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Difference between revisions of "Samper 2009 Free Radic Biol Med"

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{{Publication
{{Publication
|title=Samper E, Morgado L, Estrada JC, Bernad A, Hubbard A, Cadenas S, Melov S (2008) Increase in mitochondrial biogenesis, oxidative stress, and glycolysis in murine lymphomas. Free Radical Biology and Medicine 46 (3): 387-396.
|title=Samper E, Morgado L, Estrada JC, Bernad A, Hubbard A, Cadenas S, Melov S (2009) Increase in mitochondrial biogenesis, oxidative stress, and glycolysis in murine lymphomas. Free Radical Biology and Medicine 46 (3): 387-396.
|authors=Samper E, Morgado L, Estrada JC, Bernad A, Hubbard A, Cadenas S, Melov S
|authors=Samper E, Morgado L, Estrada JC, Bernad A, Hubbard A, Cadenas S, Melov S
|year=2008
|year=2009
|journal=Free Radical Biol. Med.
|journal=Free Radical Biol. Med.
|abstract=Lymphomas adapt to their environment by undergoing a complex series of biochemical changes that are
currently not well understood. To better define these changes, we examined the gene expression and gene
ontology profiles of thymic lymphomas from a commonly used model of carcinogenesis, the p53βˆ’/βˆ’ mouse.
These tumors show a highly significant upregulation of mitochondrial biogenesis, mitochondrial protein
translation, mtDNA copy number, reactive oxygen species, antioxidant defenses, proton transport, ATP
synthesis, hypoxia response, and glycolysis, indicating a fundamental change in the bioenergetic profile of
the transformed T cell. Our results suggest that T cell tumorigenesis involves a simultaneous upregulation of
mitochondrial biogenesis, mitochondrial respiration, and glycolytic activity. These processes would allow
cells to adapt to the stressful tumor environment by facilitating energy production and thereby promote
tumor growth. Understanding these adaptations is likely to result in improved therapeutic strategies for this
tumor type.
|keywords=Mitochondria, Reactive oxygen species, Glycolysis, Lymphoma, p53, c-myc, Free radicals
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19038329 PMID: 19038329]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19038329 PMID: 19038329]
}}
}}
{{Labeling
{{Labeling
|topics=Respiration; OXPHOS; ETS Capacity
|discipline=Biomedicine
|injuries=RONS; Oxidative Stress, Genetic Defect; Knockdown; Overexpression
|topics=Respiration; OXPHOS; ETS Capacity, Mitochondrial Biogenesis; Mitochondrial Density
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
}}
}}

Revision as of 11:28, 2 November 2010

Publications in the MiPMap
Samper E, Morgado L, Estrada JC, Bernad A, Hubbard A, Cadenas S, Melov S (2009) Increase in mitochondrial biogenesis, oxidative stress, and glycolysis in murine lymphomas. Free Radical Biology and Medicine 46 (3): 387-396.

Β» PMID: 19038329

Samper E, Morgado L, Estrada JC, Bernad A, Hubbard A, Cadenas S, Melov S (2009) Free Radical Biol. Med.

Abstract: Lymphomas adapt to their environment by undergoing a complex series of biochemical changes that are currently not well understood. To better define these changes, we examined the gene expression and gene ontology profiles of thymic lymphomas from a commonly used model of carcinogenesis, the p53βˆ’/βˆ’ mouse. These tumors show a highly significant upregulation of mitochondrial biogenesis, mitochondrial protein translation, mtDNA copy number, reactive oxygen species, antioxidant defenses, proton transport, ATP synthesis, hypoxia response, and glycolysis, indicating a fundamental change in the bioenergetic profile of the transformed T cell. Our results suggest that T cell tumorigenesis involves a simultaneous upregulation of mitochondrial biogenesis, mitochondrial respiration, and glycolytic activity. These processes would allow cells to adapt to the stressful tumor environment by facilitating energy production and thereby promote tumor growth. Understanding these adaptations is likely to result in improved therapeutic strategies for this tumor type. β€’ Keywords: Mitochondria, Reactive oxygen species, Glycolysis, Lymphoma, p53, c-myc, Free radicals


Labels:

Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property., Genetic Defect; Knockdown; Overexpression"Genetic Defect; Knockdown; Overexpression" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. 



Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property., Mitochondrial Biogenesis; Mitochondrial Density"Mitochondrial Biogenesis; Mitochondrial Density" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k