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Dysregulation or aberrant activation of such cascades can lead to inappropriate cell survival and abnormal cell proliferation in leukemia. Successful treatment of chronic myeloid leukemia (CML) with tyrosine kinase inhibitors targeting the BCR\u2010ABL fusion gene is a prime example of effectively inhibiting intracellular signaling cascades. However, even in these patients resistance can develop via emergence of mutations or feedback activation of other pathways that cause refractory disease. Constitutive activation of the phosphatidylinositol 3\u2010kinase (PI3K)\/protein kinase B (Akt)\/mammalian target of rapamycin (mTOR) signaling pathway has been observed in different types of leukemia, including CML, acute myeloid leukemia, and acute lymphoblastic leukemia. Abnormal mTOR activity may contribute to chemotherapy resistance, while it may also be effectively targeted via molecular means and\/or development of specific pharmacological inhibitors. This review discusses the role of PI3K\/Akt\/mTOR dysre\u2010gulation in leukemia and summarizes the emergence of preliminary data for the development of novel therapeutic approaches. J. Cell. Biochem. 117: 1745\u20131752, 2016. \u00a9 2016 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jcb.25559","type":"journal-article","created":{"date-parts":[[2016,3,28]],"date-time":"2016-03-28T12:01:58Z","timestamp":1459166518000},"page":"1745-1752","source":"Crossref","is-referenced-by-count":50,"title":["Targeting the mTOR Pathway in Leukemia"],"prefix":"10.1002","volume":"117","author":[{"given":"Shira","family":"Dinner","sequence":"first","affiliation":[{"name":"Division of Hematology\u2010Oncology Robert H. Lurie Comprehensive Cancer Center Feinberg School of Medicine Northwestern University Chicago Illinois 60611"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonidas C.","family":"Platanias","sequence":"additional","affiliation":[{"name":"Division of Hematology\u2010Oncology Robert H. 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