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Article: Heated tobacco product IQOS induces unique metabolic signatures in human bronchial epithelial cells.

Curley, Erin O / Abu Aboud, Omran / Chmiel, Kenneth J / Nayak, Ajay P / Fiehn, Oliver / Zeki, Amir A / Sharma, Pawan

2024 Volume 10, Issue 2

Abstract: Metabolic signatures are lacking for heated tobacco products, making it crucial to identify new biosignatures of lung damage. This will enable the establishment of product-specific guidelines and an understanding of associated toxicity. ...

Abstract	Metabolic signatures are lacking for heated tobacco products, making it crucial to identify new biosignatures of lung damage. This will enable the establishment of product-specific guidelines and an understanding of associated toxicity.
Language	English
Publishing date	2024-03-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2827830-6
ISSN	2312-0541
ISSN	2312-0541
DOI	10.1183/23120541.00805-2023
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Article: Translating L-2-HG to kidney cancer at the bench and bedside.

Aboud, Omran Abu / Weiss, Robert H

Annals of translational medicine

2019 Volume 6, Issue Suppl 2, Page(s) S103

Language	English
Publishing date	2019-01-22
Publishing country	China
Document type	Editorial ; Comment
ZDB-ID	2893931-1
ISSN	2305-5847 ; 2305-5839
ISSN (online)	2305-5847
ISSN	2305-5839
DOI	10.21037/atm.2018.11.41
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Article ; Online: Translating Metabolic Reprogramming into New Targets for Kidney Cancer.

Abu Aboud, Omran / Weiss, Robert H

Kidney cancer (Clifton, Va.)

2017 Volume 1, Issue 2, Page(s) 93–97

Abstract: In the age of bioinformatics and with the advent of high-powered computation over the past decade or so the landscape of biomedical research has become radically altered. Whereas a generation ago, investigators would study their "favorite" protein or ... ...

Abstract	In the age of bioinformatics and with the advent of high-powered computation over the past decade or so the landscape of biomedical research has become radically altered. Whereas a generation ago, investigators would study their "favorite" protein or gene and exhaustively catalog the role of this compound in their disease of interest, the appearance of omics has changed the face of medicine such that much of the cutting edge (and fundable!) medical research now evaluates the biology of the disease nearly in its entirety. Couple this with the realization that kidney cancer is a "metabolic disease" due to its multiple derangements in biochemical pathways [1, 2], and clear cell renal cell carcinoma (ccRCC) becomes ripe for data mining using multiple omics approaches.
Language	English
Publishing date	2017-11-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2961890-3
ISSN	2468-4570 ; 2468-4562
ISSN (online)	2468-4570
ISSN	2468-4562
DOI	10.3233/KCA-170014
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Article ; Online: Anti-Cancer Activity of PAK4/NAMPT Inhibitor and Programmed Cell Death Protein-1 Antibody in Kidney Cancer.

Trott, Josephine F / Aboud, Omran Abu / McLaughlin, Bridget / Anderson, Katie L / Modiano, Jaime F / Kim, Kyoungmi / Jen, Kuang-Yu / Senapedis, William / Chang, Hua / Landesman, Yosef / Baloglu, Erkan / Pili, Roberto / Weiss, Robert H

Kidney360

2022 Volume 1, Issue 5, Page(s) 376–388

Abstract: Background: Kidney cancer (or renal cell carcinoma, RCC) is the sixth most common malignancy in the United States and is increasing in incidence. Despite new therapies, including targeted therapies and immunotherapies, most RCCs are resistant to ... ...

