جستجوی مقالات مرتبط با کلیدواژه "flt3-itd" در نشریات گروه "پزشکی"

Acute myeloid leukemia (AML) is a hematopoietic malignancy caused by genetic abnormalities. These days, molecular and genetic factors are usually used as diagnostic and prognostic markers. FLT-3 is one of the most known diagnostic factors in AML. MDR1 gene belongs to the ATP binding cassette family; it is known as one of the chemotherapy-resistant causes of AML. We aimed to study FLT-3ITD mutations and their association with MDR1 gene expression in AML individuals.

For investigation, 80 AML individuals and 20 healthy controls were selected. This study was done in the cancer molecular pathology research center of Mashhad University of Medical Sciences (MUMS), Iran during 2017-2019. FLT3-ITD mutation was assessed by polymerase chain reaction (PCR); Real-time quantitative PCR was performed to measure the amount of MDR1 gene expression. Bone marrow and blood smears of patients were evaluated in terms of morphology. SPSS 16.0 was used for data analysis.

FLT3-ITD mutation and MDR1 overexpression were found in 18.8% and 23.8% of AML patients, respectively. Statistical analysis did not show any relations or association between these two markers. Cuplike morphology was observed in blast cells in 21.25% of AML cases, which was associated with FLT3-ITD mutation presence.

FLT-3 and MDR1 do not affect each other. It is suggested to perform survival studies to determine the exact role of MDR1 overexpression in drug resistance issues.

  FLT3-ITD has been recently used as a molecular prognostic marker for risk classification in acute myeloid leukemia (AML) therapy. In this study we aimed to investigate the association of FLT3-ITD gene mutation with bone marrow blast cell count, CD34 expression as malignant cell burden, cyclin D1 and Bcl-xL expressions as indexes of cell proliferation and anti-apoptosis and human equilibrative nucleoside transporter 1 (hENT1) expression as cytarabine transporter during AML treatment.

  We investigated FLT3-ITD mutations, bone marrow blast cell count, CD34, cyclin D1, Bcl-xL and hENT1 expression in bone marrow aspirates from 22 de novo AML patients in a cross sectional study.

  FLT3-ITD mutations were observed in 5 out of 22 de novo AML patients (22.7%). Patient with FLT3-ITD mutations had higher blast cell counts (79.5% vs 56.1%, p =0.004). In patients with FLT3-ITD mutations, CD34 and cyclin D1 expressions were higher (MFI 328.80 vs 25.78, p =0.003 and MFI 74.51 vs 57.15 p =0.005) than the patients without mutations. hENT1 expression in AML with FLT3-ITD mutation was lower (MFI 29.64 versus 56.32, p =0.0000) than in mutation-free AML. There was no significant difference in Bcl-xL expression between patients with and without mutations (p =0.61).

  A significant association was found between FLT3-ITD gene mutations in AML patients with bone marrow blast cell count, CD34, cyclin D1 and hENT1 expressions, however no association was obtained with Bcl-xL expression. These findings support the role of such mutation in pathogenesis of AMLand its contribution in rearrangement of standard therapy with cytarabine in management of AML.

 FLT3 gene mutation contributes worse prognosis in patients with acute myeloid leukemia (AML). Almost 67% of patients with AML with FLT3 gene mutation cannot reach complete remission after induction therapy, and  they are also at high risk of  relapse. We aimed to investigate the FLT3-ITD, -TKD (D835) gene mutation prevalence in patients with AML at Surabaya and their association with leukocyte and bone marrow blast cell count.

20 de novo patients with AML were recruited during February–July 2018. They were investigated through routine AML check-up and detection for FLT3-ITD, -TKD (D835) gene mutation. 

 Four patients with de novo AML (20%) had FLT3-ITD gene mutation, and one  patient had  FLT3-TKD (D835) gene mutation. Median leukocyte count in patients with AML with FLT3-ITD mutation was higher than wild type patients ( 146.3×103/ µL vs 16.4 x 103 / µL, P=0,002). The mean bone marrow blast cell count was higher in patients with AML with FLT3-ITD mutation than wild type patients ( 86.5% vs 57.9%, P=0,047).  The difference in leukocyte and bone marrow blast cell count in patients with FLT3-TKD (D835) mutation could not be analyzed since there was only one patient with this mutation. 

The prevalence of FLT3-ITD gene mutation in patients in AML in Surabaya was 20% and FLT3-TKD (D835) was 5%. Patients with FLT3-ITD gene mutation was associated with leukocyte and bone marrow blast cell count.