Clinical Impact of Overexpression of FOXP3 and WT1 on Disease Outcome in Egyptian Acute Myeloid Leukemia Patients
نویسندگان
چکیده
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.
منابع مشابه
The Prognostic Impact of WT1 Expression Levels, Mutations, and SNP rs16754 in AML Patients: A Retrospective Cohort Study
Background and Objective: The clinical outcomes and treatment options for acute myeloid leukemia (AML) patients are highly dependent upon molecular markers. In this study, Wilms tumor (WT1) (exons 7 and 9) mutations, SNP rs16754, and WT1 expression levels in 130 random AML patients were screened; FMs-like tyrosine kinase-3 internal tandem duplication (FLT3-ITD), nucleophosmin (NPM1), and CCAAT/...
متن کاملQuantitative Assessment of WT1 Expression by Real Time Quantitative PCR in Pediatric Patients with Acute Myeloblastic Leukemia
Background: Acute myeloid leukemia (AML) is one of myeloid malignancies which the risk increases with age increment. It is categorized based on genetic aberrations. Some of these genetic disorders can determine minimal residual diseases (MRD) and prognosis of AML patients. Wilms tumor (WT1) over expression is found in AML patients. The aim of this study was to determine the frequency of WT1 ove...
متن کاملPrognostic Value of EVI1 Expression in Pediatric Acute Myeloid Leukemia: A Systematic Review
Acute myeloid leukemia (AML) as a distortion of blood cells involves the differentiation of hematopoietic stem cells. Several studies established the irregular overexpression of specific genes is a common finding in patients with AML. The ectopic viral integration site-1 (EVI1) gene is a proto-oncogene subject to alternative splicing, and encodes a zinc-finger protein that acts as a tr...
متن کاملWilms Tumor 1 Gene Mutations in Patients with Cytogenetically Normal Acute Myeloid Leukemia
OBJECTIVE This study aimed to assess the prognostic impact of Wilms tumor 1 (WT1) mutations in cytogenetically normal acute myeloid leukemia (CN-AML) among Egyptian patients. MATERIALS AND METHODS Exons 1, 2, 3, 7, 8, and 9 of WT1 were screened for mutations in samples from 82 CN-AML patients out of 203 newly diagnosed AML patients, of age ranging from 21 to 74 years, using high-resolution ca...
متن کاملOverexpression of Wilms Tumor 1 Gene as a Negative Prognostic Indicator in Acute Myeloid Leukemia
Chromosomal aberrations are useful in assessing treatment options and clinical outcomes of acute myeloid leukemia (AML) patients. However, 40 ∼ 50% of the AML patients showed no chromosomal abnormalities, i.e., with normal cytogenetics aka the CN-AML patients. Testing of molecular aberrations such as FLT3 or NPM1 can help to define clinical outcomes in the CN-AML patients but with various succe...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 17 شماره
صفحات -
تاریخ انتشار 2016