PMID- 28479419
OWN - NLM
STAT- MEDLINE
DCOM- 20170929
LR  - 20211204
IS  - 1873-2399 (Electronic)
IS  - 0301-472X (Print)
IS  - 0301-472X (Linking)
VI  - 53
DP  - 2017 Sep
TI  - Novel tumor-suppressor function of KLF4 in pediatric T-cell acute lymphoblastic 
      leukemia.
PG  - 16-25
LID - S0301-472X(17)30141-8 [pii]
LID - 10.1016/j.exphem.2017.04.009 [doi]
AB  - Acute lymphoblastic leukemia (ALL) is the most common hematological malignancy in 
      pediatric patients. Despite advances in the treatment of this disease, many 
      children with T-cell ALL (T-ALL) die from disease relapse due to low responses to 
      standard chemotherapy and the lack of a targeted therapy that selectively 
      eradicates the chemoresistant leukemia-initiating cells (LICs) responsible for 
      disease recurrence. We reported recently that the reprogramming factor 
      Kruppel-like factor 4 (KLF4) has a tumor-suppressive function in children with 
      T-ALL. KLF4 silencing by promoter deoxyribonucleic acid (DNA) methylation in 
      patients with T-ALL leads to aberrant activation of the mitogen-activated protein 
      kinase kinase MAP2K7 and the downstream c-Jun NH(2)-terminal kinase (JNK) pathway 
      that controls the expansion of leukemia cells via c-Jun and activating 
      transcription factor 2. This pathway can be inhibited with small molecules and 
      therefore has the potential to eliminate LICs and eradicate disease in 
      combination with standard therapy for patients with refractory and relapsed 
      disease. The present review summarizes the role of the KLF4-MAP2K7 pathway in 
      T-ALL pathogenesis and the function of JNK and MAP2K7 in carcinogenesis and 
      therapy.
CI  - Copyright (c) 2017 ISEH - International Society for Experimental Hematology. 
      Published by Elsevier Inc. All rights reserved.
FAU - Shen, Ye
AU  - Shen Y
AD  - Department of Pathology and Immunology, Baylor College of Medicine, Texas 
      Children's Hospital, Houston, TX.
FAU - Chen, Taylor J
AU  - Chen TJ
AD  - Department of Pathology and Immunology, Baylor College of Medicine, Texas 
      Children's Hospital, Houston, TX.
FAU - Lacorazza, H Daniel
AU  - Lacorazza HD
AD  - Department of Pathology and Immunology, Baylor College of Medicine, Texas 
      Children's Hospital, Houston, TX. Electronic address: hdl@bcm.edu.
LA  - eng
GR  - R01 CA207086/CA/NCI NIH HHS/United States
GR  - T32 GM008231/GM/NIGMS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20170504
PL  - Netherlands
TA  - Exp Hematol
JT  - Experimental hematology
JID - 0402313
RN  - 0 (KLF4 protein, human)
RN  - 0 (Kruppel-Like Factor 4)
RN  - 0 (Kruppel-Like Transcription Factors)
RN  - 0 (Tumor Suppressor Protein p53)
RN  - 0 (Tumor Suppressor Proteins)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.12.2 (MAP Kinase Kinase 7)
RN  - EC 2.7.12.2 (MAP2K7 protein, human)
SB  - IM
MH  - Child
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/physiology
MH  - Kruppel-Like Factor 4
MH  - Kruppel-Like Transcription Factors/*physiology
MH  - MAP Kinase Kinase 7/physiology
MH  - MAP Kinase Signaling System
MH  - Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/drug therapy/*etiology
MH  - Tumor Suppressor Protein p53/physiology
MH  - Tumor Suppressor Proteins/*physiology
PMC - PMC5568468
MID - NIHMS873769
EDAT- 2017/05/10 06:00
MHDA- 2017/09/30 06:00
PMCR- 2018/09/01
CRDT- 2017/05/09 06:00
PHST- 2017/03/22 00:00 [received]
PHST- 2017/04/21 00:00 [revised]
PHST- 2017/04/22 00:00 [accepted]
PHST- 2017/05/10 06:00 [pubmed]
PHST- 2017/09/30 06:00 [medline]
PHST- 2017/05/09 06:00 [entrez]
PHST- 2018/09/01 00:00 [pmc-release]
AID - S0301-472X(17)30141-8 [pii]
AID - 10.1016/j.exphem.2017.04.009 [doi]
PST - ppublish
SO  - Exp Hematol. 2017 Sep;53:16-25. doi: 10.1016/j.exphem.2017.04.009. Epub 2017 May 
      4.