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Papers by Nashwa al-Azizi

Research paper thumbnail of Assessment of Cell-Free DNA with Microvascular Complication of Type II Diabetes Mellitus, Using PCR and Elisa

Nucleosides Nucleotides and Nucleic Acids, Mar 1, 2010

In order to assess the potential biochemical markers in the development, diagnosis, and prognosis... more In order to assess the potential biochemical markers in the development, diagnosis, and prognosis of diabetic patient with microvascular complication represented with retinopathy, we analyzed the levels of cell-free DNA by two different techniques. The levels of cell-free GAPDH assayed by quantitative PCR were significantly higher in the plasma samples of diabetic patients with and without diabetic retinopathy than in those of the control group; thus, it is a better biomarker than nucleosomes assayed by ELISA in patients with type 2 diabetes for the early detection of development of microvascular complications as retinopathy.

Research paper thumbnail of Prognostic Significance of Survivin in Pediatric Acute Lymphoblastic Leukemia

Indian Journal of Hematology and Blood Transfusion, 2011

Impaired apoptosis is mediated by members of the inhibitor of apoptosis proteins (IAP) family suc... more Impaired apoptosis is mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin. Survivin was described in number of different tumors and found to correlate with poor prognosis in a variety of cancers including hematologic malignancies. The aim of this study was to determine survivin in pediatric ALL and compare it with clinical and hematological findings, response to therapy and outcome. Flowcytometry was used for detection of intracellular survivin and determine its mean fluorescence intensity (MFI) in bone marrow mononuclear cells. Patients were followed up for 28 months after induction therapy. Survivin was detected in 63.3% of the patients BM. In spite of no association of survivin levels with established risk factors (P [ 0.05) except with high WBC, there was significant higher level of survivin expression in high risk group patients when patients were stratified into high and standard risk groups. According to response to induction therapy, there was no significant difference, in survivin level between patients who achieved CR, RD and ED. However, patients suffering relapse of the disease, had a significant higher basal level of survivin than patients still in remission. Over expression of survivin is a candidate parameter to determine poor prognosis in ALL patients and it may serve to refine treatment stratification with intensification of therapy in those patients prone to relapse.

Research paper thumbnail of Assessment of Cell-Free DNA with Microvascular Complication of Type II Diabetes Mellitus, Using PCR and Elisa

Nucleosides, Nucleotides and Nucleic Acids, 2010

In order to assess the potential biochemical markers in the development, diagnosis, and prognosis... more In order to assess the potential biochemical markers in the development, diagnosis, and prognosis of diabetic patient with microvascular complication represented with retinopathy, we analyzed the levels of cell-free DNA by two different techniques. The levels of cell-free GAPDH assayed by quantitative PCR were significantly higher in the plasma samples of diabetic patients with and without diabetic retinopathy than in those of the control group; thus, it is a better biomarker than nucleosomes assayed by ELISA in patients with type 2 diabetes for the early detection of development of microvascular complications as retinopathy.

Research paper thumbnail of Incidence of Philadelphia-chromosome in acute myelogenous leukemia and biphenotypic acute leukemia patients: And its role in their outcome

Leukemia Research, 2011

Background: Philadelphia-chromosome positive acute myeloid leukemia (Ph+ AML) is a rare entity an... more Background: Philadelphia-chromosome positive acute myeloid leukemia (Ph+ AML) is a rare entity and patient prognosis is poor, with short median survival. Biphenotypic acute leukemia (BAL) is a rare disorder that is difficult to diagnose and it displays features of both myeloid and lymphoid lineage. The aim of this study was to highlight the incidence of Philadelphia chromosome and its presence in cases of acute myeloid and biphenotypic leukemia and determine its role in the outcome of these leukemias. Subjects and methods: This study examined 464 subjects with newly diagnosed acute myeloid leukemia: 312 were males and 152 were females. All individuals were subjected to immunophenotyping and conventional karyotyping. FISH was used in failed cases of conventional cytogenetics analysis to quantify disease and to prove positive BCR-ABL fusion gene. Results: the incidence of Ph+ chromosome was found to be higher in BAL (38.4%) than in AML (1.99%). There was statistically significant difference according to the age and the median survival time between the two groups. Conclusion: Detection of specific chimeric transcripts in AML and BAL at the time of diagnosis was crucial since it plays an important role for accurate risk stratification and treatment management.

Research paper thumbnail of The prognostic impact of K-RAS mutations in adult acute myeloid leukemia patients treated with high-dose cytarabine

OncoTargets and Therapy, 2011

Background: Activating point mutation of the RAS gene has been generally accepted as an oncogenic... more Background: Activating 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. Objective: This 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 methods: The 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. Results: Mutations 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). Conclusion: It 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.

