@article{girerd_superoxide_2018,
	title = {Superoxide dismutase 2 ({SOD2}) contributes to genetic stability of native and {T315I}-mutated {BCR}-{ABL} expressing leukemic cells},
	volume = {498},
	issn = {1090-2104},
	doi = {10.1016/j.bbrc.2018.03.023},
	abstract = {Manganese Superoxide dismutase 2 (SOD2) plays a crucial role in antioxidant defense but there are no data suggesting its role in genetic instability in CML. We evaluated the effects of SOD2 silencing in human UT7 cell line expressing either non-mutated or T315I-mutated BCR-ABL. Array-CGH experiments detected in BCR-ABL-expressing cells silenced for SOD2 a major genetic instability within several chromosomal loci, especially in regions carrying the glypican family (duplicated) and β-defensin genes (deleted). In a large cohort of patients with chronic myeloid leukemia (CML), a significant decrease of SOD2 mRNA was observed. This reduction appeared inversely correlated with leukocytosis and Sokal score, high-risk patients showing lower SOD2 levels. The analysis of anti-oxidant gene expression analysis revealed a specific down-regulation of the expression of PRDX2 in UT7-BCR-ABL and UT7-T315I cells silenced for SOD2 expression. Gene set enrichment analysis performed between the two SOD2-dependent classes of CML patients revealed a significant enrichment of Reactive Oxygen Species (ROS) Pathway. Our data provide the first evidence for a link between SOD2 expression and genetic instability in CML. Consequently, SOD2 mRNA levels should be analyzed in prospective studies as patients with low SOD2 expression could be more prone to develop a mutator phenotype under TKI therapies.},
	language = {eng},
	number = {4},
	journal = {Biochemical and Biophysical Research Communications},
	author = {Girerd, Sandrine and Tosca, Lucie and Herault, Olivier and Vignon, Christine and Biard, Denis and Aggoune, Djamel and Dkhissi, Fatima and Bonnet, Marie Laure and Sorel, Nathalie and Desterke, Christophe and Bennaceur-Griscelli, Annelise and Tachdjian, Gerard and Guilhot, François and Guilhot, Joelle and Chomel, Jean-Claude and Turhan, Ali G.},
	year = {2018},
	pmid = {29550484},
	keywords = {CML, Cell Line, Tumor, Cohort Studies, Fusion Proteins, bcr-abl, Gene Expression Regulation, Leukemic, Gene Silencing, Genetic instability, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Mutation, Peroxiredoxins, Point Mutation, SOD2, Silencing, Superoxide Dismutase},
	pages = {715--722},
}

{"_id":"xeB2KdCEy7NdA3sdx","bibbaseid":"girerd-tosca-herault-vignon-biard-aggoune-dkhissi-bonnet-etal-superoxidedismutase2sod2contributestogeneticstabilityofnativeandt315imutatedbcrablexpressingleukemiccells-2018","author_short":["Girerd, S.","Tosca, L.","Herault, O.","Vignon, C.","Biard, D.","Aggoune, D.","Dkhissi, F.","Bonnet, M. L.","Sorel, N.","Desterke, C.","Bennaceur-Griscelli, A.","Tachdjian, G.","Guilhot, F.","Guilhot, J.","Chomel, J.","Turhan, A. G."],"bibdata":{"bibtype":"article","type":"article","title":"Superoxide dismutase 2 (SOD2) contributes to genetic stability of native and T315I-mutated BCR-ABL expressing leukemic cells","volume":"498","issn":"1090-2104","doi":"10.1016/j.bbrc.2018.03.023","abstract":"Manganese Superoxide dismutase 2 (SOD2) plays a crucial role in antioxidant defense but there are no data suggesting its role in genetic instability in CML. We evaluated the effects of SOD2 silencing in human UT7 cell line expressing either non-mutated or T315I-mutated BCR-ABL. Array-CGH experiments detected in BCR-ABL-expressing cells silenced for SOD2 a major genetic instability within several chromosomal loci, especially in regions carrying the glypican family (duplicated) and β-defensin genes (deleted). In a large cohort of patients with chronic myeloid leukemia (CML), a significant decrease of SOD2 mRNA was observed. This reduction appeared inversely correlated with leukocytosis and Sokal score, high-risk patients showing lower SOD2 levels. The analysis of anti-oxidant gene expression analysis revealed a specific down-regulation of the expression of PRDX2 in UT7-BCR-ABL and UT7-T315I cells silenced for SOD2 expression. Gene set enrichment analysis performed between the two SOD2-dependent classes of CML patients revealed a significant enrichment of Reactive Oxygen Species (ROS) Pathway. Our data provide the first evidence for a link between SOD2 expression and genetic instability in CML. Consequently, SOD2 mRNA levels should be analyzed in prospective studies as patients with low SOD2 expression could be more