Abstract	Background: Kidney cancer (or renal cell carcinoma, RCC) is the sixth most common malignancy in the United States and is increasing in incidence. Despite new therapies, including targeted therapies and immunotherapies, most RCCs are resistant to treatment. Thus, several laboratories have been evaluating new approaches to therapy, both with single agents as well as combinations. Although we have previously shown efficacy of the dual PAK4/nicotinamide phosphoribosyltransferase (NAMPT) inhibitor KPT-9274, and the immune checkpoint inhibitors (CPI) have shown utility in the clinic, there has been no evaluation of this combination either clinically or in an immunocompetent animal model of kidney cancer. Methods: In this study, we use the renal cell adenocarcinoma (RENCA) model of spontaneous murine kidney cancer. Male BALB/cJ mice were injected subcutaneously with RENCA cells and, after tumors were palpable, they were treated with KPT-9274 and/or anti-programmed cell death 1 (PDCD1; PD1) antibody for 21 days. Tumors were measured and then removed at animal euthanasia for subsequent studies. Results: We demonstrate a significant decrease in allograft growth with the combination treatment of KPT-9274 and anti-PD1 antibody without significant weight loss by the animals. This is associated with decreased (MOUSE) Conclusions: This study highlights the potential of the RENCA model for evaluating immunologic responses to KPT-9274 and checkpoint inhibitor (CPI) and suggests that therapy with this combination could improve efficacy in RCC beyond what is achievable with CPI alone.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/pharmacology ; Carcinoma, Renal Cell/drug therapy ; Cell Proliferation ; Kidney Neoplasms/drug therapy ; Male ; Mice ; Nicotinamide Phosphoribosyltransferase
Chemical Substances	Apoptosis Regulatory Proteins ; Nicotinamide Phosphoribosyltransferase (EC 2.4.2.12)
Language	English
Publishing date	2022-02-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2641-7650
ISSN (online)	2641-7650
DOI	10.34067/kid.0000282019
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Article ; Online: Metabolic reprogramming in clear cell renal cell carcinoma.

Wettersten, Hiromi I / Aboud, Omran Abu / Lara, Primo N / Weiss, Robert H

Nature reviews. Nephrology

2017 Volume 13, Issue 7, Page(s) 410–419

Abstract: Research in many cancers has uncovered changes in metabolic pathways that control tumour energetics and biosynthesis, so-called metabolic reprogramming. Studies in clear cell renal cell carcinoma (ccRCC) have been particularly revealing, leading to the ... ...

Abstract	Research in many cancers has uncovered changes in metabolic pathways that control tumour energetics and biosynthesis, so-called metabolic reprogramming. Studies in clear cell renal cell carcinoma (ccRCC) have been particularly revealing, leading to the concept that ccRCC is a metabolic disease. ccRCC is generally accompanied by reprogramming of glucose and fatty acid metabolism and of the tricarboxylic acid cycle. Metabolism of tryptophan, arginine and glutamine is also reprogrammed in many ccRCCs, and these changes provide opportunities for new therapeutic strategies, biomarkers and imaging modalities. In particular, metabolic reprogramming facilitates the identification of novel and repurposed drugs that could potentially be used to treat ccRCC, which when metastatic has currently limited long-term treatment options. Further research and dissemination of these concepts to nephrologists and oncologists will lead to clinical trials of therapeutics specifically targeted to tumour metabolism, rather than generally toxic to all proliferating cells. Such novel agents are highly likely to be more effective and to have far fewer adverse effects than existing drugs.
MeSH term(s)	Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Carcinoma, Renal Cell/therapy ; Humans ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Kidney Neoplasms/therapy ; Metabolic Networks and Pathways/physiology
Language	English
Publishing date	2017-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2490366-8
ISSN	1759-507X ; 1759-5061
ISSN (online)	1759-507X
ISSN	1759-5061
DOI	10.1038/nrneph.2017.59
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Article ; Online: New opportunities from the cancer metabolome.

Aboud, Omran Abu / Weiss, Robert H

Clinical chemistry

2012 Volume 59, Issue 1, Page(s) 138–146

Abstract: Background: Metabolomics, the study of all metabolites produced in the body, which often includes flora and drug metabolites, is the omics approach that can be considered most closely related to a patient's phenotype. Metabolomics has a great and ... ...

