|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
A total of 22/31 children with ALL with methylated <i>CDKN2B</i> (71.0%) and 17/41 children with ALL with unmethylated <i>CDKN2B</i> (41.46%) exhibited increased telomerase activity (>15 TPG units).
|
28454370 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
On the contrary, methylation of the p15 promoter is identified in some 50% of the patients with AML and MDS, but is less frequent in ALL.
|
27401303 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
<i>TP53</i> alterations are present in almost all cases of ALL with low hypodiploidy and are associated with alterations of the lymphoid transcription factor <i>IKZF2</i> and the tumor-suppressor gene loci <i>CDKN2A</i> and <i>CDKN2B.</i> Remarkably, more than half of <i>TP53</i> mutations in low-hypodiploid ALL in children are present in nontumor cells, indicating that low-hypodiploid ALL is a manifestation of Li-Fraumeni syndrome.
|
28003275 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The locus CDKN2A/B (9p21.3), which comprises the tumor suppressors genes CDKN2A and CDKN2B and the long noncoding RNA (lncRNA) known as ANRIL (or CDKN2B-AS), was associated with childhood acute lymphoblastic leukemia (ALL) susceptibility in several genome wide association studies (GWAS).
|
28481918 |
2017 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Children with ALL have higher levels of p15 CpG island methylation than a control group of children with ITP.
|
26501552 |
2016 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Methylation of both p15 and SHP1 genes occurred more frequently in T-ALL than in precursor B-ALL (p=0.02 and p=0.01, respectively).
|
21592569 |
2011 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
Bi-allelic CDKN2B and MTAP co-inactivation were found in 36 (16%) and 24 (11%) of patients, respectively, and did not influence the 6-year event-free survival rate either, even when the analysis was restricted to CDKN2A inactivated ALL.
|
16818274 |
2006 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
CDKN2B and/or MTAP co-deletions were highly variable in both T- and B-lineage ALL, making ALL with 9p21 a rather heterogeneous group.
|
12661005 |
2003 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
The methylation-specific polymerase chain reaction (MS-PCR) was used to analyze p15 and p16 gene methylation in 49 cases of acute lymphoblastic leukemia (ALL) and 29 cases of acute myelogenous leukemia (AML).
|
11413509 |
2001 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We also demonstrated for the first time concomitant p16 and p15 methylation in 22% (8/37) of adults with AML or ALL, exclusively in those with M2, M4, or L2 subtypes.
|
10706859 |
2000 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further, by characterizing the roles of translocation-generated fusion genes (TEL-AML 1) and tumor suppressor genes (p15INK4B and p16INK4A) in treatment response, it may be possible to identify new and selective targets and/or treatment strategies for both children and adults with ALL who are refractory to current therapies.
|
10512159 |
1999 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To determine whether alterations in these genes play a role in disease progression, we analyzed a panel of 18 matched specimen pairs collected from children with ALL at the time of initial diagnosis and first bone marrow relapse for homozygous p16 and/or p15 deletions or p15 promoter hypermethylation.
|
10090949 |
1999 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
To gain a fuller understanding of the role of deletions of chromosome 9 in the development of childhood acute lymphoblastic leukemia (ALL), we performed detailed deletional mapping of chromosome 9 in 54 primary ALL samples with matched normal DNA using 22 highly polymorphic markers; and this information was combined with our previous data concerning the presence of deletions of CDKN2/INK4A/p16 and CDKN2B/INK4B/p15 in these samples.
|
9324282 |
1997 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Furthermore our data show that although inactivation of MTS1 by deletion is common, inactivation of MTS2 by a combination of deletion and hypermethylation is more frequent in both B-ALL (20/29, 69%) and T-ALL (17/17, 100%).
|
9399648 |
1997 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Two recently described molecular abnormalities in childhood ALL are ETV6 gene rearrangements and homozygous deletions of p16(INK4A) and/or p15(INK4B).
|
9204978 |
1997 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Incidence and clinical significance of CDKN2/MTS1/P16ink4A and MTS2/P15ink4B gene deletions in childhood acute lymphoblastic leukemia.
|
9089742 |
1997 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We analyzed 60 B precursor acute lymphoblastic leukemia (ALL) primary samples and 15 cell lines for homozygous deletions of p16 and p15 genes and mutations of p16 gene.
|
8683987 |
1996 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
In hematological malignancies, homozygous deletions of p16ink4a and p15ink4b occur frequently in acute lymphoblastic leukemia (ALL) (14-40%), lymphoid type blast crisis of chronic myeloid leukemia (CML), and adult T cell leukemia (ATL), but p16ink4a deletions are more frequent than p15ink4b deletions, and hemizygous deletions of either p16ink4a and p15ink4b are rare.
|
8724524 |
1996 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Prognostic importance of p15INK4B and p16INK4 gene inactivation in childhood acute lymphocytic leukemia.
|
8622065 |
1996 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
No rearrangements or deletions of the INK4d gene were observed in Southern blot analysis of selected cases of pediatric acute lymphoblastic leukemia (ALL) containing a variant (1;19)(q23;p13) translocation that lacks rearrangement of either E2A or PBX1, or in ALL cases containing homozygous or hemizygous deletions of the related genes, INK4a and INK4b.
|
8575754 |
1995 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Homozygous deletions of the p15 gene were also very frequent in T-ALLs (9/22; 41%), and it occurred in 5 of 81 (6%) precursor-B ALL samples.
|
7606004 |
1995 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We analyzed p16INK4A and p15INK4B genes in 178 cases of primary leukemias including 81 cases of chronic lymphocytic leukemia (CLL), seven of hairy cell leukemia (HCL), seven of chronic myelogenous leukemia (CML), 43 of acute myelogenous leukemia (AML), 27 of acute lymphoblastic leukemia (ALL), and 13 of myelodysplastic syndrome (MDS) by Southern blot analyses.
|
7795238 |
1995 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Frequent deletion of p16INK4a/MTS1 and p15INK4b/MTS2 in pediatric acute lymphoblastic leukemia.
|
7727766 |
1995 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Homozygous MTS2 deletions were observed in 16 of 24 T-ALL cases and in 1 of 31 B-lineage ALLs (P < .001), all of them displaying homozygous MTS1 deletions.
|
7994022 |
1994 |