TY - JOUR
T1 - Targeting novel signaling pathways for resistant acute myeloid leukemia
AU - Sakamoto, Kathleen M.
AU - Grant, Steven
AU - Saleiro, Diana
AU - Crispino, John D.
AU - Hijiya, Nobuko
AU - Giles, Francis
AU - Platanias, Leonidas
AU - Eklund, Elizabeth A.
N1 - Funding Information:
K.M.S. is supported by the NIH ( R01 HL75826 , R01 GM087305 ), Leukemia and Lymphoma Society of America Screen to Lead Program, Hyundai Hope on Wheels , Stanford SPARK/Child Health Research Institute , S.G. is supported by the NIH ( CA142509 , CA167708 ) and Leukemia and Lymphoma Society of America (# 6472-15 ). L.C.P. is supported by grants from the NIH ( R01 CA77816 , CA155566 , CA161196 and CA121192 ) and Department of Veterans Affairs ( I01CX000916 ). J.C. is supported by the Samuel Waxman Cancer Research Foundation and NIH ( R01 CA101774 ). E.A.E. is supported by NIH ( R01 CA174205 , DK098812 ) and VA Merit Review .
Publisher Copyright:
© 2014 Elsevier Inc.
PY - 2015/3/1
Y1 - 2015/3/1
N2 - Acute myeloid leukemia (AML) is a hematologic malignancy that is the most common type of acute leukemia diagnosed in adults and the second most common type in children. The overall survival is poor and treatment is associated with significant complications and even death. In addition, a significant number of patients will not respond to therapy or relapse. In this review, several new signaling proteins aberrantly regulated in AML are described, including CREB, Triad1, Bcl-2 family members, Stat3, and mTOR/MEK. Identifying more effective and less toxic agents will provide novel approaches to treat AML.
AB - Acute myeloid leukemia (AML) is a hematologic malignancy that is the most common type of acute leukemia diagnosed in adults and the second most common type in children. The overall survival is poor and treatment is associated with significant complications and even death. In addition, a significant number of patients will not respond to therapy or relapse. In this review, several new signaling proteins aberrantly regulated in AML are described, including CREB, Triad1, Bcl-2 family members, Stat3, and mTOR/MEK. Identifying more effective and less toxic agents will provide novel approaches to treat AML.
KW - Acute myeloid leukemia
KW - Novel therapies
KW - Resistance
KW - Signaling pathways
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U2 - 10.1016/j.ymgme.2014.11.017
DO - 10.1016/j.ymgme.2014.11.017
M3 - Review article
C2 - 25533111
AN - SCOPUS:84924122265
SN - 1096-7192
VL - 114
SP - 397
EP - 402
JO - Molecular Genetics and Metabolism
JF - Molecular Genetics and Metabolism
IS - 3
ER -
