Iranian Journal of Blood and Cancer
Iranian Journal of Blood and Cancer
Medical Sciences
http://ijbc.ir
1
admin
2008-4595
2008-4609
8
10.61186/ijbc
14
2008-4595
13
en
jalali
1393
8
1
gregorian
2014
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1
7
1
online
1
fulltext
en
Dysregulation of the WNT Signaling Pathway Through Methylation of Wnt Inhibitory Factor 1 and Dickkopf-1 Genes among AML Patients at the Time of Diagnosis
Pediatric Hematology & Oncology
Pediatric Hematology & Oncology
پژوهشي
Original Article
Background: In acute myeloblastic leukemia, a large number of tumor suppressor genes are silenced through DNA
methylation such as CDKN2B & p73. Wnt inhibitory factor 1 (WIF1) and Dickkopf-3 (DKK-1) are negative regulators of
Wnt signaling pathway. In the present study, we evaluated the methylation status of WIF1 and DKK-1 genes in acute
myeloblastic leukemia patients.
Patients and Methods: Blood samples were taken from 120 AML patients and 25 healthy control subjects. DNA was
isolated, treated with sodium bisulphite, and examined using methylation-specific polymerase chain reaction (MSP)
with primers specific for methylated and unmethylated sequences of the WIF1 and DKK-1 genes.
Results: The frequency of aberrant hypermethylation of WIF1 and DKK-1 genes in acute myeloblastic leukemia
patients were determined to be 35% (42/120) and 28.3% (34/120), respectively. In addition, for all subjects in control
group, methylation of WIF1 and DKK-1 genes were negative. Patients with M0 subtype of FAB-AML had the highest
incidence of hypermethylation of WIF1 (P = 0.003) and DKK-1 (P = 0.005) genes.
Conclusion: The present study showed that, like many solid tumors, WIF1 and DKK-1 genes methylation also occurs
in acute myeloblastic leukemia. The study of other antagonists of Wnt signaling pathways are recommended.
Key words: AML, Wnt inhibitory factor 1, dickkopf, DNA methylation.
AML, Wnt inhibitory factor 1, dickkopf, DNA methylation.
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http://ijbc.ir/browse.php?a_code=A-10-9-16&slc_lang=en&sid=1
Ghasemi
A
10031947532846002642
10031947532846002642
Yes
Ghotaslou
A
10031947532846002643
10031947532846002643
No
Mohammadi
M
10031947532846002644
10031947532846002644
No
Ghaffari
K
10031947532846002645
10031947532846002645
No
Abbasian
S
10031947532846002646
10031947532846002646
No