title: Clinical Impact of Overexpression of FOXP3 and WT1 on
  Disease Outcome in Egyptian Acute Myeloid Leukemia Patients
abstract: Background: In the last decade, it has become clear that change of gene expression may alter the hematopoietic cell
  quiescent state and consequently play a major role in leukemogenesis. WT1 is known to be a player in acute myeloid
  leukemia (AML) and FOXP3 has a crucial role in regulating the immune response. Objectives: To evaluate the impact
  of overexpression of WT1and FOXP3 genes on clinical course in adult and pediatric AML patients in Egypt. Patients
  and methods: Bone marrow and peripheral blood samples were obtained from 97 de novo non M3 AML patients
  (63 adult and 34 pediatric). Real-time quantitative PCR was used to detect overexpression WT1 and FOXP3 genes.
  Patient follow up ranged from 0.2 to 39.0 months with a median of 5 months. Results: In the pediatric group; WT1
  was significantly expressed with a high total leukocyte count median 50X109/L (p=0.018). In the adult group, WT1
  had an adverse impact on complete remission induction, disease-free survival and overall survival (p=0.02, p=0.035,
  p=0.019 respectively). FOXP3 overexpression was associated with FAB subtypes AML M0 +M1 vs. M2, M4+M5 (p
  =0.039) and the presence of hepatomegaly (p=0.005). Conclusions: WT1 and FOXP3 overexpression has an adverse
  impact on clinical presentation, treatment response and survival of pediatric and adult Egyptian AML patients.
authors.affiliation: Department of Clinical Pathology, National Cancer Institute (NCI), Cairo university, Cairo, Egypt. Email: eman_kandeel@hotmail.com
authors.forename: Magda
authors.initials: M
authors.lastname: Assem
authors.forename: Ahmed
authors.initials: A
authors.lastname: Osman
authors.forename: Eman
authors.initials: E
authors.lastname: Kandeel
authors.forename: Reham
authors.initials: R
authors.lastname: Elshimy
authors.forename: Hanan
authors.initials: H
authors.lastname: Nassar
authors.forename: Radwa
authors.initials: R
authors.lastname: Ali
keywords: AML; WT1; FOXP3