prone to develop a mutator phenotype under TKI therapies.","language":"eng","number":"4","journal":"Biochemical and Biophysical Research Communications","author":[{"propositions":[],"lastnames":["Girerd"],"firstnames":["Sandrine"],"suffixes":[]},{"propositions":[],"lastnames":["Tosca"],"firstnames":["Lucie"],"suffixes":[]},{"propositions":[],"lastnames":["Herault"],"firstnames":["Olivier"],"suffixes":[]},{"propositions":[],"lastnames":["Vignon"],"firstnames":["Christine"],"suffixes":[]},{"propositions":[],"lastnames":["Biard"],"firstnames":["Denis"],"suffixes":[]},{"propositions":[],"lastnames":["Aggoune"],"firstnames":["Djamel"],"suffixes":[]},{"propositions":[],"lastnames":["Dkhissi"],"firstnames":["Fatima"],"suffixes":[]},{"propositions":[],"lastnames":["Bonnet"],"firstnames":["Marie","Laure"],"suffixes":[]},{"propositions":[],"lastnames":["Sorel"],"firstnames":["Nathalie"],"suffixes":[]},{"propositions":[],"lastnames":["Desterke"],"firstnames":["Christophe"],"suffixes":[]},{"propositions":[],"lastnames":["Bennaceur-Griscelli"],"firstnames":["Annelise"],"suffixes":[]},{"propositions":[],"lastnames":["Tachdjian"],"firstnames":["Gerard"],"suffixes":[]},{"propositions":[],"lastnames":["Guilhot"],"firstnames":["François"],"suffixes":[]},{"propositions":[],"lastnames":["Guilhot"],"firstnames":["Joelle"],"suffixes":[]},{"propositions":[],"lastnames":["Chomel"],"firstnames":["Jean-Claude"],"suffixes":[]},{"propositions":[],"lastnames":["Turhan"],"firstnames":["Ali","G."],"suffixes":[]}],"year":"2018","pmid":"29550484","keywords":"CML, Cell Line, Tumor, Cohort Studies, Fusion Proteins, bcr-abl, Gene Expression Regulation, Leukemic, Gene Silencing, Genetic instability, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Mutation, Peroxiredoxins, Point Mutation, SOD2, Silencing, Superoxide Dismutase","pages":"715–722","bibtex":"@article{girerd_superoxide_2018,\n\ttitle = {Superoxide dismutase 2 ({SOD2}) contributes to genetic stability of native and {T315I}-mutated {BCR}-{ABL} expressing leukemic cells},\n\tvolume = {498},\n\tissn = {1090-2104},\n\tdoi = {10.1016/j.bbrc.2018.03.023},\n\tabstract = {Manganese Superoxide dismutase 2 (SOD2) plays a crucial role in antioxidant defense but there are no data suggesting its role in genetic instability in CML. We evaluated the effects of SOD2 silencing in human UT7 cell line expressing either non-mutated or T315I-mutated BCR-ABL. Array-CGH experiments detected in BCR-ABL-expressing cells silenced for SOD2 a major genetic instability within several chromosomal loci, especially in regions carrying the glypican family (duplicated) and β-defensin genes (deleted). In a large cohort of patients with chronic myeloid leukemia (CML), a significant decrease of SOD2 mRNA was observed. This reduction appeared inversely correlated with leukocytosis and Sokal score, high-risk patients showing lower SOD2 levels. The analysis of anti-oxidant gene expression analysis revealed a specific down-regulation of the expression of PRDX2 in UT7-BCR-ABL and UT7-T315I cells silenced for SOD2 expression. Gene set enrichment analysis performed between the two SOD2-dependent classes of CML patients revealed a significant enrichment of Reactive Oxygen Species (ROS) Pathway. Our data provide the first evidence for a link between SOD2 expression and genetic instability in CML. Consequently, SOD2 mRNA levels should be analyzed in prospective studies as patients with low SOD2 expression could be more prone to develop a mutator phenotype under TKI therapies.},\n\tlanguage = {eng},\n\tnumber = {4},\n\tjournal = {Biochemical and Biophysical Research Communications},\n\tauthor = {Girerd, Sandrine and Tosca, Lucie and Herault, Olivier and Vignon, Christine and Biard, Denis and Aggoune, Djamel and Dkhissi, Fatima and Bonnet, Marie Laure and Sorel, Nathalie and Desterke, Christophe and Bennaceur-Griscelli, Annelise and Tachdjian, Gerard and Guilhot, François and Guilhot, Joelle and Chomel, Jean-Claude and Turhan, Ali G.},\n\tyear = {2018},\n\tpmid = {29550484},\n\tkeywords = {CML, Cell Line, Tumor, Cohort Studies, Fusion Proteins, bcr-abl, Gene Expression Regulation, Leukemic, Gene Silencing, Genetic instability, Humans, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Mutation, Peroxiredoxins, Point Mutation, SOD2, Silencing, Superoxide Dismutase},\n\tpages = {715--722},\n}\n\n","author_short":["Girerd, S.","Tosca, L.","Herault, O.","Vignon, C.","Biard, D.","Aggoune, D.","Dkhissi, F.","Bonnet, M. 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