PMID- 22665066
OWN - NLM
STAT- MEDLINE
DCOM- 20130524
LR  - 20131121
IS  - 1476-5594 (Electronic)
IS  - 0950-9232 (Linking)
VI  - 32
IP  - 13
DP  - 2013 Mar 28
TI  - BCR-ABL regulates death receptor expression for TNF-related apoptosis-inducing 
      ligand (TRAIL) in Philadelphia chromosome-positive leukemia.
PG  - 1670-81
LID - 10.1038/onc.2012.186 [doi]
AB  - Allogeneic stem cell transplantation (allo-SCT) is a potentially curative therapy 
      for chronic myeloid leukemia and Philadelphia chromosome-positive (Ph(+)) acute 
      lymphoblastic leukemia, and the graft-vs-leukemia (GVL) effect can eradicate 
      residual leukemia after allo-SCT. Ph(+) leukemia cells frequently express 
      death-inducing receptors (DR4 and DR5) for tumor necrosis factor-related 
      apoptosis-inducing ligand (TRAIL), which is one of the cytotoxic ligands 
      expressed on cytotoxic T cells and natural killer cells mediating the GVL effect. 
      Here we demonstrate that imatinib specifically downregulated DR4 and DR5 
      expression in cell lines and clinical samples of Ph(+) leukemia. 
      Second-generation tyrosine kinase inhibitors (dasatinib and nilotinib) and short 
      hairpin RNA against bcr-abl also downregulated DR4 and DR5 expression in Ph(+) 
      leukemia cells, and transfection of bcr-abl into a Ph(-) leukemia cell line 
      induced DR4 and DR5 expression, which was abrogated by imatinib treatment. 
      Accordingly, Ph(+) leukemia cells that had been pretreated with imatinib showed 
      resistance to the pro-apoptotic activity of recombinant human soluble TRAIL. 
      These observations demonstrate that BCR-ABL is critically involved in the 
      leukemia-specific expression of DR4 and DR5 and in the susceptibility of Ph(+) 
      leukemia to TRAIL-mediated anti-leukemic activity, providing new insight into the 
      mechanisms of the tumor-specific cytotoxic activities of TRAIL.
FAU - Kuroda, I
AU  - Kuroda I
AD  - Department of Pediatrics, School of Medicine, University of Yamanashi, Yamanashi, 
      Japan.
FAU - Inukai, T
AU  - Inukai T
FAU - Zhang, X
AU  - Zhang X
FAU - Kikuchi, J
AU  - Kikuchi J
FAU - Furukawa, Y
AU  - Furukawa Y
FAU - Nemoto, A
AU  - Nemoto A
FAU - Akahane, K
AU  - Akahane K
FAU - Hirose, K
AU  - Hirose K
FAU - Honna-Oshiro, H
AU  - Honna-Oshiro H
FAU - Goi, K
AU  - Goi K
FAU - Kagami, K
AU  - Kagami K
FAU - Yagita, H
AU  - Yagita H
FAU - Tauchi, T
AU  - Tauchi T
FAU - Maeda, Y
AU  - Maeda Y
FAU - Sugita, K
AU  - Sugita K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120604
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (RNA, Small Interfering)
RN  - 0 (Receptors, Death Domain)
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (TNFRSF10A protein, human)
RN  - EC 2.7.10.2 (Fusion Proteins, bcr-abl)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
SB  - IM
MH  - Cell Line, Tumor
MH  - Fusion Proteins, bcr-abl/genetics/*physiology
MH  - Gene Expression Regulation, Leukemic/*drug effects
MH  - Humans
MH  - Leukemia, Myelogenous, Chronic, BCR-ABL Positive/*genetics/pathology
MH  - MAP Kinase Signaling System/physiology
MH  - Mitogen-Activated Protein Kinase 3/antagonists & inhibitors/genetics
MH  - Philadelphia Chromosome
MH  - Protein Kinase Inhibitors/pharmacology
MH  - RNA, Small Interfering/pharmacology
MH  - Receptors, Death Domain/*genetics/metabolism
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/genetics/metabolism
MH  - TNF-Related Apoptosis-Inducing Ligand/*pharmacology
EDAT- 2012/06/06 06:00
MHDA- 2013/05/28 06:00
CRDT- 2012/06/06 06:00
PHST- 2012/06/06 06:00 [entrez]
PHST- 2012/06/06 06:00 [pubmed]
PHST- 2013/05/28 06:00 [medline]
AID - onc2012186 [pii]
AID - 10.1038/onc.2012.186 [doi]
PST - ppublish
SO  - Oncogene. 2013 Mar 28;32(13):1670-81. doi: 10.1038/onc.2012.186. Epub 2012 Jun 4.