Methylation status of Wnt signaling pathway genes affects the clinical outcome of Philadelphia-positive acute lymphoblastic leukemia
Palabras clave : 
Materias Investigacion::Ciencias de la Salud::Oncología
Fecha incorporación: 
2008
Editorial : 
Wiley-Blackwell
ISSN: 
1347-9032
Cita: 
Martin, V., Agirre, X., Jimenez-Velasco, A., San Jose-Eneriz, E. et al. Methylation status of Wnt signaling pathway genes affects the clinical outcome of Philadelphia-positive acute lymphoblastic leukemia. Cancer Scie 2008; 99 (9): 1865–1868
Resumen
The clinical significance of aberrant promoter methylation of the canonical Wnt pathway antagonist genes (sFRP1, sFRP2, sFRP4, sFRP5, Wif1, Dkk3, and Hdpr1) and also putative tumor-suppressor gene Wnt5a, belonging to the non-canonical Wnt signaling pathway, was investigated in a large series of 75 patients with Philadelphia chromosome-positive acute lymphoblastic leukemia by methylationspecific polymerase chain reaction. At least one methylated gene was observed in cells from 66% (49/75) of patients (methylated group). Disease-free survival and overall survival at 9 years were 51 and 40%, respectively, for the unmethylated group and 3 and 2%, respectively, for the methylated group (both P < 0.0001). Multivariate analysis demonstrated that the Wnt methylation profile was an independent prognostic factor predicting disease-free survival (P = 0.007) and overall survival (P = 0.039). Abnormal DNA methylation of promoter-associated CpG islands in the Wnt signaling pathway is very common in Philadelphia chromosome-positive acute lymphoblastic leukemia and potentially defines subgroups with distinct clinical characteristics.

Ficheros en este registro:
Fichero: 
2008_Cancer Science_Martin_Methylation status of Wnt signaling pathway genes affects the clinical outcome of Philadelphia-positive acute lymphoblastic leukemia.pdf
Descripción: 
Tamaño: 
98,91 kB
Formato: 
Adobe PDF


Los ítems de Dadun están protegidos por copyright, con todos los derechos reservados, a menos que se indique lo contrario.