Research paper thumbnail of Assessment of Cell-Free DNA with Microvascular Complication of Type II Diabetes Mellitus, Using PCR and Elisa

Nucleosides Nucleotides and Nucleic Acids, Mar 1, 2010

In order to assess the potential biochemical markers in the development, diagnosis, and prognosis... more In order to assess the potential biochemical markers in the development, diagnosis, and prognosis of diabetic patient with microvascular complication represented with retinopathy, we analyzed the levels of cell-free DNA by two different techniques. The levels of cell-free GAPDH assayed by quantitative PCR were significantly higher in the plasma samples of diabetic patients with and without diabetic retinopathy than in those of the control group; thus, it is a better biomarker than nucleosomes assayed by ELISA in patients with type 2 diabetes for the early detection of development of microvascular complications as retinopathy.

Research paper thumbnail of Prognostic Significance of Survivin in Pediatric Acute Lymphoblastic Leukemia

Indian Journal of Hematology and Blood Transfusion, 2011

Impaired apoptosis is mediated by members of the inhibitor of apoptosis proteins (IAP) family suc... more Impaired apoptosis is mediated by members of the inhibitor of apoptosis proteins (IAP) family such as survivin. Survivin was described in number of different tumors and found to correlate with poor prognosis in a variety of cancers including hematologic malignancies. The aim of this study was to determine survivin in pediatric ALL and compare it with clinical and hematological findings, response to therapy and outcome. Flowcytometry was used for detection of intracellular survivin and determine its mean fluorescence intensity (MFI) in bone marrow mononuclear cells. Patients were followed up for 28 months after induction therapy. Survivin was detected in 63.3% of the patients BM. In spite of no association of survivin levels with established risk factors (P [ 0.05) except with high WBC, there was significant higher level of survivin expression in high risk group patients when patients were stratified into high and standard risk groups. According to response to induction therapy, there was no significant difference, in survivin level between patients who achieved CR, RD and ED. However, patients suffering relapse of the disease, had a significant higher basal level of survivin than patients still in remission. Over expression of survivin is a candidate parameter to determine poor prognosis in ALL patients and it may serve to refine treatment stratification with intensification of therapy in those patients prone to relapse.

Research paper thumbnail of Assessment of Cell-Free DNA with Microvascular Complication of Type II Diabetes Mellitus, Using PCR and Elisa

Nucleosides, Nucleotides and Nucleic Acids, 2010

In order to assess the potential biochemical markers in the development, diagnosis, and prognosis... more In order to assess the potential biochemical markers in the development, diagnosis, and prognosis of diabetic patient with microvascular complication represented with retinopathy, we analyzed the levels of cell-free DNA by two different techniques. The levels of cell-free GAPDH assayed by quantitative PCR were significantly higher in the plasma samples of diabetic patients with and without diabetic retinopathy than in those of the control group; thus, it is a better biomarker than nucleosomes assayed by ELISA in patients with type 2 diabetes for the early detection of development of microvascular complications as retinopathy.

Research paper thumbnail of Incidence of Philadelphia-chromosome in acute myelogenous leukemia and biphenotypic acute leukemia patients: And its role in their outcome

Leukemia Research, 2011

Background: Philadelphia-chromosome positive acute myeloid leukemia (Ph+ AML) is a rare entity an... more Background: Philadelphia-chromosome positive acute myeloid leukemia (Ph+ AML) is a rare entity and patient prognosis is poor, with short median survival. Biphenotypic acute leukemia (BAL) is a rare disorder that is difficult to diagnose and it displays features of both myeloid and lymphoid lineage. The aim of this study was to highlight the incidence of Philadelphia chromosome and its presence in cases of acute myeloid and biphenotypic leukemia and determine its role in the outcome of these leukemias. Subjects and methods: This study examined 464 subjects with newly diagnosed acute myeloid leukemia: 312 were males and 152 were females. All individuals were subjected to immunophenotyping and conventional karyotyping. FISH was used in failed cases of conventional cytogenetics analysis to quantify disease and to prove positive BCR-ABL fusion gene. Results: the incidence of Ph+ chromosome was found to be higher in BAL (38.4%) than in AML (1.99%). There was statistically significant difference according to the age and the median survival time between the two groups. Conclusion: Detection of specific chimeric transcripts in AML and BAL at the time of diagnosis was crucial since it plays an important role for accurate risk stratification and treatment management.

Research paper thumbnail of The prognostic impact of K-RAS mutations in adult acute myeloid leukemia patients treated with high-dose cytarabine

OncoTargets and Therapy, 2011

Background: Activating point mutation of the RAS gene has been generally accepted as an oncogenic... more Background: Activating 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. Objective: This 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 methods: The 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. Results: Mutations 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). Conclusion: It 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.