Abstract	Background: Metabolomics, the study of all metabolites produced in the body, which often includes flora and drug metabolites, is the omics approach that can be considered most closely related to a patient's phenotype. Metabolomics has a great and largely untapped potential in the field of oncology, and the analysis of the cancer metabolome to identify biofluid markers and novel druggable targets can now be undertaken in many research laboratories. Content: The cancer metabolome has been used to identify and begin to evaluate potential biomarkers and therapeutic targets in a variety of malignancies, including breast, prostate, and kidney cancer. We discuss the several standard techniques for metabolite separation and identification, with their potential problems and drawbacks. Validation of biomarkers and targets may entail intensive use of labor and technology and generally requires a large number of study participants as well as laboratory validation studies. The field of pharmacometabolomics, in which specific therapies are chosen on the basis of a patient's metabolomic profile, has shown some promise in the translation of metabolomics into the arena of personalized medicine. Summary: The relatively new approach using metabolomics has just begun to enter the mainstream of cancer diagnostics and therapeutics. As this field advances, metabolomics will take its well-deserved place next to genomics, transcriptomics, and proteomics in both clinical and basic research in oncology.
MeSH term(s)	Biomarkers, Tumor/metabolism ; Early Diagnosis ; Humans ; Metabolome ; Neoplasms/diagnosis ; Neoplasms/metabolism ; Neoplasms/radiotherapy ; Precision Medicine
Chemical Substances	Biomarkers, Tumor
Language	English
Publishing date	2012-11-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	80102-1
ISSN	1530-8561 ; 0009-9147
ISSN (online)	1530-8561
ISSN	0009-9147
DOI	10.1373/clinchem.2012.184598
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Article ; Online: Inhibition of PPARα induces cell cycle arrest and apoptosis, and synergizes with glycolysis inhibition in kidney cancer cells.

Abu Aboud, Omran / Wettersten, Hiromi I / Weiss, Robert H

PloS one

2013 Volume 8, Issue 8, Page(s) e71115

Abstract: Renal cell carcinoma (RCC) is the sixth most common cancer in the US. While RCC is highly metastatic, there are few therapeutics options available for patients with metastatic RCC, and progression-free survival of patients even with the newest targeted ... ...

Abstract	Renal cell carcinoma (RCC) is the sixth most common cancer in the US. While RCC is highly metastatic, there are few therapeutics options available for patients with metastatic RCC, and progression-free survival of patients even with the newest targeted therapeutics is only up to two years. Thus, novel therapeutic targets for this disease are desperately needed. Based on our previous metabolomics studies showing alteration of peroxisome proliferator-activated receptor α (PPARα) related events in both RCC patient and xenograft mice materials, this pathway was further examined in the current study in the setting of RCC. PPARα is a nuclear receptor protein that functions as a transcription factor for genes including those encoding enzymes involved in energy metabolism; while PPARα has been reported to regulate tumor growth in several cancers, it has not been evaluated in RCC. A specific PPARα antagonist, GW6471, induced both apoptosis and cell cycle arrest at G0/G1 in VHL(+) and VHL(-) RCC cell lines (786-O and Caki-1) associated with attenuation of the cell cycle regulatory proteins c-Myc, Cyclin D1, and CDK4; this data was confirmed as specific to PPARα antagonism by siRNA methods. Interestingly, when glycolysis was blocked by several methods, the cytotoxicity of GW6471 was synergistically increased, suggesting a switch to fatty acid oxidation from glycolysis and providing an entirely novel therapeutic approach for RCC.
MeSH term(s)	Apoptosis/drug effects ; Apoptosis/genetics ; Apoptosis/physiology ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Carcinoma, Renal Cell/pathology ; Cell Cycle Checkpoints/drug effects ; Cell Cycle Checkpoints/genetics ; Cell Cycle Checkpoints/physiology ; Cell Line ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/genetics ; Cell Survival/physiology ; Cyclin D1/metabolism ; Cyclin-Dependent Kinase 4/metabolism ; Deoxyglucose/pharmacology ; G1 Phase/drug effects ; G1 Phase/genetics ; G1 Phase/physiology ; Glucose/metabolism ; Glucose/pharmacology ; Glycolysis/drug effects ; Glycolysis/genetics ; Glycolysis/physiology ; Humans ; Immunoblotting ; Immunohistochemistry ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Oxazoles/pharmacology ; PPAR alpha/antagonists & inhibitors ; PPAR alpha/genetics ; PPAR alpha/metabolism ; Proto-Oncogene Proteins c-myc/metabolism ; RNA Interference ; Resting Phase, Cell Cycle/drug effects ; Resting Phase, Cell Cycle/genetics ; Resting Phase, Cell Cycle/physiology ; Tyrosine/analogs & derivatives ; Tyrosine/pharmacology
Chemical Substances	GW 6471 ; Oxazoles ; PPAR alpha ; Proto-Oncogene Proteins c-myc ; Cyclin D1 (136601-57-5) ; Tyrosine (42HK56048U) ; Deoxyglucose (9G2MP84A8W) ; Cyclin-Dependent Kinase 4 (EC 2.7.11.22) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2013-08-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0071115
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Article ; Online: Dual and Specific Inhibition of NAMPT and PAK4 By KPT-9274 Decreases Kidney Cancer Growth.

