Identifying Leukemia-associated Immunophenotypes in Acute Myeloid Leukemia Patients Using Multiparameter Flow Cytometry.

Objectives: We sought to identify leukemia-associated immunophenotypes (LAIPs) in 50 acute myeloid leukemia (AML) patients at diagnosis using an eight-color multiparameter flow cytometry (MFC) panel and to detect if they showed any alteration in relapsed/refractory cases.

Methods: We used the eight-color MFC panel with CD45/side scatter log gating strategy to analyze LAIPs in 50 AML patients presenting to Alexandria University Hospitals, Egypt at diagnosis and relapse and refractory cases. Twenty age and sex matched bone marrow samples from patients performing bone marrow aspirate for non-malignant hematological indications were included as controls.

The prognostic impact of loss of chromosome 7 material detected by fluorescence in situ hybridization (FISH) in myeloid malignancies.

Background: Monosomy 7 (-7) or deletion in its long arm [del(7q)] is among the most common chromosomal abnormalities in myeloid malignancies. There are prognostic variations between -7 and del(7q) in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS).

Aim: To describe the clinical characteristics, response to treatment, and survival of patients with primary AML and MDS having -7 or del(7q) detected by fluorescence in situ hybridization (FISH).

Telomerase activity in Philadelphia positive chronic myeloid leukaemia.

Telomerase is a specialized type of reverse transcriptase that catalyzes the synthesis and extension of telomeric DNA. Activation of telomerase and stabilization of telomeres are considered necessary for immortalization of tumor cells. Chronic Myeloid Leukaemia (CML) is a good example to investigate the reactivation of telomerase as; after a variable period in chronic phase, CML undergoes further evolution.

A novel gene, FGA7, is fused to RUNX1/AML1 in a t(4;21)(q28;q22) in a patient with T-cell acute lymphoblastic leukemia.

AML1 is among the most frequent targets of chromosomal rearrangements in human leukemias. We report here the molecular analysis of a t(4;21)(q28;q22) that has disrupted AML1 in a patient with de novo T-cell acute lymphoblastic leukemia. By using 3'-RACE analysis, we show that this rearrangement results in the fusion of a novel gene immediately downstream of exon 5 or exon 6 of AML1, indicating that the AML1 breakpoint lies in intron 6 and that alternative fusion splice variants are generated.

A new translocation that rearranges the AML1 gene in a patient with T-cell acute lymphoblastic leukemia.

The AML1 gene (also known as RUNX1 or CBFA2), located in chromosome band 21q22, encodes a transcription factor which heterodimerizes with the CBFbeta protein forming a complex called human core binding factor (CBF). The CBF complex appears to regulate a number of genes important for hematopoiesis. AML1 is one of the most common targets of chromosomal rearrangements in human leukemias and has been involved in 14 chromosomal translocations to date.