2. Academic Validation
  3. Targeting nonclassical oncogenes for therapy in T-ALL

Targeting nonclassical oncogenes for therapy in T-ALL

  • Cancer Cell. 2012 Apr 17;21(4):459-72. doi: 10.1016/j.ccr.2012.02.029.
Prem S Subramaniam 1,  Dosh W Whye,  Evgeni Efimenko,  Jianchung Chen,  Valeria Tosello,  Kim De Keersmaecker,  Adam Kashishian,  Mary Ann Thompson,  Mireia Castillo,  Carlos Cordon-Cardo,  Utpal P Davé,  Adolfo Ferrando,  Brian J Lannutti,  Thomas G Diacovo
Affiliations

Affiliation

  • 1 Department of Pediatrics, Columbia University Medical Center, New York, NY 10032, USA.
PMID: 22516257 DOI: 10.1016/j.ccr.2012.02.029
Abstract

Constitutive phosphoinositide 3-kinase (PI3K)/Akt activation is common in T cell acute lymphoblastic leukemia (T-ALL). Although four distinct class I PI3K isoforms (α, β, γ, δ) could participate in T-ALL pathogenesis, none has been implicated in this process. We report that in the absence of PTEN Phosphatase tumor suppressor function, PI3Kγ or PI3Kδ alone can support leukemogenesis, whereas inactivation of both isoforms suppressed tumor formation. The reliance of PTEN null T-ALL on the combined activities of PI3Kγ/δ was further demonstrated by the ability of a dual inhibitor to reduce disease burden and prolong survival in mice as well as prevent proliferation and promote activation of proapoptotic pathways in human tumors. These results support combined inhibition of PI3Kγ/δ as therapy for T-ALL.

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