|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Response to Comment on "PP2A inhibition sensitizes cancer stem cells to ABL tyrosine kinase inhibitors in BCR-ABL<sup>+</sup> human leukemia".
|
31316004 |
2019 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Comment on "PP2A inhibition sensitizes cancer stem cells to ABL tyrosine kinase inhibitors in BCR-ABL human leukemia".
|
31316003 |
2019 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The NEDD8-activating enzyme inhibitor MLN4924 induces DNA damage in Ph+ leukemia and sensitizes for ABL kinase inhibitors.
|
31349760 |
2019 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
PP2A inhibition sensitizes cancer stem cells to ABL tyrosine kinase inhibitors in BCR-ABL<sup>+</sup> human leukemia.
|
29437150 |
2018 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Treatment of BCR-ABL+ human leukemia has been significantly improved by ABL tyrosine kinase inhibitors (TKIs), but they are not curative for most patients and relapses are frequently associated with BCR-ABL mutations, warranting new targets for improved treatments.
|
28599273 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results are consistent with our <i>in vivo</i> findings using a functional pre-clinical mouse model of chronic myeloid leukemia (CML), whereby we demonstrated the ability of NOX-A12, combined with the ABL kinase inhibitor, nilotinib, to reduce the leukemia burden in mice to a greater extent than either agent alone.
|
29299123 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
As with ABL, translocations that fuse ARG to ETV6/TEL have been identified in patients with leukemia.
|
28386107 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, ABL TKIs cannot eradicate leukemia stem cells.
|
27437766 |
2016 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
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 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
This breakthrough revolutionized our knowledge related to leukemia biology and contemporary studies revealed that chromosomal translocation resulted in the fusion between the 5' segment of BCR gene and 3' segment of the ABL gene to form BCR/ABL fusion gene.
|
27894413 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, treatments combining ABL TKIs with additional drugs may be a promising strategy in the treatment of leukemia.
|
24586514 |
2014 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with nilotinib against BCR-ABL-positive leukemia cells involves the ABL kinase domain mutation.
|
24100660 |
2014 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The literature on Ph-positive leukemia lacking ABL exon 2 was also reviewed.
|
18253707 |
2008 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
ABL kinase inhibitors have been spectacularly successful in treating CML, but disease persistence and acquired drug resistance can prevent eradication and cure of the leukemia.
|
17353369 |
2007 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
ABL kinase domain mutations have been implicated in the resistance to the BCR-ABL inhibitor imatinib mesylate of Philadelphia-positive (Ph+) leukemia patients.
|
17189410 |
2006 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
As an oral, nontoxic compound with a mechanism of action distinct from that of ABL tyrosine kinase inhibition, FTI SCH66336 shows promise for the treatment of BCR/ABL-induced leukemia.
|
11222387 |
2001 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Oligomerization of the ABL tyrosine kinase by the Ets protein TEL in human leukemia.
|
8754809 |
1996 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The apparent nonrandom contribution of the paternally-derived chromosome 9 and the maternally-derived chromosome 22 to the leukemia-specific translocation t(9;22)(q34;q11) obtained by cytogenetic analysis suggested that the two genes affected by this rearrangement, namely ABL and BCR, are imprinted.
|
7723413 |
1995 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Joining of the BCR and ABL genes is an essential feature of the group of human leukemias characterized by the Philadelphia chromosome and there is recent evidence that the human BCR-ABL fusion gene induces leukemia in experimental animals.
|
1756491 |
1991 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Entire ABL gene is joined with 5'-BCR in some patients with Philadelphia-positive leukemia.
|
1868241 |
1991 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The ABL proto-oncogene on the Philadelphia chromosome is 'activated' by its translocation in a manner similar to its activation by the murine Abelson leukemia virus--with the formation of a fusion protein with a new N-terminus and enhanced tyrosine kinase activity.
|
3289649 |
1988 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Activation of the abl gene and its involvement in human leukemia is one of the most thoroughly characterized examples of the structural alterations of chromosomes associated with the conversion of a normal cell into a cancer cell.
|
3129652 |
1988 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The Philadelphia translocation, t(9;22), fuses the BCR and ABL genes resulting in the expression of leukemia-specific, chimeric BCR-ABL messenger RNAs.
|
3165197 |
1988 |