Abu Aboud, Omran / Chen, Ching-Hsien / Senapedis, William / Baloglu, Erkan / Argueta, Christian / Weiss, Robert H

Molecular cancer therapeutics

2016 Volume 15, Issue 9, Page(s) 2119–2129

Abstract: Kidney cancer (or renal cell carcinoma, RCC) is the sixth most common malignancy in the United States and one of the relatively few whose incidence is increasing. Because of the near universal resistance which occurs with the use of current treatment ... ...

Abstract	Kidney cancer (or renal cell carcinoma, RCC) is the sixth most common malignancy in the United States and one of the relatively few whose incidence is increasing. Because of the near universal resistance which occurs with the use of current treatment regimens, reprogrammed metabolic pathways are being investigated as potential targets for novel therapies of this disease. Borrowing from studies on other malignancies, we have identified the PAK4 and NAD biosynthetic pathways as being essential for RCC growth. We now show, using the dual PAK4/NAMPT inhibitor KPT-9274, that interference with these signaling pathways results in reduction of G2-M transit as well as induction of apoptosis and decrease in cell invasion and migration in several human RCC cell lines. Mechanistic studies demonstrate that inhibition of the PAK4 pathway by KPT-9274 attenuates nuclear β-catenin as well as the Wnt/β-catenin targets cyclin D1 and c-Myc. Furthermore, NAPRT1 downregulation, which we show occurs in all RCC cell lines tested, makes this tumor highly dependent on NAMPT for its NAD requirements, such that inhibition of NAMPT by KPT-9274 leads to decreased survival of these rapidly proliferating cells. When KPT-9274 was administered in vivo to a 786-O (VHL-mut) human RCC xenograft model, there was dose-dependent inhibition of tumor growth with no apparent toxicity; KPT-9274 demonstrated the expected on-target effects in this mouse model. KPT-9274 is being evaluated in a phase I human clinical trial in solid tumors and lymphomas, which will allow this data to be rapidly translated into the clinic for the treatment of RCC. Mol Cancer Ther; 15(9); 2119-29. ©2016 AACR.
MeSH term(s)	Acrylamides/pharmacology ; Aminopyridines/pharmacology ; Animals ; Antibodies, Monoclonal/pharmacology ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Disease Models, Animal ; Humans ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/metabolism ; Kidney Neoplasms/pathology ; Male ; Mice ; Molecular Targeted Therapy ; NAD/metabolism ; Nicotinamide Phosphoribosyltransferase/antagonists & inhibitors ; Nicotinamide Phosphoribosyltransferase/genetics ; Nicotinamide Phosphoribosyltransferase/metabolism ; Signal Transduction/drug effects ; Tumor Burden/drug effects ; Xenograft Model Antitumor Assays ; beta Catenin/metabolism ; p21-Activated Kinases/antagonists & inhibitors ; p21-Activated Kinases/genetics ; p21-Activated Kinases/metabolism
Chemical Substances	Acrylamides ; Aminopyridines ; Antibodies, Monoclonal ; Antineoplastic Agents ; KPT-9274 ; beta Catenin ; NAD (0U46U6E8UK) ; Nicotinamide Phosphoribosyltransferase (EC 2.4.2.12) ; PAK4 protein, human (EC 2.7.1.11) ; p21-Activated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2016-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-16-0197
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Article ; Online: Glutamine Addiction in Kidney Cancer Suppresses Oxidative Stress and Can Be Exploited for Real-Time Imaging.

