To identify gene alterations that cooperate with STAT5 activation to initiate leukemia, the authors crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only in B cells. High-throughput sequencing approaches were used to identify genes frequently targeted by the T2/Onc transposon. They observe among others expression of Sos1 and Kdm2a, and activation of p38, correlated with survival, underscoring the role these genes and associated pathways have in B-ALL.
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To identify gene alterations that cooperate with STAT5 activation to initiate leukemia, the authors crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only in B cells. High-throughput sequencing approaches were used to identify genes frequently targeted by the T2/Onc transposon. They observe among others expression of Sos1 and Kdm2a, and activation of p38, correlated with survival, underscoring the role these genes and associated pathways have in B-ALL.
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