|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
TOPK inhibitor OTS514 suppressed proliferation of BCR/ABL‑positive cell lines and colony formation of CD34‑positive cells from patients with CML compared with lymphoma patients without bone marrow involvement.
|
30864683 |
2019 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results showed that CP-CML CD34+ progenitors were characterized by significant lower phosphorylation of proteins involved in the regulation of growth and cell survival, such as tyrosine kinases of the Src family and members of STAT family, and by a significant higher phosphorylation of p53 (Ser15), compared to normal CD34+ cells from healthy donors.
|
29774100 |
2018 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We show several mRNAs up- or downregulated in CD34-CML during the chronic phase.
|
28905209 |
2018 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The analysis of molecular circuitry of AHR signaling in CML showed a transcriptional signature in CML derived CD34+ CD38- primitive cells with either low or high levels of AHR, with an upregulation of myeloid genes involved in differentiation in the "AHR low" fraction and an upregulation of genes involved in stem cell maintenance in the "AHR high" fraction.
|
30091999 |
2018 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Ivermectin is significantly more effective in inducing caspase-dependent apoptosis in CML cell line K562 and primary CML CD34 than normal bone marrow (NBM) CD34 cells.
|
29428725 |
2018 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Several evidence suggests that CML stem cells are intrinsically resistant to Tyrosine Kinase Inhibitors (TKI), and therefore they represent the most likely candidate responsible for disease relapse.In this work, we investigated the microRNA (miRNA) expression profile of different subpopulations of CML Leukemic Stem Cells (LSCs): Lin-CD34+CD38- and Lin-CD34-CD38- cells.
|
28533480 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We have now demonstrated that protein expression of human estrogen receptor alpha 36 (ERα36), an alternative splicing variant of human estrogen receptor alpha 66 (ERα66), is highly increased in TKI-insensitive CD34+ chronic myeloid leukemia (CML) cells and BCR-ABL-T315I mutant cells, and is abnormally localized in plasma membrane and cytoplasm.
|
28599273 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
<i>Materials and methods</i> We compared DNA methylation of 1,505 selected promoter CpGs in chronic myelogenous leukemia (CML), acute lymphoblastic leukemia (ALL) with and without the Philadelphia chromosome t(9:22), CD34+ hematopoietic stem cells transfected with <i>BCR-ABL</i>, and other tumors without <i>BCR-ABL</i> (acute promyelocytic leukemia (APL) and gastrointestinal stromal tumors (GIST).
|
28730166 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The results of the present study indicated that primary CML CD34<sup>+</sup> blasts were able to release MVs, which were selectively enriched with the surface markers CD34 and CD123, and functional miRNAs from parental cells.
|
28789422 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although separate IFNγ or IM treatment only slightly upregulated BCL6 expression, combined treatment induced remarkable BCL6 upregulation in CML lines and primary human CD34+ CML stem cells.
|
28368400 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Combination of propofol and dasatinib significantly eliminates CML CD34 without affecting NBM CD34 cells.
|
28962554 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Bone marrow samples of newly diagnosed children with chronic-phase chronic myeloid leukemia (CML) were obtained at diagnosis and after imatinib initiation and stained with anti-human CD34, CD38, CD123, CD45RA, cMpl, and lineage antibodies.
|
28233439 |
2017 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
In contrast to normal hematopoietic stem cells, CD34(+)/CD38(-)CML LSCs expressed the IL-2 receptor alpha chain, IL-2RA (CD25).
|
26607600 |
2016 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
BLT2 inhibition induces apoptosis, inhibits proliferation, colony formation and self-renewal capacity of CD34(+) cells from TKI-resistant BP-CML patients.
|
26966074 |
2016 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, the enhanced apoptosis observed with the combination of cysmethynil and imatinib is significant only in primary CML CD34+ progenitor cells, not normal cord blood progenitor cells.
|
26706195 |
2016 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The model facilitates the evaluation of the frequency of leukemic stem cells with long-term leukemia-initiating activity, a critical subcellular population that causes disease relapse and progression, through the utilization of primary CD34(+) CML stem/progenitor cells obtained from CML patients at diagnosis and prior to drug treatment.
|
27581149 |
2016 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Microvessels in pre-CML, highlighted by CD34, were tortuous with abnormal branching, although to a lesser extent than those found in CML-CP.
|
27040932 |
2016 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The capacity of Flk1(+)CD31(-)CD34(-) MSCs from CML patients to inhibit T lymphocyte activation and proliferation was impaired in vitro.
|
25837664 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using microarray-based miRNA profiling, we found that miRNA 486 (miR-486) is significantly upregulated in chronic myeloid leukemia (CML) compared with normal CD34(+) cells, particularly in the megakaryocyte-erythroid progenitor population. miR-486-5p expression increased during erythroid differentiation of both CML and normal CD34(+) cells.
|
25515961 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found significant upregulation (p<0.05) of Notch1, Notch2 and Hes1 on the most primitive CD34+Thy+ subset of CML CD34+ cells suggesting that active Notch signalling in CML primitive progenitors.
|
25849484 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The primary CD34(+) CML cells from this patient showed increased sensitivity to the combination of ponatinib and ABT-263, a BCL2 inhibitor with a negligible effect against the normal CD34(+) cells.
|
25712455 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, BAP1 protein levels are low or undetectable in CD34(+) cells from CML patients at diagnosis as compared with CD34(+) cells from normal donors.
|
26118501 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Bosutinib/PF-00477736 co-treatment also potentiated cell death in CD34(+) CML patient samples, including dasatinib-resistant blast crisis cells exhibiting both T315I and E355G mutations, but was minimally toxic to normal CD34(+) cells.
|
25465126 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
A similar mechanism was found to operate in primary CML CD34(+) cells.
|
25965880 |
2015 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The 41 and 39 genes were significantly upregulated in CML CD34(+) cells (HINT1, TXN, SERBP1) and granulocytes, respectively.
|
26460262 |
2015 |