author_facet Ahangari, G.
Shamsodin, N.
Chavoshzadeh, Z.
Moghadam, K.A.
Ghavamzadeh, A.
Nazarian, S.H.
Ahangari, G.
Shamsodin, N.
Chavoshzadeh, Z.
Moghadam, K.A.
Ghavamzadeh, A.
Nazarian, S.H.
author Ahangari, G.
Shamsodin, N.
Chavoshzadeh, Z.
Moghadam, K.A.
Ghavamzadeh, A.
Nazarian, S.H.
spellingShingle Ahangari, G.
Shamsodin, N.
Chavoshzadeh, Z.
Moghadam, K.A.
Ghavamzadeh, A.
Nazarian, S.H.
European Journal of Inflammation
Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
General Medicine
Immunology
Immunology and Allergy
author_sort ahangari, g.
spelling Ahangari, G. Shamsodin, N. Chavoshzadeh, Z. Moghadam, K.A. Ghavamzadeh, A. Nazarian, S.H. 2058-7392 2058-7392 SAGE Publications General Medicine Immunology Immunology and Allergy http://dx.doi.org/10.1177/1721727x0800600204 <jats:p> Acute myeloblastic leukemia (AML) is characterized by uncontrolled proliferation with the bone marrow (BM) of malignant myeloid progenitors arrested in their maturation process and the egress of these abnormal cells into the circulation. There is evidence that neutrophil production is a balance between the proliferative action of granulocyte-colony-stimulating factor (G-CSF) and a negative feedback from mature neutrophils. Recently, there have been reports on mutations in neutrophil elastase (ELA2) gene in genomic DNA of cyclic neutropenia. These patients developed acute myeloblastic leukemia. Therefore, we hypothesized that elastase may play role in the abnormal AML. Peripheral blood was obtained from 42 patients with acute myeloblastic leukemia and 30 healthy individuals. Total RNA was isolated using RNA standard techniques from freshly separated cells by polymorphoprep. RNA was analyzed by employing PCR amplification of reverse transcribed using a total of ten specific primers. We amplified five exons of ELA2 gene separately and sequenced each exon. Mutational analysis was carried out by directed capillary sequencing method. We found no mutation in 42 Acute myeloblastic leukemia patients compared to healthy individuals. Interestingly, we found heterozygote 50% single nucleotide polymorphism (SNP) in exon II codon 44 of healthy individuals but not in AML patients. It was a silent mutation G to A substitution but no changes in amino acid sequences. The codon sequence was GCG that changed to GCA. </jats:p> Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia European Journal of Inflammation
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title Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_unstemmed Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_full Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_fullStr Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_full_unstemmed Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_short Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_sort elastase ii gene encoding as inflammatory molecules in acute myeloblastic leukemia
topic General Medicine
Immunology
Immunology and Allergy
url http://dx.doi.org/10.1177/1721727x0800600204
publishDate 2008
physical 73-79
description <jats:p> Acute myeloblastic leukemia (AML) is characterized by uncontrolled proliferation with the bone marrow (BM) of malignant myeloid progenitors arrested in their maturation process and the egress of these abnormal cells into the circulation. There is evidence that neutrophil production is a balance between the proliferative action of granulocyte-colony-stimulating factor (G-CSF) and a negative feedback from mature neutrophils. Recently, there have been reports on mutations in neutrophil elastase (ELA2) gene in genomic DNA of cyclic neutropenia. These patients developed acute myeloblastic leukemia. Therefore, we hypothesized that elastase may play role in the abnormal AML. Peripheral blood was obtained from 42 patients with acute myeloblastic leukemia and 30 healthy individuals. Total RNA was isolated using RNA standard techniques from freshly separated cells by polymorphoprep. RNA was analyzed by employing PCR amplification of reverse transcribed using a total of ten specific primers. We amplified five exons of ELA2 gene separately and sequenced each exon. Mutational analysis was carried out by directed capillary sequencing method. We found no mutation in 42 Acute myeloblastic leukemia patients compared to healthy individuals. Interestingly, we found heterozygote 50% single nucleotide polymorphism (SNP) in exon II codon 44 of healthy individuals but not in AML patients. It was a silent mutation G to A substitution but no changes in amino acid sequences. The codon sequence was GCG that changed to GCA. </jats:p>
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author Ahangari, G., Shamsodin, N., Chavoshzadeh, Z., Moghadam, K.A., Ghavamzadeh, A., Nazarian, S.H.
