Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Patients with t(12;21)/(ETV6-RUNX1) or hyperdiploidy >50 ALL had the best prognosis; those with a negative MRD on day 19 had a particularly low risk of relapse: 1.9% and 3.8%, respectively.
|
27560110 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
NRAS mutations were associated with a higher frequency of hyperdiploidy (P = 0.01) and lower frequency of ETV6-RUNX1 (P < 0.01), whereas KRAS mutations were associated with younger age (P < 0.01), a higher frequency of KMT2A rearranged (P < 0.01) but no significant difference if infants with ALL were excluded, and inferior event-free survival (66.6% vs. 80.5%, P = 0.04).
|
28853218 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Clinical parameters and ETV6-RUNX1 status (using FISH technique) of pALL patients attending the Pediatric Oncology Clinic, King Abdulaziz Medical City, Riyadh from 2006 to 2011 were studied.
|
26625756 |
2015 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Aberrant expression of tumor suppressor genes WT 1, RB 1, p53, homozygous deletion of p16 gene and their relationship with expression of oncogenes BCR-ABL, TEL-AML 1, MLL-AF 4, E2A-PBX 1, SIL-TAL 1 were determined in bone marrow samples of children with de novo B-lineage (n=170) and T-lineage (n=25) acute lymphoblastic leukemia (ALL).
|
15878620 |
2005 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our data provide new insight on TEL-AML1 function and may offer a new therapeutic opportunity for B-ALL.
|
25893288 |
2015 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study provides novel mechanistic insights regarding the chemosensitivity of TEL-AML1(+) ALL cells and provides a cogent explanation for the excellent leukemia-free survival outcome of children with TEL-AML1(+) ALL treated on contemporary chemotherapy programs.
|
11378579 |
2001 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We observed a consistently higher (2.8-fold) expression of OPAL1 in TEL-AML1-positive ALL compared with TEL-AML1-negative ALL in both cohorts, but higher OPAL1 expression was not consistently associated with other favorable prognostic indicators such as age and white blood cell count, or ALL genetic subtype.
|
16709928 |
2006 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
We evaluated the prevalence of BCR/ABL, MLL, and ETV6/RUNX1 rearrangements as well as CDKN2A (alias p16) deletion in a group of Mexican children with acute lymphoblastic leukemia (ALL) to determine whether the changes coexist, and to compare the incidences found with other reports in the literature.
|
18617057 |
2008 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The coexpression of myelocytic and B-lymphoid antigens was found in 3 of the 11 of TEL-AML1 fusion positive-ALL.
|
12850377 |
2003 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
These data infer that IGF2BP1 is a potent regulator of ETV6/RUNX1 mRNA stability and potentially link this evolutionary-highly conserved protein to cell transformation events in ETV6/RUNX1-mediated leukemogenesis of t(12;21)(p13;q22)-positive ALL.
|
26852652 |
2016 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Of 35 ALL patients, we found an incidence of 8.6% of TEL/AML1 translocation in ALL patients (12% of B-lineage ALL), which is lower than that reported in caucasians but is similar to that reported in Japanese and Koreans.
|
15104290 |
2004 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
KOR-SA3544 expression over 3% was detected in the majority of TEL/AML1-negative patients with newly diagnosed common or preB ALL (19 of 31) and not in TEL/AML1-positive patients (0 of 18, P < 0.0001).
|
9665191 |
1998 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Although deletion of ETV6 and t(12;21) were associated in most patients, in eight cases (six B lineage and two T-ALL) LOH was detected at the ETV6 locus without ETV6-AML1 hybrid RNA.
|
9305598 |
1997 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
The genes p16 (or MTS1) and TEL/AML1 are now respectively recognized as the most common tumor suppressor and fusion genes in childhood acute lymphoblastic leukemia.
|
9372085 |
1996 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
TEL-AML1 fusion precedes differentiation to pre-B cells in childhood acute lymphoblastic leukemia.
|
12526921 |
2003 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
Importantly, hypermethylation of DLX3 significantly reduces its expression in MLL-AF4 rearranged leukemias while methylation is almost absent in TEL-AML1 positive ALL specimens.
|
17611665 |
2007 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Two supervised methods of analysis were used to identify the 20 best discriminating genes between the following cohorts: acute myelogenous leukemia (AML) versus acute lymphoblastic leukemia (ALL); B-lineage versus T-lineage ALL; newly diagnosed B-lineage standard-risk versus high-risk ALL; and B-lineage leukemia harboring the TEL-AML 1 fusion versus patients without a molecularly characterized translocation.
|
12374679 |
2002 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
This high level of AML1 expression could be an important factor contributing to the pathogenesis and progression of childhood ALL.
|
11960347 |
2002 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
In comparison with Western cohorts, the incidence of BCR-ABL1 (5.94%) was much higher in our series, while the occurrence of ETV6-RUNX1 (13.19%) was significantly lower in pediatric B-ALL patients in our study than in Western reports.
|
30125757 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
In initial and validation analyses, SLX4IP deletions were significantly associated with male gender and ETV6/RUNX1-rearranged ALL (both overall P < 0.0001).
|
24045615 |
2014 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Patients with near-triploidy or near-tetraploidy were more likely than those with high-hyperdiploidy (51-67 chromosomes) (n = 159) to be female (P = 0.05) and have T-lineage ALL (P = 0.02), L2 morphology (P < 0.0001), or the ETV6-RUNX1 fusion (P < 0.0001).
|
16875937 |
2006 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
We also provided preliminary evidence that the deletion of the nontranslocated TEL allele may adversely influence the clinical course of TEL/AML1+ ALL.
|
15356655 |
2004 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Structure and possible mechanisms of TEL-AML1 gene fusions in childhood acute lymphoblastic leukemia.
|
10463610 |
1999 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
Biomarker
|
disease |
BEFREE |
AML1 amplification in a case of childhood acute lymphoblastic leukemia.
|
12393286 |
2002 |
Childhood Acute Lymphoblastic Leukemia
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
B-cell precursor childhood acute lymphoblastic leukemia with ETV6-RUNX1 (TEL-AML1) fusion has an overall good prognosis, but relapses occur, usually after cessation of treatment and occasionally many years later.
|
21482711 |
2011 |