Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
BCR-ABL, a common molecular defect in adult ALL, is a valuable tumor marker whose detection influences prognosis and clinical management decisions.
|
12707370 |
2003 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Bcr-Abl proteins are effective inducers of the leukemic phenotype in chronic myeloid leukemia (CML) and distinct variants of acute lymphoblastic leukemia (ALL).
|
12750174 |
2003 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
BCR-ABL breakpoints were identified in p190 ALL (n=25), p210 ALL (n=25) and p210 CML (n=32); reciprocal breakpoints were identified in 54 cases.
|
20703256 |
2010 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
BCR-ABL fusion gene typically causes a type of acute lymphoblastic leukemia (ALL), known as Ph+ ALL.
|
24112092 |
2014 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
A 35-year-old man was diagnosed as ALL because of the infiltration of CD10(+)CD19(+)CD33(+)CD34(+) lymphoblasts in the bone marrow and the expression of p190-type BCR/ABL fusion transcript.
|
16979235 |
2007 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
A minor breakpoint region (m-bcr) BCR/ABL rearrangement, corresponding to the fusion product gene p190, was detected by interphase FISH in 3 of these cases, Immunophenotyping analysis classified five of the 6 cases as B-lineage ALL.
|
16938575 |
2006 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
A split ABL FISH signal without the involvement of BCR does not represent a t(9;22) translocation, and prognostic implications of this apparent subgroup of ALL cases have not been determined.
|
16157197 |
2005 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Aberrant expression of KOR-SA3544 has been invariably found in BCR/ABL-positive acute lymphoblastic leukemia (ALL) and in some BCR/ABL-negative ALL.
|
9665191 |
1998 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Adult patients with acute lymphoblastic leukemia (ALL) were evaluated to determine whether presence/absence of BCR-ABL induced differences in activation of Src, PI3K/Akt and NF-κB or in the expression of anti-apoptotic proteins such as BCL-2 and c-IAP1.
|
22591684 |
2012 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
ALL cells carrying a SNX2-ABL1 fusion exhibited a BCR-ABL1+ ALL-like gene expression profile.
|
24215620 |
2014 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
All the BCR-ABL+ ALL cases showed CD66 expression.
|
17909799 |
2008 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Also, targeted therapeutic strategies are continuously expanding as illustrated by the tyrosine kinase inhibitor (TKI) imatinib for BCR-ABL positive ALL.
|
19817644 |
2009 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Although "paired box 5" (PAX5)-related fusion genes are well documented in childhood B-cell precursor acute lymphoblastic leukemia (ALL), these types of fusion with the exception of PAX5-JAK2 are rarely seen in patients with gene expression profiles similar to those of BCR-ABL1 (Philadelphia)-positive ALL (Ph-like ALL).
|
27870151 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Although non-tumor-cell-autonomous mechanisms can prevent full eradication of dasatinib-refractory ALL in this clinically relevant model, the emergence of resistance to BCR-ABL kinase inhibitors can be effectively circumvented by the addition of "conventional" chemotherapeutic agents with alternate antileukemic mechanisms of action.
|
21263154 |
2011 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Although the number of patients is small and the observation period is too short, the combination therapy is very promising and produces high-quality CR for most newly diagnosed patients with BCR-ABL-positive ALL.
|
15315963 |
2004 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Analysis of primary ALL samples revealed a significant increase in GPR132 expression in IKZF1-deleted BCR-ABL negative patients, suggesting that levels of wild-type Ikaros may influence the regulation of G2A in B-ALL.
|
27588474 |
2016 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
CTD_human |
Antileukaemia effect of rapamycin alone or in combination with daunorubicin on Ph+ acute lymphoblastic leukaemia cell line.
|
21898527 |
2012 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
At the extreme end of the risk spectrum, the t(4;11)/MLL-AF4 and t(9;22)/BCR-ABL almost always confer a dire prognosis in both children and adults with ALL, who warrant high-dose chemotherapy and hematopoietic stem cell rescue to sustain or even induce first remission.
|
11071360 |
2000 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Basically two types of BCR-ABL1 chimeric mRNA transcripts have been observed: (1) e13a2/e14a2 transcripts in CML and ALL, resulting from chromosomal breaks in the major breakpoint cluster region (M-bcr) of the BCR gene and (2) e1a2 transcripts in ALL resulting from breaks in the minor breakpoint cluster region (m-bcr) of the BCR gene.
|
21944569 |
2011 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
BCR-ABL1 signal patterns were analyzed using FISH in 243 CML-chronic phase (CML-CP), 17 CML-blast phase (CML-BP) and 52 BCR-ABL1 positive acute lymphoblastic leukemia (ALL) patients.
|
31594548 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Both retained the Ph1 chromosome and expressed the ALL type bcr/abl chimeric mRNA containing the junction of the first exon of BCR gene (e1) and second exon of c-abl gene (a2).
|
8428799 |
1993 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Cases of precursor B cell ALL lacking the PH/BCR/ABL genotype exhibited a pronounced age-dependent, gender prevalence with a modal age in the sixth decade for females compared to the second decade for males.
|
19322628 |
2009 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Chronic myelogenous leukemia (CML) and Philadelphia chromosome-positive (Ph(+)) acute lymphoblastic leukemia (ALL) are associated with fusion of the BCR and ABL1 genes by chromosome translocation.
|
22749885 |
2012 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) are hematopoietic malignancies caused by the constitutive activation of BCR-ABL tyrosine kinase.
|
29859988 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Compared to several other learning algorithms, MDR gives the greatest AUC (area under the ROC curve) for the classifications of prostate cancer, acute lymphoblastic leukemia (ALL) and four ALL subtypes: BCR-ABL, E2A-PBX1, MALL and TALL.
|
18831787 |
2008 |