|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The possibility of tumor‑derived exosomes enrichment was confirmed, and for the first time, to the best of our knowledge, the detection of the BCR‑ABL1 transcript highlighted the presence of active leukemic cells in patients with CP‑CML.
|
31638195 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ETV6-ABL1 fusion is a rare but recurrent genetic aberration found in various hematologic malignancies involving both the lymphoid and myeloid lineage, but to the best of our knowledge, CMML is an exceptionally rare presentation of ETV6-ABL1 rearranged neoplasm.
|
31425923 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Correction: ABL kinase inhibition sensitizes primary lung adenocarcinomas to chemotherapy by promoting tumor cell differentiation.
|
31666936 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Unexpectedly, we found that treatment of tumor-bearing mice with an ABL allosteric inhibitor promoted differentiation of lung adenocarcinomas from poorly differentiated tumors expressing basal cell markers to tumors expressing terminal differentiation markers <i>in vivo</i>, which rendered lung adenocarcinomas susceptible to chemotherapy.
|
30956771 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our efforts have yielded SIAIS178 (<b>19</b>), which induces proper interaction between BCR-ABL and VHL ligase leading to effective degradation of BCR-ABL protein, achieves significant growth inhibition of BCR-ABL<sup>+</sup> leukemic cells in vitro, and induces substantial tumor regression against K562 xenograft tumors in vivo.
|
31539241 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Atypical chronic myeloid leukemia (aCML) is a BCR-ABL1 negative myelodysplastic (MDS)/myeloproliferative (MPN) neoplasm with poor overall survival.
|
30078497 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
miR-96 acts as a tumor suppressor via targeting the BCR-ABL1 oncogene in chronic myeloid leukemia blastic transformation.
|
31518872 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Previous study has revealed that H19 expression is required for efficient tumor growth induced by BCR-ABL in chronic myeloid leukemia (CML).
|
28776669 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Using a mouse xenograft model we demonstrate that, while primary tumor size is not affected by ABL kinase inhibitors, the <i>in vivo</i> matrix metalloproteinase (MMP) activity, tumor cell invasion, and consequent spontaneous metastasis to lungs are significantly impaired in inhibitor-treated mice.
|
29774130 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
BCR-ABL1-like B-lymphoblastic leukemia/lymphoma (BCR-ABL1-like B-ALL), also known as Philadelphia-like (Ph-like) ALL, is a neoplasm of B-lineage lymphoblasts characterized by a pattern of gene expression similar to that of B-ALL with the BCR-ABL1 translocation but lacking the BCR-ABL1 fusion protein.
|
29696694 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Recent work indicates that <i>FH<sup>-/-</sup></i> PRCC cells have increased activation of ABL1, which promotes tumor growth, but how ABL1 is activated remains unclear.
|
30297534 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This study intended to establish a droplet digital PCR (dd-PCR) for monitoring minimal residual disease (MRD) in patients with BCR/ABL (P210)-positive chronic myeloid leukemia (CML), thereby achieving deep-level monitoring of tumor load and determining the efficacy for guided clinically individualized treatment.
|
29691899 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Using a genetic loss-of-function approach and bone marrow transplantation models for CML and BCR-ABL1<sup>+</sup> B-ALL, we show that SHP2 is required for BCR-ABL1-evoked myeloid and lymphoid neoplasia.
|
28804122 |
2018 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Atypical chronic myeloid leukemia (aCML) and chronic neutrophilic leukemia (CNL) are rare BCR-ABL1 fusion gene-negative myeloid neoplasms with a predominance of neutrophils.
|
30458320 |
2018 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In 6 patients, we detected mutations in 6 genes commonly mutated in other myeloid neoplasms: ABL1, ASXL1, DNMT3A, IDH1, SETBP1, and TP63.
|
28667884 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
BCR/ABL-edited cells developed smaller tumors than those originating from unedited Boff-p210 parental cells.
|
28212528 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Genetic deletion of Fos and Dusp1 suppressed tumor growth in a BCR-ABL fusion protein kinase-induced mouse model of chronic myeloid leukemia (CML).
|
28319094 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Myeloid neoplasms with concurrent BCR-ABL1 and CBFB rearrangements: A series of 10 cases of a clinically aggressive neoplasm.
|
28253536 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Consistent with structural modeling, we demonstrate that mutations in ABL1 identified in primary NSCLC tumors and a lung cancer cell line increase downstream pathway activation compared to wild-type ABL1.
|
26758680 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Western blot assays showed complete activation of downstream signal pathways up to p-SRC proto-oncogene tyrosine-protein kinase, and p-focal adhesion kinase recruitment in MET and ALK-coamplified tumors only, whereas isolated MET amplification, MET and ALK borderline amplification (5%-10% of tumor cells with ≥15 copies of the relevant gene), or negative tumors showing eusomy or chromosome polysomy were confined to p-mitogen-activated protein kinase, p-protein kinase B, and/or p-MET activation.
|
26804638 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Chronic Myeloid Leukemia (CML) could be considered as the paradigm for non-genomic loss of function of tumor suppressors due to the ability of BCR-ABL to directly promote functionally inactivation of several tumor suppressors.
|
27184141 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Therefore, we postulate that normal ABL1 kinase behaves like a tumor suppressor and therapeutic target in leukemias expressing oncogenic forms of the kinase.
|
26864341 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
BCR-ABL negative myeloproliferative neoplasia: a review of involved molecular mechanisms.
|
25196073 |
2015 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
C61-LNP plus low dose TBI also yielded progression-free survival, tumor-free survival and overall survival outcomes in CD22ΔE12 × BCR-ABL double transgenic mice with advanced stage, radiation-resistant BPL with lymphomatous features that were significantly superior to those of mice treated with TBI alone or C61-LNP alone.
|
26285772 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
SH2-containing tyrosine phosphatase 1 (SHP-1) is reported to bind to p210BCR‑ABL1 and to function as a tumor suppressor.
|
24647617 |
2014 |