|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
For the existence of Philadelphia chromosome and BCR-ABL1 fusion gene together with complex chromosome abnormalities, a diagnosis of Philadelphia-positive acute myeloid leukemia was made, although the type (de novo or blast crisis) remained unclear.
|
28550639 |
2017 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The effect of the additional cytogenetic abnormalities on major molecular response and BCR-ABL kinase domain mutations in long-term follow-up chronic myeloid leukemia patients, a cross sectional study.
|
27924671 |
2017 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Approximately 5-10% of chronic myeloid leukemia (CML) patients are found to have structural or numerical additional chromosomal abnormality (ACAs) in addition to the characteristic t(9;22)(q34;q11.2) BCR/ABL1 at the time of diagnosis.
|
27810077 |
2016 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Specifically, it is associated to a particular cytogenetic abnormality, known as Philadelphia chromosome (Ph), which results from a fusion between part of the BCR ("breakpoint cluster region") gene from chromosome 22 and the Abelson (ABL) gene on chromosome 9 and leads to the formation a new gene leukemia-specific, the BCR-ABL.
|
27281463 |
2016 |
|
Congenital chromosomal disease
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Studies on CML have led to the identification of the first cancer-associated chromosomal abnormality and the subsequent development of tyrosine kinase inhibitors (TKIs) that inhibit BCR-ABL kinase activity in CML.
|
27581135 |
2016 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
In this paper gene sets differentially expressed between acute lymphoblastic leukaemia (ALL) with BCR-ABL and those with no observed cytogenetic abnormalities were determined by GSA methods.
|
23679247 |
2013 |
|
Congenital chromosomal disease
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These studies involve the identification of the first cancer-associated chromosomal abnormality and the subsequent development of tyrosine kinase inhibitors (TKIs) that inhibit BCR-ABL kinase activity in CML.
|
23483480 |
2013 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression.
|
23543457 |
2013 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
MRC-cIII-generated ROS promote oxidative DNA damage to trigger genomic instability, resulting in an accumulation of chromosomal aberrations and tyrosine kinase inhibitor-resistant BCR-ABL1 mutants.
|
22411871 |
2012 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Chronic myeloid leukemia in chronic phase (CML-CP) stem cells (LSCs) produce high levels of mitochondrial ROS, causing oxidative DNA damage, resulting in genomic instability, generating imatinib-resistant BCR-ABL1 kinase mutants and additional chromosomal aberrations.
|
22616753 |
2012 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Various types of BCR-ABL hybrid transcripts were compared with phases of CML and cytogenetic abnormalities.
|
22382182 |
2012 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Specific subsets of MPAL are defined by chromosomal anomalies such as the t(9;22) Philadelphia chromosome BCR-ABL1 or involvement of the MLL gene on chromosome 11q23.
|
22372202 |
2012 |
|
Congenital chromosomal disease
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Although the major BCR/ABL transcript is present in majority of CML patients, the minor BCR/ABL transcript is rarely reported as an additional chromosomal abnormality related to the progression of CML.
|
22057509 |
2011 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
T-cell, MLL-rearranged, TEL-AML1-positive, E2A-PBX1-positive and hyperdiploid acute lymphoblastic leukemia, with the exception of BCR-ABL-positive and 'B-other' acute lymphoblastic leukemias (defined as precursor B-cell acute lymphoblastic leukemia not carrying the foregoing cytogenetic aberrations), were found to have unique microRNA-signatures that differed from each other and from those of healthy hematopoietic cells.
|
21242186 |
2011 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The appearance of chromosomal aberrations in patients with CML BC has led to many attempts to elucidate a mechanism whereby BCR-ABL affects DNA damage and repair.
|
20445577 |
2010 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Among 53 patients with a median follow-up of 16 months, of whom 38, 5 and 10 were in chronic phase, accelerated phase and blast crisis, respectively, 19 (36%) had additional chromosomal aberrations and 20 (38%) had BCR-ABL kinase domain mutations.
|
20015884 |
2010 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We report a rare cryptic ins(12;9)(p13;q34q34), a chromosomal abnormality involving the ABL1 (9q34) and the ETV6 (alias TEL; 12p13) genes, detectable only by fluorescence in situ hybridization (FISH), in a patient with Philadelphia-negative chronic myeloid leukemia (CML).
|
19480935 |
2009 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
In the present case, cytogenetic and fluorescence in situ hybridization analyses revealed multiple chromosomal aberrations, including a del(9)(q21qter) and a marker chromosome ish der(9)(ABL+).
|
19215794 |
2009 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
These findings suggest that the t(7;14)(p22;q13) translocation had a crucial role in the progression to CML-AP, and that the resistance to imatinib may be due to the additional cytogenetic abnormalities, including der(17)t(1;17)(q25;p13), but not to BCR/ABL mutations.
|
18474303 |
2008 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In acute lymphoblastic leukemia, besides age and white cell count at diagnosis, the cytogenetic abnormalities t(9;22)/BCR-ABL and t(4;11)/MLL-AF4 are important prognostic markers and are often included in the treatment stratification of patients with adult acute lymphoblastic leukemia.
|
18728022 |
2008 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The BCR/ABL tyrosine kinase inhibitor imatinib mesylate produces a high rate of cytogenetic responses in patients with Philadelphia (Ph)-positive chronic myeloid leukemia (CML), but secondary clonal chromosome abnormalities may develop in Ph-negative cells, and acute myeloid leukemia (AML) has been reported in patients with secondary chromosome abnormalities.
|
17391756 |
2007 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Thus, ectopic p185/p190 BCR-ABL expression, such as p210 BCR-ABL, PML-RARA, or C-MYC transduction, may induce an increased chromosomal instability leading to clonal karyotypic evolution, which may mimic secondary chromosome aberrations in human Ph-positive ALL.
|
16080957 |
2005 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Association of cytogenetic abnormalities with detection of BCR-ABL fusion transcripts in children with T-lineage lymphoproliferative diseases (T-ALL and T-NHL).
|
14752867 |
2004 |
|
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The ABL gene on chromosome band 9q34 is a proto-oncogene and is the well-known translocation partner of the BCR gene on 22q11 giving rise to t(9;22)(q34;q11), which is the hallmark of chronic myeloid leukemia and is the most common chromosomal abnormality in adult acute lymphoblastic leukemia (ALL).
|
15282669 |
2004 |
|
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The median duration of imatinib treatment before the identification of cytogenetic abnormalities in BCR-ABL-negative cells was 13 months.
|
12646934 |
2003 |