|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
In this study methylation Specific Melting Curve Analysis (MS-MCA) and real time PCR was used to assess the CDKN2B promoter hyper-methylation and gene expression in 59 Iranian acute myeloid leukemia (AML) patients.
|
29552069 |
2017 |
|
Leukemia, Myelocytic, Acute
|
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 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
CD93 expression is functionally required for engraftment of primary human AML LSCs and leukemogenesis, and it regulates LSC self-renewal predominantly by silencing CDKN2B, a major tumor suppressor in AML.
|
26387756 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Assessing of the methylation status of p15 and MGMT genes may allow stratification of patients with AML into distinct groups with potentially different prognosis.
|
22772967 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Strategies to re-express epigenetically silenced p15(INK4b) and p21(WAF1) genes in acute myeloid leukemia.
|
21124069 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
ALL-specific recurrent abnormalities were RB1 (n=3), PAX5 (n=4), and CDKN2B (n=3) deletions; AML-specific recurrent abnormalities were HOXA9 and HOXA10 (n=2) deletions and NOTCH1 duplication (n=2).
|
20193845 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Reactivation of p15INK4b expression in AML cell lines and patient blasts using 5-aza-2'-deoxycytidine (decitabine) and trichostatin A increased H3K4me3 and maintained H3K27me3 enrichment at p15INK4b.
|
20190193 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
In this report, MS-qFRET is validated in cell lines and then used to detect the status of p15(INK4B) methylation in clinical samples from eight patients with acute myeloid leukemia.
|
20362674 |
2010 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, the methylation dynamics of 4 TSGs (p15(INK4B), CDH-1, DAPK-1, and SOCS-1) were studied in sequential bone marrow samples from 30 patients with myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML) who completed a minimum of 4 cycles of therapy with 5-azacytidine and entinostat.
|
19546476 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
These results suggest perturbed modifications of histone H3 around the p15 CpG island region in AML.
|
17074388 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, this study (a) establishes that the gene encoding the tumor suppressor p15(INK4b) is a target of CBFbeta-SMMHC, a finding relevant to the leukemogenesis process, and (b) indicates that, in patients with inv(16)-containing AML, reexpression from the INK4b locus in the leukemia would not be predicted to occur using hypomethylating drugs.
|
17283131 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Zebularine is an effective inhibitor of p15INK4B methylation and cell growth in human AML in vitro.
|
17258075 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
LHGDN |
These results suggest perturbed modifications of histone H3 around the p15 CpG island region in AML.
|
17074388 |
2007 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
In contrast to these genetic alterations, epigenetic lesions, e.g., promoter silencing by hypermethylation of the p15/INK4b and other genes, are increasingly recognized as important in the pathogenesis of AML.
|
17019734 |
2006 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although FHIT and p15(INK4B) methylations were not correlated in MDS and AML, increased FHIT methylation at the relapse in AML was associated with p15(INK4B) methylation.
|
15902282 |
2005 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Furthermore, two patients with PBC-ALL and 11 acute myeloblastic leukemia (AML) were quantitatively examined for p15 gene methylation using bisulfite genomic sequencing.
|
15755508 |
2005 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We interpret these data to mean that dysfunction of the cell cycle and/or the cell-cell adhesion molecule plays a role in the pathogenesis of acute myeloid leukemia and that analysis of the methylation of p15(INK4b) and E-cadherin genes can provide clinically important evidence on which to base treatment.
|
15863205 |
2005 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Methylation of E-cadherin and RARbeta occurs preferentially in AMLs with high methylation index (MI), while epigenetic lesions in SOCS1, DAP-kinase, and p15 appear to be independent.
|
15495254 |
2004 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Aberrant p15 gene promoter methylation in therapy-related myelodysplastic syndrome and acute myeloid leukaemia: clinicopathological and karyotypic associations.
|
12648079 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
At diagnosis, p15 methylation occurred in 29 (58%) AML patients, and 10 (40.0%) ALL patients. p16 methylation occurred in two (4%) AML and two (8%) ALL patients.
|
14513284 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
The important cell cycle regulatory gene p15(INK4b) has been shown to be inactivated in acute myeloid leukemia and myelodysplastic syndrome.
|
12750705 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
LHGDN |
Methylation of p15 was less common in t-AML of subtype M5 than in other FAB subtypes (P=0.03).
|
12970781 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Methylation of p15 was less common in t-AML of subtype M5 than in other FAB subtypes (P=0.03).
|
12970781 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
At presentation, 93 % of cases of AML (8 of 8 M1, 10 of 11 M2, 2 of 2 M4, 5 of 6 M5, and 2 of 2 M6; French-American-British classification system) showed p15 methylation, but none showed p16 methylation.
|
11413509 |
2001 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Interestingly, KG-1 and KG-1a model the methylation of p15 observed in AML, where KG-1 methylation is variegated and KG-1a methylation is complete.
|
11532526 |
2001 |