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.

BackgroundActivating point mutation of the RAS gene has been generally accepted as an oncogenic event in a variety of malignancies. It represents one of the most common genetic alterations in acute myeloid leukemia (AML). However, little is known about its clinical relevance in the treatment outcome for this leukemia.ObjectiveThis study aimed to clarify the biologic and prognostic impact of K-RAS mutations in relation to the dose of cytarabine (ara-C) used in postinduction consolidation chemotherapy in adult AML patients.Patients and methodsThe study comprised of 71 de novo AML patients with male/ female ratio 1.4:1; their ages ranged from 21–59 years with a median of 37 years. They were subjected to full clinical evaluation, routine laboratory investigations, cytogenetic studies by G-banding (Giemsa staining), and K-RAS mutation detection using real-time polymerase chain reaction. The patients were randomized into two groups according to the ara-C dose used in consolidation treatment, the high the dose ara-C (HDAC) group receiving 400 mg ara-C and-low-dose ara-C (LDAC) group receiving 100 mg ara-C; they were followed over a period of five years.ResultsMutations in the K-RAS gene (mutRAS) were detected in 23 patients (32%) with the remaining 48 patients (68%) having wild-type RAS (wtRAS). The percent of blast cells was significantly lower in mutRAS compared to wtRAS patients (P ≤ 0.001) while M4 subtype of AML and Inv(16) frequencies were significantly higher in mutRAS compared to wtRAS patients (P = 0.015) and (P = 0.003), respectively. The patients were followed up for a median of 43 months (range 11–57 months). There was no significant difference in overall survival (OS) between mutRAS and wtRAS (P = 0.326). Within the mutRAS patients treated with HDAC, cumulative OS was significantly higher than those treated with LDAC (P = 0.001). This was not the case in the wtRAS group (P = 0.285). There was no significant difference in disease-free survival (DFS) between mutRAS and wtRAS groups (P = 0.923). mutRAS patients treated with HDAC had a statistically higher cumulative DFS than mutRAS patients treated with LDAC (P = 0.001). Patients with wtRAS also benefited from HDAC, but to a lesser extent. Among patients with wtRAS, those treated with HDAC showed higher cumulative and median DFS than patients treated with LDAC (P = 0.031).ConclusionIt was concluded that adult AML patients carrying mutations in the K-RAS gene benefit from higher ara-C doses more than wtRAS patients, so pretreatment mutation detection could be an important predictor for treatment strategy and survival of adult AML patients. These findings counter the prevailing bias that oncogene mutations lead to more aggressive behavior in human malignancies.

Background and study aim: MicroRNAs were evaluated as biomarkers for liver injury in various liver diseases. This study aimed to evaluate the serum miRNA-122 as a potential biomarker for diagnosis and monitoring different stages of disease in chronic hepatitis C patients. Patients and Methods: A case-control study included 45 subjects, divided into three groups: control group, compensated, and decompensated cirrhotic patients groups. All participants were subjected to full history taking, clinical assessment, routine lab investigations, hepatitis B surface antigen, HCV antibodies, HCV-RNA using PCR, and determination of serum expression of miRNA-122 using real-time PCR. Results: The miRNA-122 expression levels among the two groups with liver disease were significantly higher than the control group. Among cirrhotic patients, the expression levels were significantly higher in the compensated subjects compared to the decompensated group. The miRNA-122 levels decreased with the progression of liver disease (from Child-Pugh class A to C) but without significant difference. Patients with ascites had a significantly lower expression of miR-122 compared to those without ascites. Patients with gastrointestinal bleeding and hepatic encephalopathy had statistically insignificant lower expression of miRNA 122 compared to subjects without these complications. As regards all patients groups there were significant positive correlations between miRNA-122 expression and (AST, ALT, albumin, and viral load) and a significant negative correlation as regard INR. Conclusion: Serum miRNA-122 expression levels decreased with the progression of liver disease and at a cutoff value ≤ 2.74 fold change could predict the occurrence of hepatic decompensation. So Serum miRNA-122 seems to be a useful new diagnostic marker in hepatitis C patients with different stages of the disease.

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