|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Mice that express a NUP98-HOXD13 (NHD13) transgene develop multiple types of leukemia, including myeloid and T and B lymphocyte.
|
31622281 |
2019 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Furthermore, <i>Mof</i> inactivation suppressed leukemia development in an <i>NUP98-HOXA9</i>-driven AML model.
|
28202522 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.
|
28210005 |
2017 |
|
Childhood Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
2222-2234) provides new mechanistic insight into the molecular basis by which Nup98 promotes gene activation in normal hematopoietic cells and how that process is altered by translocations to cause excess expression of developmental genes in leukemia.
|
29284709 |
2017 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, such aberrations were not only observed in transiently transfected HeLa cells but also in mouse bone marrow cells immortalized by Nup98 fusions and in cells derived from leukemia patients harboring Nup98 fusions.
|
27031510 |
2016 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Critical role of retinoid/rexinoid signaling in mediating transformation and therapeutic response of NUP98-RARG leukemia.
|
25510432 |
2015 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, the age-associated accumulation of somatic mutations that occurs in the Nup98-HOXD13 (NHD13) mouse model of leukemia progression was significantly elevated by co-expression of a PKR transgene, whereas knockout of PKR expression or pharmacologic inhibition of PKR activity reduced the frequency of spontaneous mutations in vivo.
|
26202421 |
2015 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In contrast, neither NUP98-NSD1 nor FLT3-ITD single transduced cells were able to initiate leukemia.
|
24951466 |
2014 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
NUP98 is known to be fused to at least 28 different partner genes in patients with hematopoietic malignancies, including acute myeloid leukemia, chronic myeloid leukemia in blast crisis, myelodysplastic syndrome, acute lymphoblastic leukemia, and bilineage/biphenotypic leukemia.
|
21948299 |
2011 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, these findings reveal a major role for Smad4 in the negative regulation of leukemia initiation and maintenance induced by HOXA9/NUP98-HOXA9 and provide strong evidence that antagonizing Smad4 stabilization by these oncoproteins might be a promising novel therapeutic approach in leukemia.
|
21471525 |
2011 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Rearrangements of the NUP98 gene in human leukemia result in the expression of numerous fusion oncoproteins whose effect on nucleocytoplasmic trafficking is poorly understood.
|
20233715 |
2010 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
NUP98 has been involved in multiple recurrent chromosome rearrangements in leukemia.
|
18084320 |
2008 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Some of these genes (Hoxa5, Hoxa9, Flt3) are deregulated in NUP98/HHEX-induced murine leukemia as well as in human blasts carrying this fusion and might represent bona fide therapeutic targets.
|
18388181 |
2008 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
To elucidate the leukemogenic potential of NUP98-PMX1, we compared the effects of PMX1 and NUP98-PMX1 and, through strategic mutations, the involvement of the SRE in NUP98-PMX1-mediated leukemia.
|
18604245 |
2008 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interestingly, an engineered NUP98-HOXA10 (NA10) fusion can induce a several hundred-fold expansion of HSCs in vitro and NA10 and the AML-associated fusion gene NUP98-HOXD13 (ND13) have a virtually indistinguishable ability to transform myeloid progenitor cells in vitro and to induce leukemia in collaboration with MEIS1 in vivo.
|
17712416 |
2007 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Retroviral integration site analysis identifies ICSBP as a collaborating tumor suppressor gene in NUP98-TOP1-induced leukemia.
|
16939812 |
2006 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
NUP98 fusion in human leukemia: dysregulation of the nuclear pore and homeodomain proteins.
|
16105755 |
2005 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Clinical findings are reviewed here, along with the findings of several in vivo and in vitro models have been employed to investigate the mechanisms by which NUP98 fusion genes contribute to the pathogenesis of leukemia.
|
15359631 |
2004 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data confirm the previous findings that NUP98 is a recurrent target in various types of leukemia.
|
15390187 |
2004 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, the ability of Hox genes to induce leukemia as NUP98 fusion partners, although apparently redundant for Abd-B-like activity, is not restricted to this group, but rather is determined by the intrinsic leukemogenic potential of the Hox partner.
|
14966272 |
2004 |
|
Childhood Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Induction of acute myeloid leukemia in mice by the human leukemia-specific fusion gene NUP98-HOXD13 in concert with Meis1.
|
12543865 |
2003 |
|
Childhood Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
NUP98 is a nucleoporin that composes the nuclear pore complex and is the target gene in leukemia with the t(7;11)(p15;p15).
|
10222653 |
1999 |