|
rs121913488
|
|
|
0.740 |
GeneticVariation |
BEFREE |
The FLT3 receptor tyrosine kinase plays an integral role in hematopoiesis, and one third of AML diagnoses exhibit gain-of-function mutations in FLT3, with the juxtamembrane domain internal tandem duplication (ITD) and the kinase domain D835Y variants observed most frequently.
|
30541869 |
2019 |
|
rs121913488
|
|
|
0.740 |
GeneticVariation |
BEFREE |
Retroviral expression of FLT3-N676K in myeloid 32D cells induced AML in syngeneic C3H/HeJ mice (n = 11/13, median latency 58 days), with a transforming activity similar to FLT3-internal tandem duplication (ITD) (n = 8/8), FLT3-TKD D835Y (n = 8/9), and FLT3-ITD-N676K (n = 9/9) mutations.
|
26891877 |
2016 |
|
rs121913488
|
|
|
0.740 |
GeneticVariation |
BEFREE |
In addition, crenolanib inhibited drug-resistant AML primary blasts with FLT3-ITD and D835H/Y mutations.
|
24046014 |
2013 |
|
rs121913488
|
|
|
0.740 |
GeneticVariation |
BEFREE |
Our FLT3-Aurora kinase inhibitor, CCT137690, successfully inhibited growth of FLT3-ITD-D835Y cells in vitro and in vivo, suggesting that dual FLT3-Aurora inhibition may overcome selective FLT3 inhibitor resistance, in part due to inhibition of Aurora kinase, and may benefit patients with FLT3-mutated AML.
|
22354205 |
2012 |
|
rs1057519766
|
|
|
0.720 |
GeneticVariation |
BEFREE |
Gene expression analysis of AML patients with CBFB/MYH11 rearrangement and FLT3 N676K mutation showed a trend toward a specific expression profile.
|
23878140 |
2013 |
|
rs1057519766
|
|
|
0.720 |
GeneticVariation |
BEFREE |
Moreover, further experiments investigating molecular mechanisms for leukemogenesis induced by FLT3-N676K mutation and clinical evaluation of FLT3 inhibitors in FLT3-N676K-positive AML seem warranted.
|
26891877 |
2016 |
|
rs1057519764
|
|
|
0.710 |
GeneticVariation |
BEFREE |
Targeted next-generation sequencing at the time of AML progression on gilteritinib identified treatment-emergent mutations that activate RAS/MAPK pathway signaling, most commonly in <i>NRAS</i> or <i>KRAS.</i> Less frequently, secondary <i>FLT3</i>-F691L gatekeeper mutations or <i>BCR-ABL1</i> fusions were identified at progression.
|
31088841 |
2019 |
|
rs1057520026
|
|
|
0.710 |
GeneticVariation |
BEFREE |
The other novel mutation, FLT3 K663Q, is the first AML-associated gain-of-function mutation located outside the JM and AL domains.
|
16990784 |
2006 |
|
rs121913232
|
|
|
0.710 |
GeneticVariation |
BEFREE |
Recently, novel mutations within the activation loop were identified in patients with AML: deletion of isoleucine 836 (Ile836del) and an exchange of isoleucine 836 to methionine plus an arginine insertion (Ile836Met+Arg).
|
12663439 |
2003 |
|
rs376588714
|
|
|
0.710 |
GeneticVariation |
BEFREE |
Identification of a novel activating mutation (Y842C) within the activation loop of FLT3 in patients with acute myeloid leukemia (AML).
|
15345593 |
2005 |
|
rs1244282842
|
|
|
0.010 |
GeneticVariation |
BEFREE |
From Six Gene Polymorphisms of the Antioxidant System, Only GPX Pro198Leu and GSTP1 Ile105Val Modulate the Risk of Acute Myeloid Leukemia.
|
26823947 |
2016 |
|
rs35602083
|
|
|
0.010 |
GeneticVariation |
BEFREE |
The FLT3 D324N variant was present in 42 cases (6.4%), but it was not associated with a specific AML subtype and did not show an elevated leukocyte count, as do other FLT3 mutations.
|
16320249 |
2006 |
|
rs374234147
|
|
|
0.010 |
GeneticVariation |
BEFREE |
We identified five IDH1 mutations that were novel to AML: (1) c.299 G>A, p.R100Q; (2) c.311G>T, p.G104V; (3) c.322T>C, p.F108L; (4) c.356G>A, p.R119Q; and (5) c.388A>G, p.I130V.
|
24376688 |
2013 |
|
rs759272576
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Targeted next-generation sequencing at the time of AML progression on gilteritinib identified treatment-emergent mutations that activate RAS/MAPK pathway signaling, most commonly in <i>NRAS</i> or <i>KRAS.</i> Less frequently, secondary <i>FLT3</i>-F691L gatekeeper mutations or <i>BCR-ABL1</i> fusions were identified at progression.
|
31088841 |
2019 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Prospective evaluation of gene mutations and minimal residual disease in patients with core binding factor acute myeloid leukemia.
|
23321257 |
2013 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Activating mutation of D835 within the activation loop of FLT3 in human hematologic malignancies.
|
11290608 |
2001 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Crowding induces live cell extrusion to maintain homeostatic cell numbers in epithelia.
|
22504183 |
2012 |
|
rs121913487
|
|
C |
0.800 |
CausalMutation |
CLINVAR |
A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy.
|
16857985 |
2006 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Prospective enterprise-level molecular genotyping of a cohort of cancer patients.
|
25157968 |
2014 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Phase IIB trial of oral Midostaurin (PKC412), the FMS-like tyrosine kinase 3 receptor (FLT3) and multi-targeted kinase inhibitor, in patients with acute myeloid leukemia and high-risk myelodysplastic syndrome with either wild-type or mutated FLT3.
|
20733134 |
2010 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.
|
23430109 |
2013 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Recurring mutations found by sequencing an acute myeloid leukemia genome.
|
19657110 |
2009 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Validation of ITD mutations in FLT3 as a therapeutic target in human acute myeloid leukaemia.
|
22504184 |
2012 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
A phase 2 trial of the FLT3 inhibitor lestaurtinib (CEP701) as first-line treatment for older patients with acute myeloid leukemia not considered fit for intensive chemotherapy.
|
16857985 |
2006 |
|
rs121913487
|
|
T |
0.800 |
CausalMutation |
CLINVAR |
Sorafenib treatment of FLT3-ITD(+) acute myeloid leukemia: favorable initial outcome and mechanisms of subsequent nonresponsiveness associated with the emergence of a D835 mutation.
|
22368270 |
2012 |