Abu Aboud, Omran / Habib, Samy L / Trott, Josephine / Stewart, Benjamin / Liang, Sitai / Chaudhari, Abhijit J / Sutcliffe, Julie / Weiss, Robert H

Cancer research

2017 Volume 77, Issue 23, Page(s) 6746–6758

Abstract: Many cancers appear to activate intrinsic antioxidant systems as a means to counteract oxidative stress. Some cancers, such as clear cell renal cell carcinoma (ccRCC), require exogenous glutamine for growth and exhibit reprogrammed glutamine metabolism, ... ...

Abstract	Many cancers appear to activate intrinsic antioxidant systems as a means to counteract oxidative stress. Some cancers, such as clear cell renal cell carcinoma (ccRCC), require exogenous glutamine for growth and exhibit reprogrammed glutamine metabolism, at least in part due to the glutathione pathway, an efficient cellular buffering system that counteracts reactive oxygen species and other oxidants. We show here that ccRCC xenograft tumors under the renal capsule exhibit enhanced oxidative stress compared with adjacent normal tissue and the contralateral kidney. Upon glutaminase inhibition with CB-839 or BPTES, the RCC cell lines SN12PM-6-1 (SN12) and 786-O exhibited decreased survival and pronounced apoptosis associated with a decreased GSH/GSSG ratio, augmented nuclear factor erythroid-related factor 2, and increased 8-oxo-7,8-dihydro-2'-deoxyguanosine, a marker of DNA damage. SN12 tumor xenografts showed decreased growth when treated with CB-839. Furthermore, PET imaging confirmed that ccRCC tumors exhibited increased tumoral uptake of
MeSH term(s)	8-Hydroxy-2'-Deoxyguanosine ; Animals ; Antineoplastic Agents/pharmacology ; Antioxidants/pharmacology ; Apoptosis/physiology ; Benzeneacetamides/pharmacology ; Carcinoma, Renal Cell/drug therapy ; Carcinoma, Renal Cell/pathology ; Deoxyguanosine/analogs & derivatives ; Deoxyguanosine/metabolism ; Glutaminase/antagonists & inhibitors ; Glutamine/metabolism ; Humans ; Kidney Neoplasms/drug therapy ; Kidney Neoplasms/pathology ; Mice ; NF-E2 Transcription Factor/metabolism ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Thiadiazoles/pharmacology ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents ; Antioxidants ; Benzeneacetamides ; CB-839 ; NF-E2 Transcription Factor ; Reactive Oxygen Species ; Thiadiazoles ; Glutamine (0RH81L854J) ; 8-Hydroxy-2'-Deoxyguanosine (88847-89-6) ; Glutaminase (EC 3.5.1.2) ; Deoxyguanosine (G9481N71RO)
Language	English
Publishing date	2017-10-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-0930
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Article ; Online: Inhibition of PPARα induces cell cycle arrest and apoptosis, and synergizes with glycolysis inhibition in kidney cancer cells.

Omran Abu Aboud / Hiromi I Wettersten / Robert H Weiss

PLoS ONE, Vol 8, Iss 8, p e

2013 Volume 71115

Abstract	Renal cell carcinoma (RCC) is the sixth most common cancer in the US. While RCC is highly metastatic, there are few therapeutics options available for patients with metastatic RCC, and progression-free survival of patients even with the newest targeted therapeutics is only up to two years. Thus, novel therapeutic targets for this disease are desperately needed. Based on our previous metabolomics studies showing alteration of peroxisome proliferator-activated receptor α (PPARα) related events in both RCC patient and xenograft mice materials, this pathway was further examined in the current study in the setting of RCC. PPARα is a nuclear receptor protein that functions as a transcription factor for genes including those encoding enzymes involved in energy metabolism; while PPARα has been reported to regulate tumor growth in several cancers, it has not been evaluated in RCC. A specific PPARα antagonist, GW6471, induced both apoptosis and cell cycle arrest at G0/G1 in VHL(+) and VHL(-) RCC cell lines (786-O and Caki-1) associated with attenuation of the cell cycle regulatory proteins c-Myc, Cyclin D1, and CDK4; this data was confirmed as specific to PPARα antagonism by siRNA methods. Interestingly, when glycolysis was blocked by several methods, the cytotoxicity of GW6471 was synergistically increased, suggesting a switch to fatty acid oxidation from glycolysis and providing an entirely novel therapeutic approach for RCC.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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