|
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 |
|
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 |
|
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 |
|
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 |
|
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 |
|
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 |
|
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 |
|
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 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, ABL TKIs cannot eradicate leukemia stem cells.
|
27437766 |
2016 |
|
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 |
|
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 |
|
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 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The SRC-ABL inhibitor bosutinib is one of the five tyrosine kinase inhibitors currently approved for the treatment of Philadelphia chromosome-positive leukemias.
|
24490604 |
2014 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
CML comprises approximately 20% of all leukemias and is characterized by a balanced (9;22) chromosomal translocation that results in the formation of a chimeric gene comprised of the BCR (breakpoint cluster region) gene and the ABL oncogene (BCR-ABL fusion gene).
|
20300999 |
2010 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The literature on Ph-positive leukemia lacking ABL exon 2 was also reviewed.
|
18253707 |
2008 |
|
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 |
|
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 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This case has implications for the design of future studies using STI571 in leukemias involving ABL-encoded fusion proteins other than BCR-ABL.
|
11964320 |
2002 |
|
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 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Frequent jumping translocations of chromosomal segments involving the ABL oncogene alone or in combination with CD3-MLL genes in secondary leukemias.
|
9002963 |
1997 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Oligomerization of the ABL tyrosine kinase by the Ets protein TEL in human leukemia.
|
8754809 |
1996 |
|
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 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Because these two chromosomes are translocated with breakpoints within the BCR and ABL genes in Philadelphia chromosome-positive leukemias, knowledge of these sequences also might provide insight into the validity of various theories of chromosomal rearrangements.
|
7665185 |
1995 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The significance of the finding that a part of the SH3 region of ABL protein is missing in some Philadelphia chromosome-positive leukemias is discussed in reference to the cases reported previously.
|
7934165 |
1994 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Third, recent advances in understanding the functions of the normal ABL protein have given clues to the mechanism(s) of ABL-induced leukemias and approaches to blocking this process.
|
8464245 |
1993 |