We aimed to explore the expression of CD34 and its impact on the disease outcome in patients with APL. The study comprised 40 de novo APL patients. Diagnostic tools included peripheral blood and bone marrow morphology and cytochemistry, immunophenotyping, cytogenetic studies, and PML/RARα fusion gene detection using RT-PCR. CD34 was expressed in 13 (32.5%) of cases with higher expression in M3v compared to M3 subtype. All M3v cases were CD34+, while only 7.4% of M3 cases were CD34+. CD34+ cases were associated with significant higher white blood cell count and peripheral blood promyelocytes. No significant association was found between PML/RAR-α isoform and molecular remission. CD34+ expression was significantly associated with decreased incidence of molecular remission and increased incidence of early death. The overall survival of patients with WBC count >11 × 103/μl was inferior to patients with WBC count <11 × 103/μl, but no significant differences were observed in overall survival between CD34- and CD34+ or between bcr1 and bcr3 groups. Immunophenotypic analysis for CD34 could distinguish an APL subset with different biological characteristics and adverse prognostic outcome.
Background: Acute Myelogenous Leukemia (AML) is a malignant disease of haematopoietic stem cells. C-kit is a Tyrosine Kinase Receptor class III (RTK) which is expressed on early hematopoietic progenitor cells and shares in hematopoietic stem cell proliferation, differentiation and survival. c-kit is a proto-oncogene, so activating c-kit mutations may contribute in the pathogenesis of leukemia in humans. Exon 11 of c-Kit gene is the frequent site for mutations in different kinds of tumors. Objectives: We aim to screen the mutation status of exon 11 of c-kit gene and further evaluation of these mutations as a prognostic marker in AML cases. Methodology: To determine the frequency of exon 11 mutations in 60 de novo AML cases, we have done polymerase chain reaction followed by direct DNA sequencing. Results: The c-kit mutations in exon 11 were detected in (14/60) 23.3% in AML cases. Two different missense mutations were detected. Those included Pro121Gln and another mutation, Pro171His. There was significant decrease in the rate of achievement of complete remission (CR) in the mutated group compared to the wild group (P=0.02). In addition, the one year survival (OS) was less in the mutated group compared to the wild group (P=0.02). Conclusion: Mutations in exon 11 of the c-kit gene can be involved in pathogenesis and is a useful predictive genetic marker in AML.
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