltransferase (EC 2.3.1.57) ; Purine-Nucleoside Phosphorylase (EC 2.4.2.1) ; 5'-methylthioadenosine phosphorylase (EC 2.4.2.28) ; Adenine (JAC85A2161)
Language	English
Publishing date	2020-01-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-019-13950-4
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Article ; Online: Dietary folate levels alter the kinetics and molecular mechanism of prostate cancer recurrence in the CWR22 model.

Affronti, Hayley C / Long, Mark D / Rosario, Spencer R / Gillard, Bryan M / Karasik, Ellen / Boerlin, Christoph S / Pellerite, Anthony J / Foster, Barbara A / Attwood, Kristopher / Pili, Roberto / Wilton, John H / Campbell, Moray J / Smiraglia, Dominic J

Oncotarget

2017 Volume 8, Issue 61, Page(s) 103758–103774

Abstract: Folate impacts the genome and epigenome by feeding into one-carbon metabolism to produce critical metabolites, deoxythymidine monophosphate and s-adenosylmethionine. The impact of folate exposure and intervention timing on cancer progression remains ... ...

Abstract	Folate impacts the genome and epigenome by feeding into one-carbon metabolism to produce critical metabolites, deoxythymidine monophosphate and s-adenosylmethionine. The impact of folate exposure and intervention timing on cancer progression remains controversial. Due to polyamine metabolism's extraordinary biosynthetic flux in prostate cancer (CaP) we demonstrated androgen stimulated CaP is susceptible to dietary folate deficiency. We hypothesized dietary folate levels may also affect castration recurrent CaP. We used the CWR22 human xenograft model which recurs following androgen withdrawal. Engrafted mice were fed a folate depleted or supplemented diet beginning at androgen withdrawal, or prior to xenograft implantation. Both folate depletion and supplementation at the time of withdrawal significantly decreased recurrence incidence. Folate supplementation prior to xenograft implantation increased time to recurrence, suggesting a protective role. By contrast, folate depleted recurrent tumors exhibited transcriptional adaptive responses that maintained high polyamine levels at the expense of increased DNA damage and DNA methylation alterations. Mining of publically available data demonstrated folate related pathways are exceptionally dysregulated in human CaP, which correlated with decreased time to biochemical recurrence. These findings highlight the potential for novel therapeutic interventions that target these metabolic pathways in CaP and provide a rationale to apply such strategies alongside androgen withdrawal.
Language	English
Publishing date	2017-10-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.21911
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Article ; Online: GRM1 is An Androgen-Regulated Gene and its Expression Correlates with Prostate Cancer Progression in Pre-Clinical Models.

Shourideh, Mojgan / Azabdaftari, Gissou / Attwood, Kristopher / DePriest, Adam / Wadosky, Kristine M / Gillard, Bryan M / Karasik, Ellen / Heemers, Hannelore / Kyprianou, Natasha / Gelman, Irwin H / Corey, Eva / Vessella, Robert L / Mohler, James L / Koochekpour, Shahriar

publication RETRACTED

Clinical cancer research : an official journal of the American Association for Cancer Research

2016

Abstract: Purpose: We recently demonstrated that glutamate receptor GRM1 was expressed at high levels in castration-resistant prostate cancer (CR-PCa) tissues and cells. Herein, we determined the relationship between GRM1 and AR, PSA, and tumor growth, remission, ...

