|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data define STAT5B as major STAT5 isoform driving BCR/ABL<sup>+</sup> leukemia.
|
30679796 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Chronic myeloid leukemia (CML) is characterized by the presence of a constitutively activated tyrosine kinase (Breakpoint Cluster Region - Abelson murine leukemia viral oncogene homolog1, BCR-ABL).
|
31358779 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data showed that complex BCR-ABL1 signal patterns were associated with leukemic clonal evolution and poorer prognosis in BCR-ABL1 positive leukemia.
|
31594548 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
<b>Conclusion:</b> HNRNPA1-mediated exosomal transfer of miR-320 from leukemia cells to BMMSC is an important mediator of leukemia progression and is a potential therapeutic target for CML.
|
31534508 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Leukemia stem cells contribute to drug-resistance and relapse in chronic myeloid leukemia and BCR-ABL1 inhibitor monotherapy fails to eliminate them, thereby necessitating alternate therapeutic strategies.
|
31371410 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study demonstrates that FAM168A may act as a linker protein that binds to BCR-ABL1 and AKT1, which further mediates the downstream signaling pathways in CML.
|
31291942 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, to clarify whether the epigenetic silencing is affected by BCR-ABL1 inhibition, we assessed the methylation status in the patients at different time intervals following the tyrosine kinase inhibition using imatinib therapy, as the first-line treatment for this type of leukemia.
|
31014357 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
A kinase-independent role for CDK8 in BCR-ABL1<sup>+</sup> leukemia.
|
31628323 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
CML is a highly treatable form of leukemia with multiple orally available small molecule inhibitors of the activated BCR-ABL1 (breakpoint cluster region-ABL1) kinase.
|
30608253 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We observed higher frequency of <i>KIR A</i> homozygosity among 745 healthy Chinese Southern Han than 836 adult patients representing three types of leukemia: ALL (OR = 0.68, 95% CI = 0.52-0.89, <i>p</i> = 0.004), AML (OR = 0.76, 95% CI = 0.59-0.98, <i>p</i> = 0.034), and CML (OR = 0.72 95% CI = 0.51-1.0, ns).
|
31379844 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
BCR-ABL1-positive leukemias have historically been classified as either chronic myelogenous leukemia or Ph+ acute lymphoblastic leukemia.
|
31136068 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Starting from this observation, we extended our study to a panel of human leukemic cells carrying genetic lesions distinctive of different types of leukemias and myeloproliferative disorders (the BCR-ABL1 translocation and the JAK2V617F amino acid substitution) to dissect the cellular events induced by SOX6.
|
30833651 |
2019 |
|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
BCR-ABL1 tyrosine kinase inhibitor K0706 exhibits preclinical activity in Philadelphia chromosome-positive leukemia.
|
31493432 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The summary RR per 5 kg/m2 increase in BMI were 1.12 [95% confidence interval (CI): 1.05-1.20] for HL, 1.05 (95% CI: 1.03-1.08) for NHL, 1.11 (95% CI: 1.05-1.16) for DLBCL, 1.06 (95% CI: 1.03-1.09) for ML, 1.09 (95% CI: 1.03-1.15) for leukaemia, 1.13 (95% CI: 1.04-1.24) for AML, 1.13 (95% CI: 1.05-1.22) for CML and 1.04 (95% CI: 1.00-1.09) for CLL, and were1.12 (95% CI: 1.05-1.19) for NHL, 1.22 (95% CI: 1.09-1.37) for DLBCL, and 1.19 (95% CI: 1.03-1.38) for FL for BMI in early adulthood analysis.
|
30753270 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, the identification and control of downstream molecules/ signaling route of the BCR-ABL1 that are involved in the survival and self-renewal of leukemia stem cells can be an effective treatment strategy to eliminate leukemia stem cells, which supposed to be cured by Musashi2-Numb signaling pathway.
|
31231484 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Comparison of <i>BCR-ABL</i> Transcript Variants Between Patients With Chronic Myeloid Leukaemia and Leukaemia Cell Lines.
|
31280200 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
BCR-ABL1 point mutation-mediated resistance to tyrosine kinase inhibitor (TKI) therapy in Philadelphia chromosome-positive (Ph<sup>+</sup>) leukemia is effectively managed with several approved drugs, including ponatinib for BCR-ABL1<sup>T315I</sup>-mutant disease.
|
31543464 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate that SIAIS178 as efficacious BCR-ABL degrader warrants extensive further investigation for the treatment of BCR-ABL<sup>+</sup> leukemia.
|
31539241 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In this study, we show that the relatively rapid onset of this leukemia is potentially related to oncogenic domains within the BCR component.
|
30413411 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
A t(9;22) chromosomal translocation which forms the chimeric tyrosine kinase breakpoint cluster region (BCR)‑Abelson murine leukemia viral oncogene homolog 1 (ABL) is a key mechanism underlying the pathogenesis of chronic myelogenous leukemia (CML).
|
31115499 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conclude that the Q-LAMP assay may represent a faster and valid alternative to the qualitative BIOMED-1 RT-PCR for the diagnosis at <i>BCR-ABL1</i>-positive leukemias, especially when samples are analyzed in centers with restricted resources and/or limited technical expertise.
|
31817063 |
2019 |
|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We describe and validate a <i>Drosophila</i> leukemia model based on inducible human BCR-ABL1 expression controlled by tissue-specific promoters.
|
30409797 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Recent studies have demonstrated the existence of a subset of BCR-ABL1 like leukemias (~10-15% of Bimmunophenotype ALL), whose blast cells have a gene expression profile similar to that of BCR-ABL1 despite the absence of t(9;22)(q34;q11.2).
|
28748759 |
2018 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Monocyte subsets and their phenotypes during treatment with BCR-ABL1 tyrosine kinase inhibitors for Philadelphia chromosome-positive leukemia.
|
29431866 |
2018 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Thus, the aim of this study was to investigate the effects of Shb knockout on the development of leukemia in three additional models, that is, colony stimulating factor 3 receptor-T618I-induced neutrophilic leukemia, p190 Breakpoint cluster region-cAbl oncogene 1 tyrosine kinase-induced B-cell leukemia, and G12D-Kras-induced T-cell leukemia/thymic lymphoma.
|
29792386 |
2018 |