|
Neoplasms
|
0.200 |
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
|
0.200 |
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
|
0.200 |
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
|
0.200 |
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
|
0.200 |
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
|
0.200 |
Biomarker
|
group |
BEFREE |
The study concluded that siRNA/PEI-αLA nanoparticles enabled silencing of the BCR-ABL gene and BCR-ABL protein, which consequently reduced growth on CML K562 cells in vitro and arrested the growth of localized tumors in a localized CML mouse model.
|
29913272 |
2018 |
|
Neoplasms
|
0.200 |
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
|
0.200 |
Biomarker
|
group |
BEFREE |
We performed integrated genome-wide chromatin and expression analyses and identified Ikaros target genes in mouse and human BCR-ABL1<sup>+</sup> pre-B ALL, revealing novel conserved gene pathways associated with Ikaros tumor suppressor function.
|
28190001 |
2017 |
|
Neoplasms
|
0.200 |
GeneticVariation
|
group |
BEFREE |
It is important to recognize that neoplasms carrying the t(8;22)/BCR-FGFR1, although rare, can commonly with B lymphoblastic leukemia at the initial diagnosis, which could distract one from recognizing a possible underlying 8p11 myeloproliferative syndrome.
|
28551329 |
2017 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
In vivo studies indicated that SHC004-221A1 suppressed BCR-ALB<sup>T315I</sup>-driven tumor growth in mice.
|
28595903 |
2017 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Given the distinct clinical and pathological characteristics, we believe that hematological neoplasms harboring BCR-JAK2 should be included as an additional distinct entity to the current WHO category of "myeloid and lymphoid neoplasms with eosinophilia and abnormalities of PDGFRA, PDGFRB, or FGFR", and testing for a JAK2 fusion should be pursued in neoplasms with a karyotypic 9p24 abnormality.
|
27134074 |
2016 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
We will suggest control experiments and outline further methods that are required to allow for assessment of disease development upon tumor suppressor knockout in CML.
|
27581141 |
2016 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Novel fusion between the breakpoint cluster region and platelet-derived growth factor receptor-alpha genes in a patient with chronic myeloid leukemia-like neoplasm: undetectable residual disease after imatinib therapy.
|
25941032 |
2015 |
|
Neoplasms
|
0.200 |
AlteredExpression
|
group |
BEFREE |
Thus, wild-type IKAROS restrains stemness properties and has tumor suppressor activity in BCR-ABL1-initiated leukemia.
|
24791856 |
2015 |
|
Neoplasms
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Limited duration of complete remission on ruxolitinib in myeloid neoplasms with PCM1-JAK2 and BCR-JAK2 fusion genes.
|
25260694 |
2015 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Finally, when administered intraperitoneally, ART inhibited p38, ERK, STAT5, and CREB activation in tumor tissues and the growth of human CML xenograft tumors in mice without exhibiting any significant adverse effects.
|
25738364 |
2015 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Non genomic loss of function of tumor suppressors in CML: BCR-ABL promotes IκBα mediated p53 nuclear exclusion.
|
26295305 |
2015 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
We conclude that BCR-ABL1 kinase-dependent and -independent mechanisms convert p27 from a nuclear tumor suppressor to a cytoplasmic oncogene.
|
25293778 |
2014 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Dasatinib, a dual Src/Abl kinase inhibitor approved for the treatment of CML, is under investigation as monotherapy for tumors with abnormal Src signaling, such as melanoma.
|
24281418 |
2014 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
We investigated adhesion pathways that contribute to engraftment of breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferative neoplasia in a mouse retroviral transduction/transplantation model.
|
24394666 |
2014 |
|
Neoplasms
|
0.200 |
GeneticVariation
|
group |
BEFREE |
Genes relatively hypermethylated in HR+, luminal A, or p53 wild-type breast cancers included FABP3, FGF2, FZD9, GAS7, HDAC9, HOXA11, MME, PAX6, POMC, PTGS2, RASSF1, RBP1, and SCGB3A1, whereas those more highly methylated in HR-, basal-like, or p53 mutant tumors included BCR, C4B, DAB2IP, MEST, RARA, SEPT5, TFF1, THY1, and SERPINA5.
|
25287138 |
2014 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
The discovery of the JAK2V617F mutation followed by the discovery of other genetic abnormalities allowed important progress in the understanding of the pathogenesis and management of myeloproliferative neoplasms (MPN)s. Classical Breakpoint cluster region-Abelson (BCR-ABL)-negative neoplasms include 3 main disorders: essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF).
|
25486952 |
2014 |
|
Neoplasms
|
0.200 |
AlteredExpression
|
group |
BEFREE |
PTEN tumor suppressor gene is downregulated by BCR-ABL1 in CML stem cells and its deletion is associated with acceleration of disease.
|
24091144 |
2014 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Studies involving BCR transgenic mice indicated that B cells inhibit anti-tumor T cell responses through antigen non-specific mechanisms.
|
24293009 |
2013 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
Among these cancers are chronic neutrophilic leukemia (CNL) and atypical (BCR-ABL1-negative) chronic myeloid leukemia (CML), both of which are diagnosed on the basis of neoplastic expansion of granulocytic cells and exclusion of genetic drivers that are known to occur in other myeloproliferative neoplasms and myeloproliferative-myelodysplastic overlap neoplasms.
|
23656643 |
2013 |