|
Neoplasms
|
0.200 |
Biomarker
|
group |
HPO |
|
|
|
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
CML has provided a model for the genetic basis of human neoplasia.
|
2182595 |
1990 |
|
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 |
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 |
|
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 |
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 |
Cytogenetic and molecular genetic analysis are important in the diagnosis of CML and are becoming increasingly important in the diagnosis of chronic LPDs and other haematological neoplasms.
|
7665691 |
1995 |
|
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 |
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 |
First, four independent synteny breaks were found within the CER1 telomeric breakpoint cluster region, comparing human, dog, and chicken genomes, and two independent synteny breaks within the CER1 centromeric breakpoint cluster region, comparing human, mouse, and chicken genomes, suggesting a nonrandom involvement of tumor breakpoint regions in chromosome evolution.
|
15913951 |
2005 |
|
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 |
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 |
However, the development of an extramedullary tumor in chronic-phase CML generally indicates a poor prognosis, because it commonly consists of blast proliferation and is followed by blast crisis in the marrow within a few months.
|
15389905 |
2004 |
|
Neoplasms
|
0.200 |
AlteredExpression
|
group |
BEFREE |
In K562 leukemia cells, overexpression of miR-30a reduced ABL1 and BCR-ABL1 protein expression, decreased proliferation, and arrested cell cycle progression between G1 and S. These findings strongly suggest that miR-30a acts as a tumor suppressor by downregulating ABL1 and BCR-ABL1 expression.
|
23287430 |
2013 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
In this particular review we discuss the oncogenes and tumor suppressors comprising the regulatory network upstream and downstream of BCR-ABL1 and dismantle how derailed BCR-ABL1 signaling provides cell a selective growth advantage.
|
23575065 |
2013 |
|
Neoplasms
|
0.200 |
Biomarker
|
group |
BEFREE |
In this respect, the rather clear description of CML in cytogenetic, clinical, and laboratory terms, the relatively long chronic phase of the disease, and the association of the blastic phase with nonrandom chromosome changes (at least in the initial phases of the disease) make Ph-positive CML an excellent candidate for a model for the study of molecular events in human neoplasia.
|
3004697 |
1986 |
|
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 |
Intra-tumour genetic heterogeneity has been reported in both leukaemias and solid tumours and is implicated in the development of drug resistance in CML and AML.
|
21063398 |
2011 |
|
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 |
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 |
New understanding of the pathogenesis of CML: a prototype of early neoplasia.
|
9305592 |
1997 |
|
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 |
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 |
Biomarker
|
group |
BEFREE |
Our data, together with the already published information considering BCR function suggest that BCR can be considered as a candidate tumor suppressor gene localized on chromosome 22q which may be involved in meningioma pathogenesis.
|
18474292 |
2008 |
|
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 |