author_facet Ahangari, G., Shamsodin, N., Chavoshzadeh, Z., Moghadam, K.A., Ghavamzadeh, A., Nazarian, S.H., Ahangari, G., Shamsodin, N., Chavoshzadeh, Z., Moghadam, K.A., Ghavamzadeh, A., Nazarian, S.H.
author_sort ahangari, g.
container_issue 2
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container_title European Journal of Inflammation
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description <jats:p> Acute myeloblastic leukemia (AML) is characterized by uncontrolled proliferation with the bone marrow (BM) of malignant myeloid progenitors arrested in their maturation process and the egress of these abnormal cells into the circulation. There is evidence that neutrophil production is a balance between the proliferative action of granulocyte-colony-stimulating factor (G-CSF) and a negative feedback from mature neutrophils. Recently, there have been reports on mutations in neutrophil elastase (ELA2) gene in genomic DNA of cyclic neutropenia. These patients developed acute myeloblastic leukemia. Therefore, we hypothesized that elastase may play role in the abnormal AML. Peripheral blood was obtained from 42 patients with acute myeloblastic leukemia and 30 healthy individuals. Total RNA was isolated using RNA standard techniques from freshly separated cells by polymorphoprep. RNA was analyzed by employing PCR amplification of reverse transcribed using a total of ten specific primers. We amplified five exons of ELA2 gene separately and sequenced each exon. Mutational analysis was carried out by directed capillary sequencing method. We found no mutation in 42 Acute myeloblastic leukemia patients compared to healthy individuals. Interestingly, we found heterozygote 50% single nucleotide polymorphism (SNP) in exon II codon 44 of healthy individuals but not in AML patients. It was a silent mutation G to A substitution but no changes in amino acid sequences. The codon sequence was GCG that changed to GCA. </jats:p>
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spelling Ahangari, G. Shamsodin, N. Chavoshzadeh, Z. Moghadam, K.A. Ghavamzadeh, A. Nazarian, S.H. 2058-7392 2058-7392 SAGE Publications General Medicine Immunology Immunology and Allergy http://dx.doi.org/10.1177/1721727x0800600204 <jats:p> Acute myeloblastic leukemia (AML) is characterized by uncontrolled proliferation with the bone marrow (BM) of malignant myeloid progenitors arrested in their maturation process and the egress of these abnormal cells into the circulation. There is evidence that neutrophil production is a balance between the proliferative action of granulocyte-colony-stimulating factor (G-CSF) and a negative feedback from mature neutrophils. Recently, there have been reports on mutations in neutrophil elastase (ELA2) gene in genomic DNA of cyclic neutropenia. These patients developed acute myeloblastic leukemia. Therefore, we hypothesized that elastase may play role in the abnormal AML. Peripheral blood was obtained from 42 patients with acute myeloblastic leukemia and 30 healthy individuals. Total RNA was isolated using RNA standard techniques from freshly separated cells by polymorphoprep. RNA was analyzed by employing PCR amplification of reverse transcribed using a total of ten specific primers. We amplified five exons of ELA2 gene separately and sequenced each exon. Mutational analysis was carried out by directed capillary sequencing method. We found no mutation in 42 Acute myeloblastic leukemia patients compared to healthy individuals. Interestingly, we found heterozygote 50% single nucleotide polymorphism (SNP) in exon II codon 44 of healthy individuals but not in AML patients. It was a silent mutation G to A substitution but no changes in amino acid sequences. The codon sequence was GCG that changed to GCA. </jats:p> Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia European Journal of Inflammation
spellingShingle Ahangari, G., Shamsodin, N., Chavoshzadeh, Z., Moghadam, K.A., Ghavamzadeh, A., Nazarian, S.H., European Journal of Inflammation, Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia, General Medicine, Immunology, Immunology and Allergy
title Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_full Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_fullStr Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_full_unstemmed Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_short Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
title_sort elastase ii gene encoding as inflammatory molecules in acute myeloblastic leukemia
title_unstemmed Elastase II Gene Encoding as Inflammatory Molecules in Acute Myeloblastic Leukemia
topic General Medicine, Immunology, Immunology and Allergy
url http://dx.doi.org/10.1177/1721727x0800600204