Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Our findings demonstrate a higher penetrance of the CDKN2A risk locus in DS and serve as a basis for further biological insights into DS-ALL etiology.
|
31350265 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
Common CNAs involved CDKN2A/2B (30.3%), IKZF1 (27.3%), PAX5 (9.1%), RB1 (9.1%), BTG1 (6.7%), and ETV6 (6.7%), which regulate cell cycle, B lymphopoiesis, or act as tumor suppressors in ALL.
|
31112375 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Our findings suggested that CDKN2A/B deletions were associated with poor prognosis independently in both adult and childhood ALL patients.
|
30592434 |
2019 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Previous studies involving CDKN2A/B gene deletions have shown mixed associations with survival outcome in childhood ALL.
|
29446543 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The prognostic value of deletions in the CDKN2A/B locus in ALL is controversial in part due to the limitations of the methodologies used.
|
27960642 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
<i>CDKN2A/2B</i> deletions were associated with poor 2-year OS (P=0.045) and RFS (P=0.071) rates in Philadelphia chromosome positive (Ph<sup>+</sup>) B-ALL patients, as well as in the high risk (HR) B-ALL group (P=0.037 and P=0.047, respectively).
|
29552179 |
2018 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The IKZF1 SNPs, rs10235796 and rs6964969, and the CDKN2A SNP rs3731246 (previously unreported) could serve as risk markers for ALL susceptibility in Yemeni children.
|
28768142 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
GENOMICS_ENGLAND |
Biallelic loss of CDKN2A is associated with poor response to treatment in pediatric acute lymphoblastic leukemia.
|
27756164 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
The present study examines the incidence of IKZF1, CDKN2A/B, PAX5, EBF1, ETV6, BTG1, RB1, JAK2, and Xp22.33 gene deletions/duplications associated with pediatric ALL in Iran and investigates the possible effect of these mutations on drug resistance.
|
28886309 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
These results provide evidence for the influence of genetic variants at CDKN2A/B locus with the risk of developing B-ALL.
|
28481918 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
We investigated in vitro BTZ sensitivity in a large panel of ALL cell lines that acted as a model system for refractory ALL, and found that Philadelphia chromosome-positive (Ph+) ALL, IKZF1 deletion, and biallelic loss of CDKN2A were associated with favorable response.
|
29236701 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The prevalence of p16 deletion was 39.7% in B-lineage ALL and 33.3% in T-lineage ALL.
|
27967319 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
Biallelic loss of CDKN2A is associated with poor response to treatment in pediatric acute lymphoblastic leukemia.
|
27756164 |
2017 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Recent genome-wide association studies (GWAS) focusing on pediatric acute lymphoblastic leukemia (ALL), the most common malignancy in children younger than 15 years old, have found evidence that single-nucleotide polymorphisms (SNPs) in IKZF1 (7p12.2), ARID5B (10q21.2), CDKN2A (9p21.3), and CEBPE (14q11.2) are strongly associated to the risk of developing pediatric ALL.
|
27184773 |
2016 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
These SNPs are located at CDKN2A (rs3731217) and IKZF1 (rs4132601), genes frequently lost in ALL, and at CEBPE (rs2239633), ARID5B (rs7089424), PIP4K2A (rs10764338), and GATA3 (rs3824662), genes located on chromosomes gained in high-hyperdiploid ALL.
|
26575185 |
2015 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
Deletions of EBF1, IKZF1, and CDKN2A/B have an independent adverse prognosis for adolescents and adults with B-precursor ALL, and this suggests that these CNAs should be included in the initial risk assessment of ALL.
|
26194343 |
2015 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Notably, the CDKN2A variant was not significantly associated with melanoma, glioblastoma, or pancreatic cancer risk, implying that this polymorphism specifically confers ALL risk but not general cancer risk.
|
26527286 |
2015 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
To determine the prevalence and prognostic impact of significant acute lymphoblastic leukemia (ALL) -related genes: CRLF2 deregulation (CRLF2-d), IGH@ translocations (IGH@-t), and deletions of CDKN2A/B, IKZF1, PAX5, ETV6, RB1, BTG1, and EBF1 in adolescents and adults.
|
22851563 |
2012 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
Recent studies have shown that SNPs mapping to 7p12.2 (IKZF1), 9p21 (CDKN2A), 10q21.2 (ARID5B), and 14q11.2 (CEBPE) and carrier status for recessively inherited Nijmegen Breakage syndrome (NBS) influence childhood acute lymphoblastic leukemia (ALL) risk.
|
21889209 |
2011 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
We hypothesized that this association reflects the capability of some ANRIL polymorphisms to contribute to its transcription changes responsible for alterations of CDKN2A/B expression profiles, thus leading to abnormal proliferative boosts and consequent increased ALL susceptibility.
|
21414664 |
2011 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
The 9p instability was detected in 19% of the patients with ALL and always included homozygous loss of CDKN2A along with loss of CDKN2B.
|
20013897 |
2010 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk.
|
20453839 |
2010 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
CTD_human |
Variation in CDKN2A at 9p21.3 influences childhood acute lymphoblastic leukemia risk.
|
20453839 |
2010 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
GeneticVariation
|
disease |
BEFREE |
In conclusion, CDKN2A deletion is a significant secondary abnormality in childhood ALL strongly correlated with phenotype and genotype.
|
18838613 |
2009 |
Childhood Acute Lymphoblastic Leukemia
|
0.600 |
Biomarker
|
disease |
BEFREE |
In vitro ALLs with INK4A/ARF, p210 bcr/abl, or p190 bcr/abl mutations remained sensitive to anti-mHA cytolytic T cells.
|
18489987 |
2008 |