Abstract	Purpose: We recently demonstrated that glutamate receptor GRM1 was expressed at high levels in castration-resistant prostate cancer (CR-PCa) tissues and cells. Herein, we determined the relationship between GRM1 and AR, PSA, and tumor growth, remission, and recurrence in preclinical PCa models. The effect of alterations in GRM1 expression was also investigated on PCa cell growth, migration and invasion. Experimental design: We used quantitative gene expression and immunohistochemistry to define the temporal association between GRM1 expression and AR, PSA, and tumor growth during CR progression in CWR22 (n = 59) and LuCaP 35 (n = 12) PCa xenografts. The effect of alterations in GRM1 expression levels on growth, migration, and invasion was investigated in GRM1-overexpressed or -silenced PCa cell lines. The effect of DHT on GRM1 expression was determined in the presence or absence of the antiandrogen bicalutamide. Results: We found that GRM1 transcript and tissue expression directly correlated with growth and AR and PSA expression in hormone-sensitive (HS), castrated, and CR tumor xenografts. GRM1 overexpression or silencing directly correlated with PCa cell proliferation, migration, and invasion. DHT increased GRM1 expression via an AR-dependent manner in HS- and CR-PCa cell lines. Conclusions: This is a first report of GRM1 as an androgen and AR-target gene. GRM1 expression directly correlated with tumor growth, regression, and recurrence and may contribute to CR-progression of PCa in preclinical models. Further studies are needed to define the utility of GRM1 as a druggable target or biomarker for PCa.
Language	English
Publishing date	2016-07-25
Publishing country	United States
Document type	Journal Article ; Retracted Publication
ZDB-ID	1225457-5
ISSN	1557-3265 ; 1078-0432
ISSN (online)	1557-3265
ISSN	1078-0432
DOI	10.1158/1078-0432.CCR-16-0137
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Zs.A 4223: Show issues

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Article ; Online: Role of vitamin D receptor in the antiproliferative effects of calcitriol in tumor-derived endothelial cells and tumor angiogenesis in vivo.

Chung, Ivy / Han, Guangzhou / Seshadri, Mukund / Gillard, Bryan M / Yu, Wei-dong / Foster, Barbara A / Trump, Donald L / Johnson, Candace S

Cancer research

2009 Volume 69, Issue 3, Page(s) 967–975

Abstract: Calcitriol (1,25-dihydroxycholecalciferol), the major active form of vitamin D, is antiproliferative in tumor cells and tumor-derived endothelial cells (TDEC). These actions of calcitriol are mediated at least in part by vitamin D receptor (VDR), which ... ...

Abstract	Calcitriol (1,25-dihydroxycholecalciferol), the major active form of vitamin D, is antiproliferative in tumor cells and tumor-derived endothelial cells (TDEC). These actions of calcitriol are mediated at least in part by vitamin D receptor (VDR), which is expressed in many tissues including endothelial cells. To investigate the role of VDR in calcitriol effects on tumor vasculature, we established TRAMP-2 tumors subcutaneously into either VDR wild-type (WT) or knockout (KO) mice. Within 30 days post-inoculation, tumors in KO mice were larger than those in WT (P < 0.001). TDEC from WT expressed VDR and were able to transactivate a reporter gene whereas TDEC from KO mice were not. Treatment with calcitriol resulted in growth inhibition in TDEC expressing VDR. However, TDEC from KO mice were relatively resistant, suggesting that calcitriol-mediated growth inhibition on TDEC is VDR-dependent. Further analysis of the TRAMP-C2 tumor sections revealed that the vessels in KO mice were enlarged and had less pericyte coverage compared with WT (P < 0.001). Contrast-enhanced magnetic resonance imaging showed an increase in vascular volume of TRAMP tumors grown in VDR KO mice compared with WT mice (P < 0.001) and FITC-dextran permeability assay suggested a higher extent of vascular leakage in tumors from KO mice. Using ELISA and Western blot analysis, there was an increase of hypoxia-inducible factor-1alpha, vascular endothelial growth factor, angiopoietin 1, and platelet-derived growth factor-BB levels observed in tumors from KO mice. These results indicate that calcitriol-mediated antiproliferative effects on TDEC are VDR-dependent and loss of VDR can lead to abnormal tumor angiogenesis.
MeSH term(s)	Adenocarcinoma/blood supply ; Adenocarcinoma/drug therapy ; Adenocarcinoma/pathology ; Angiopoietin-1/biosynthesis ; Animals ; Calcitriol/pharmacology ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Hypoxia-Inducible Factor 1, alpha Subunit/biosynthesis ; Male ; Mice ; Mice, Knockout ; Neovascularization, Pathologic/drug therapy ; Neovascularization, Pathologic/metabolism ; Neovascularization, Pathologic/pathology ; Prostatic Neoplasms/blood supply ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Proto-Oncogene Proteins c-sis/biosynthesis ; Receptors, Calcitriol/biosynthesis ; Receptors, Calcitriol/deficiency ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Vascular Endothelial Growth Factor A/biosynthesis
Chemical Substances	Angiopoietin-1 ; Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Proto-Oncogene Proteins c-sis ; Receptors, Calcitriol ; Vascular Endothelial Growth Factor A ; Calcitriol (FXC9231JVH)
Language	English
Publishing date	2009-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-08-2307
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Article ; Online: Lack of evidence for green tea polyphenols as DNA methylation inhibitors in murine prostate.

