PMID- 24639110
OWN - NLM
STAT- MEDLINE
DCOM- 20150903
LR  - 20161125
IS  - 1559-0283 (Electronic)
IS  - 1085-9195 (Linking)
VI  - 70
IP  - 1
DP  - 2014 Sep
TI  - Hypothesis: Tim-3/galectin-9, a new pathway for leukemia stem cells survival by 
      promoting expansion of myeloid-derived suppressor cells and differentiating into 
      tumor-associated macrophages.
PG  - 273-7
LID - 10.1007/s12013-014-9900-0 [doi]
AB  - Despite the improvements in chemotherapy, about 60 % of acute myeloid leukemia 
      (AML) remission patients still relapse. Leukemic stem cells (LSCs) are the main 
      causes for the relapse and refractory. T cell immunoglobulin mucin-3 (TIM-3), a 
      specific surface molecule expressed on LSCs in most types of AML, is a candidate 
      for AML LSC-targeted therapies. It is important to know how this molecule 
      functions in the maintenance of LSCs and suppression of anti-tumor immunity. 
      Recent data have shown that Tim-3 which expresses on T cells can suppress immune 
      responses indirectly by inducing expansion of myeloid-derived suppressor cells 
      (MDSCs). MDSCs at the leukemia site can also differentiate into tumor-associated 
      macrophages (TAMs). TAMs can promote proliferation and survival of LSCs by the 
      diversion of adaptive immunity and the facilitation of extracellular matrix 
      remodeling, angiogenesis, and lymphangiogenesis. Our previous study in AML 
      patient bone marrow samples showed CD68(+) macrophages around AML clone. Based on 
      the known evidence and our experimental findings, we hypothesize that Tim-3, 
      which specifically expresses on LSCs, is beneficial for LSCs survival and AML 
      progression by promoting expansion of MDSCs and differentiating into TAMs at the 
      leukemia site.
FAU - Gao, Lei
AU  - Gao L
AD  - Department of Hematology, Xinqiao Hospital, Third Military Medical University, 
      Chongqing, 400037, China, gaolei7765@163.com.
FAU - Yu, Shicang
AU  - Yu S
FAU - Zhang, Xi
AU  - Zhang X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cell Biochem Biophys
JT  - Cell biochemistry and biophysics
JID - 9701934
RN  - 0 (Galectins)
RN  - 0 (HAVCR2 protein, human)
RN  - 0 (Hepatitis A Virus Cellular Receptor 2)
RN  - 0 (LGALS9 protein, human)
RN  - 0 (Membrane Proteins)
SB  - IM
MH  - *Cell Differentiation
MH  - Cell Line, Tumor
MH  - Cell Survival
MH  - Galectins/*metabolism
MH  - Hepatitis A Virus Cellular Receptor 2
MH  - Humans
MH  - Leukemia, Myeloid, Acute/metabolism/*pathology
MH  - Macrophages/*cytology
MH  - Membrane Proteins/*metabolism
MH  - Neoplastic Stem Cells/*pathology
MH  - *Signal Transduction
EDAT- 2014/03/19 06:00
MHDA- 2015/09/04 06:00
CRDT- 2014/03/19 06:00
PHST- 2014/03/19 06:00 [entrez]
PHST- 2014/03/19 06:00 [pubmed]
PHST- 2015/09/04 06:00 [medline]
AID - 10.1007/s12013-014-9900-0 [doi]
PST - ppublish
SO  - Cell Biochem Biophys. 2014 Sep;70(1):273-7. doi: 10.1007/s12013-014-9900-0.