|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, morphine alleviated the inhibitory effects of BCR-ABL TKIs in cell survival, colony formation and replating capacity in BP-CML CD34 <sup>+</sup> stem/progenitor cells.
|
31615652 |
2019 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
CML transformation to lymphoid blast phase (BP) is associated with copy number abnormalities, characteristic of BCR-ABL1 positive acute lymphoblastic leukemia, but not of CML in the chronic phase.
|
30511400 |
2019 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Despite the efficacy of BCR-ABL tyrosine kinase inhibitors (TKIs) in chronic phase-chronic myeloid leukemia, the management of blast phase-chronic myeloid leukemia (BP-CML) remains a challenge.
|
31276961 |
2019 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
Bosutinib, a BCR-ABL1 tyrosine kinase inhibitor (TKI), has been available for several years as a treatment for chronic-, accelerated-, and blast-phase chronic myeloid leukemia (CML), for patients with resistance or intolerance to prior therapy.
|
30587215 |
2018 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Among the study group analyzed, a significantly higher frequency of BCR/ABL1 gene rearrangements that is consistent with der(9) deletion were observed in the blast crisis (BC) phase at 41.67%, followed by the accelerated phase (AP) at 36.84%, the imatinib mesylate (IM)-resistant chronic phase (CP) at 23.08%, and the lowest incidence was found in de novo CP at 16.61%.
|
30055547 |
2018 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, for a proportion of them, BCR-ABL1 inhibition will become ineffective at treating the disease, and CML will progress to blast crisis (BC) CML with poor prognosis.
|
29683667 |
2018 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
This case illustrates the major interest of interphase FISH for BCR-ABL1 rearrangement on blood neutrophils as a decisive method to discriminate a lymphoid blast crisis of CML from a de novo BCR-ABL1 positive ALL.
|
28444777 |
2018 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Imatinib, an ABL tyrosine kinase inhibitor, is dramatically effective in CML patients; however, 30% of CML patients will need further treatment due to progression of CML to blast crisis (BC).
|
27908728 |
2017 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
Drug resistance to BCR-ABL1 tyrosine kinase inhibitor (TKI) and disease progression to blast crisis (BC) are major clinical problems in chronic myeloid leukemia (CML); however, underlying mechanisms governing this process remain to be elucidated.
|
28232743 |
2017 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
ARDAP derivative <b>10</b> inhibited the proliferation of BCR/ABL-expressing KU812 and LAMA84 cells from chronic myeloid leukemia (CML) patients in blast crisis and of hematopoietic cells ectopically expressing the imatinib mesylate (IM)-sensitive KBM5-WT or its IM-resistant KBM5-T315I mutation.
|
28523104 |
2017 |
|
Blast Phase
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here, we show that the expression of WASP decreases with the progression of CML, inversely correlates with the expression of BCR-ABL1 and is particularly low in blast crisis.
|
29022901 |
2017 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
According to the 2008 World Health Organization (WHO) Classification of Tumors of the Haematopoietic and Lymphoid Tissues, the finding of B lymphoblasts in the blood or bone marrow of a patient with chronic myelogenous leukemia, BCR-ABL1+ (CML) should raise a concern for progression of the disease to B-lymphoblastic blast phase.
|
25916436 |
2017 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We demonstrated that expression of the Ik6 transcript, which lacked exons 3-6, was observed exclusively in BCR-ABL1(+) B ALL and lymphoid blast crisis CML (BC-CML) patients harbouring the IKZF1 Δ3-6 deletion.
|
27198500 |
2016 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
In patients who achieved BCR-ABL1 ≤ 10% at 3 months (dasatinib, 84%; imatinib, 64%), improvements in progression-free and overall survival and lower rates of transformation to accelerated/blast phase were reported compared with patients with BCR-ABL1 greater than 10% at 3 months.
|
27217448 |
2016 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
BCR-ABL1-Abl1(-/-) cells generated highly aggressive chronic myeloid leukemia (CML)-blast phase-like disease in mice compared with less malignant CML-chronic phase-like disease from BCR-ABL1-Abl1(+/+) cells.
|
26864341 |
2016 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
A phase I study of danusertib (PHA-739358) in adult patients with accelerated or blastic phase chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant or intolerant to imatinib and/or other second generation c-ABL therapy.
|
25887498 |
2015 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In this study, we investigated the distribution and clonality of the TCR Vβ repertoire in 4 cases with imatinib-resistant CML in blast crisis (BC-CML) with abelson murine leukemia viral oncogene homolog 1 (ABL1) kinase domain mutations (KDMs).
|
26423566 |
2015 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Whereas the chronic phase of CML is dependent on BCR-ABL, additional mutations are required for progression to BC.
|
26304963 |
2015 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, oligomycin-A enhanced elimination of BCR-ABL(+) leukemia cells by TKI in a mouse model and in primary blast crisis CML samples.
|
25547679 |
2015 |
|
Blast Phase
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Both the presence and the levels of BCR/ABL1 expression seem to be critical for CML progression from chronic phase (CP) to blast crisis (BC).
|
26179066 |
2015 |
|
Blast Phase
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Adults with Ph+ chronic phase (CP)-, accelerated phase (AP)- or blast phase (BP)-CML, or ALL and documented BCR-ABL T315I mutation were treated with a 5-day continuous infusion of MK-0457 administered every 14 days at 40 mg/m(2)/h, 32 mg/m(2)/h or 24 mg/m(2)/h.
|
25127392 |
2014 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
Before treatment, CML-CP patients showed lower BCR-ABL relative concentrations with a higher proportion of M-bcr (42.7%) compared to CML-BP and ALL patients while ALL patients had a higher BCR-ABL relative concentration with high expression of m-bcr (51.4%).
|
25520136 |
2014 |
|
Blast Phase
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Whereas higher BCR-ABL expression has been described as a pre-requisite for malignant CML stem cell transformation and CML progression to blast crisis, recent evidence suggests that during persistence TKI select for CML precursors with low BCR-ABL expression.
|
24500518 |
2014 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
The BCR-ABL1 fusion gene, encoding a constitutively active tyrosine kinase, is thought to be sufficient to cause chronic phase (CP) CML, whereas additional genetic lesions are needed for progression into CML BC.
|
25501026 |
2014 |
|
Blast Phase
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chronic myeloid leukemia responds well to therapy targeting the oncogenic fusion protein BCR-ABL1 in chronic phase, but is resistant to treatment after it progresses to blast crisis (BC).
|
23737503 |
2013 |