Morey Kinney, Shannon R / Zhang, Wa / Pascual, Marien / Greally, John M / Gillard, Bryan M / Karasik, Ellen / Foster, Barbara A / Karpf, Adam R

Cancer prevention research (Philadelphia, Pa.)

2009 Volume 2, Issue 12, Page(s) 1065–1075

Abstract: Green tea polyphenols (GTP) have been reported to inhibit DNA methylation in cultured cells. Here, we tested whether oral consumption of GTPs affects normal or cancer-specific DNA methylation in vivo, using mice. Wild-type (WT) and transgenic ... ...

Abstract	Green tea polyphenols (GTP) have been reported to inhibit DNA methylation in cultured cells. Here, we tested whether oral consumption of GTPs affects normal or cancer-specific DNA methylation in vivo, using mice. Wild-type (WT) and transgenic adenocarcinoma of mouse prostate (TRAMP) mice were given 0.3% GTPs in drinking water beginning at 4 weeks of age. To monitor DNA methylation, we measured 5-methyl-deoxycytidine (5mdC) levels, methylation of the B1 repetitive element, and methylation of the Mage-a8 gene. Each of these parameters were unchanged in prostate, gut, and liver from WT mice at both 12 and 24 weeks of age, with the single exception of a decrease of 5mdC in the liver at 12 weeks. In GTP-treated TRAMP mice, 5mdC levels and the methylation status of four loci hypermethylated during tumor progression were unaltered in TRAMP prostates at 12 or 24 weeks. Quite surprisingly, GTP treatment did not inhibit tumor progression in TRAMP mice, although known pharmacodynamic markers of GTPs were altered in both WT and TRAMP prostates. We also administered 0.1%, 0.3%, or 0.6% GTPs to TRAMP mice for 12 weeks and measured 5mdC levels and methylation of B1 and Mage-a8 in prostate, gut, and liver tissues. No dose-dependent alterations in DNA methylation status were observed. Genome-wide DNA methylation profiling using the HpaII tiny fragment enrichment by ligation-mediated PCR assay also revealed no significant hypomethylating effect of GTP. These data indicate that oral administration of GTPs does not affect normal or cancer-specific DNA methylation in the murine prostate.
MeSH term(s)	Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Animals ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/physiology ; DNA Methylation ; Flavonoids/pharmacokinetics ; Flavonoids/pharmacology ; Guanosine Triphosphate/metabolism ; Immunoenzyme Techniques ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Phenols/pharmacokinetics ; Phenols/pharmacology ; Polyphenols ; Prostate/metabolism ; Prostate/pathology ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tea ; Tissue Distribution
Chemical Substances	Flavonoids ; Phenols ; Polyphenols ; RNA, Messenger ; Tea ; Guanosine Triphosphate (86-01-1) ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37)
Language	English
Publishing date	2009-11-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2434717-6
ISSN	1940-6215 ; 1940-6207
ISSN (online)	1940-6215
ISSN	1940-6207
DOI	10.1158/1940-6207.CAPR-09-0010
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