|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Translocations and deregulation of the <i>MSI2</i> gene are diagnostic of certain cancers, including chronic myeloid leukemia (CML) with translocation t(7;17), acute myeloid leukemia (AML) with translocation t(10;17), and some cases of B-precursor acute lymphoblastic leukemia (pB-ALL).
|
30126842 |
2018 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Enhanced co-expression of MDR1, survivin, and Bcl-2 proteins, supposedly involved in IM-resistance and CML-SC survival, was detected in both CD34+/CD38- and CD34+/CD38+ cells.
|
30017934 |
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 |
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 |
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 |
Biomarker
|
disease |
BEFREE |
In order to understand the role of Cyclin Dependent Kinase Inhibitors in CML LSC permanence after TKI treatment, in this study we analyzed cell cycle status, the levels of several CDKIs and the subcellular localization of such molecules in different CML cell lines, as well as primary CD34(+)CD38(-)lin(-) LSC and HSC.
|
26985855 |
2016 |
|
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 |
The high levels of CD25 expression in the CD34(+)CD38(-) fraction of human CML cells indicate that CD25(+) LICs constitute an "LIC-derived niche" that could be preferentially targeted in therapy for CML.
|
24574458 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
We have identified the cytokine-targeting surface enzyme dipeptidylpeptidase-IV (DPPIV/CD26) as a novel, specific and pathogenetically relevant biomarker of CD34(+)/CD38(─) CML LSC.
|
24778155 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
High levels of CD38 reduced intracellular nicotinamide adenine dinucleotide (NAD+) levels and blocked acquired resistance by inhibiting the activity of the NAD+-dependent SIRT1 deacetylase that we have previously shown to promote resistance in CML cells by facilitating error-prone DNA damage repair.
|
24967705 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
The putative targets: PROTEINASE 3, SURVIVIN, and hTERT were expressed only at relatively low levels by the CD34(+)CD38(-)ALDH(high) CML cells, similar to the normal CD34(+)CD38(-)ALDH(high) cells and less than in the total CML CD34(+) cells.
|
21132730 |
2011 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, peptide inhibition of BCL6 in human CML cells compromises colony formation and leukemia initiation in transplant recipients and selectively eradicates CD34(+) CD38(-) LICs in patient-derived CML samples.
|
21911423 |
2011 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
We evaluated BCR-ABL expression in CD34(+)CD38(+) (38(+)) committed progenitors and CD34(+)CD38(-) (38(-)) stem/primitive progenitor cells in samples from CML patients on imatinib treatment for at least 4 years with cytogenetic and molecular response.
|
21931114 |
2011 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, by generating an anti-IL1RAP antibody, we provide proof of concept that IL1RAP can be used as a target on CML CD34(+)CD38(-) cells to induce antibody-dependent cell-mediated cytotoxicity.
|
20805474 |
2010 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Lineage-negative (i.e., immature) CD34+ CD38- CML stem cell-enriched populations were isolated from five patients with chronic phase CML samples by fluorescence-activated cell sorting.
|
17470736 |
2007 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Second, the number of committed (CD34+/CD38+) and non-committed (CD34+/CD38-) stem cells, expressing the chimeric fusion gene p210 BCR/ABL in the autograft from a patient with chronic myeloid leukemia (CML), was determined.
|
9789216 |
1998 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
SCF, as a single agent, supported the survival and expansion of colony-forming unit-granulocyte-macrophage (CFU-GM) from CML CD34(+)CD38(+) cells and the more primitive CML CD34(+)CD38(-) cells.
|
9746786 |
1998 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
We also separated CD34+ CML cell populations into HLA-DR(hi) and HLA-DR(lo) fractions and CD38(hi) and CD38(lo) fractions by flow cytometry.
|
9305602 |
1997 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results indicate that benign progenitors in CML are enriched within the CD34+ cells with low DR antigen expression, but not low CD38 expression.
|
7541674 |
1995 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
New complex Ph' translocation t (10; 14; 22) in bone marrow cells and in PHA-stimulated peripheral blood cultures in chronic myelocytic leukaemia.
|
6933152 |
1980 |