Source:http://linkedlifedata.com/resource/pubmed/id/15863205
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
2005-5-2
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| pubmed:abstractText |
Hypermethylation of CpG islands is a common mechanism by which tumor suppressor genes are inactivated. The tumor suppressor gene p15(INK4b) is important component of cell cycles, whereas E-cadherin gene is often termed a metastasis suppressor gene. We have studied the feasibility of detecting tumor-associated aberrant p15(INK4b) and E-cadherin methylation in acute myeloid leukemia (AML) using methylation-specific PCR. Aberrant methylation of p15(INK4b) was detected in 31 of 61 (51%) AML patients. On the other hand, E-cadherin hypermethylation was detected in 36 of 61 (56%) AML patients. We have examined the methylation pattern of these genes and the prognosis in AML patients using a log-rank test. Methylation of p15(INK4b) gene significantly correlated with prognosis (p=0.0012), and methylation of E-cadherin gene more significantly correlated with prognosis (p=0.0004). When both were methylated, there was even more significant unfavorable prognosis compared to either of the methylated genes (p<0.0001). 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.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CDKN2B protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Cadherins,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclin-Dependent Kinase Inhibitor...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Suppressor Proteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jun
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| pubmed:issn |
0145-2126
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
29
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
653-9
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:15863205-Adolescent,
pubmed-meshheading:15863205-Adult,
pubmed-meshheading:15863205-Aged,
pubmed-meshheading:15863205-Cadherins,
pubmed-meshheading:15863205-Cell Cycle Proteins,
pubmed-meshheading:15863205-Cyclin-Dependent Kinase Inhibitor p15,
pubmed-meshheading:15863205-Cytogenetic Analysis,
pubmed-meshheading:15863205-DNA Methylation,
pubmed-meshheading:15863205-Female,
pubmed-meshheading:15863205-Follow-Up Studies,
pubmed-meshheading:15863205-Humans,
pubmed-meshheading:15863205-Immunophenotyping,
pubmed-meshheading:15863205-Leukemia, Myeloid, Acute,
pubmed-meshheading:15863205-Male,
pubmed-meshheading:15863205-Middle Aged,
pubmed-meshheading:15863205-Prognosis,
pubmed-meshheading:15863205-Retrospective Studies,
pubmed-meshheading:15863205-Survival Analysis,
pubmed-meshheading:15863205-Treatment Outcome,
pubmed-meshheading:15863205-Tumor Suppressor Proteins
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| pubmed:year |
2005
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| pubmed:articleTitle |
Methylation of p15(INK4b) and E-cadherin genes is independently correlated with poor prognosis in acute myeloid leukemia.
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| pubmed:affiliation |
First Department of Internal Medicine, Tokyo Medical University, 6-7-1, Nishishinjuku, Shinjuku-ku, Tokyo 160-0023, Japan.
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| pubmed:publicationType |
Journal Article
|