|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
Study on the treatment of the p15 gene combined with Bcr-abl-specific siRNA and STI571 for chronic myeloid leukemia.
|
24938701 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, our study may provide new insights into the role of p15INK4B in CML and a potential therapeutic target for overcoming tyrosine kinase inhibitor resistance in CML.
|
25387678 |
2014 |
|
Myeloid Leukemia, Chronic
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
p14ARF, p15INK4b and p16INK4a methylation status in chronic myelogenous leukemia.
|
15370242 |
2004 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Using a quantitative assay, methylation-sensitive single nucleotide primer extension (MS-SNuPE), we have analyzed the methylation levels of promoter and exonic (coding region) CpG islands of two cyclin-dependent kinase inhibitors [p15(INK4B) and p16(INK4A)] and the PAX6 gene, which encodes a transcriptional factor involved in neuronal proliferation, in DNA samples taken from patients with chronic myelogenous leukemia, acute myelogenous leukemia, myelodysplastic syndrome, and colorectal cancer.
|
11584062 |
2001 |
|
Myeloid Leukemia, Chronic
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
We conclude that de novo methylation of c-abl and p15 both occur in CML, and analysis of DNA methylation changes using the bisulfite-based MS-SNuPE assay allows both a sensitive and quantitative assessment of these molecular events compared to other methods currently utilized.(Blood.2000;95:2990-2992)
|
10779450 |
2000 |
|
Myeloid Leukemia, Chronic
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In contrast, neither p15INK4B nor p16INK4A were inactivated in any stage of chronic myelogenous leukemia.
|
9041182 |
1997 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
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 |
|
Myeloid Leukemia, Chronic
|
0.100 |
Biomarker
|
disease |
BEFREE |
In order to determine whether these genes are more widely involved in haematological malignancies, we have investigated a total of 84 samples that did not have homozygous p16 or p15 deletions from patients with acute lymphoid leukaemia (n=13), acute myeloid leukaemia (n=24) and chronic myeloid leukaemia in blast crisis (n=43) as well as four haemopoietic cell lines. p15 and p16 exon 1 and exon 2 were amplified by polymerase chain reaction (PCR), analysed by single-stranded conformation polymorphism (SSCP) and subsequently by sequencing.
|
8616035 |
1996 |
|
Myeloid Leukemia, Chronic
|
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 |
|
Myeloid Leukemia, Chronic
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We found that a part or the whole of the CDK4I gene was homozygously deleted in 14 of the 37 (38%) cell lines and 4 of 72 (6%) samples from leukemia patients, including 45 with acute myelocytic leukemia, 14 with acute lymphocytic leukemia (ALL), and 13 with chronic myelocytic leukemia in blastic crisis.
|
7919362 |
1994 |