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Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

Antineoplastic effects of pharmacological inhibitors of aurora kinases in CSF3R < sup > T618I < /sup > -driven cells
Blood Cells Mol Dis. 2023 Oct 9;104:102799. doi: 10.1016/j.bcmd.2023.102799. Online ahead of print.ABSTRACTMyeloproliferative neoplasms (MPN) are consolidated as a relevant group of diseases derived from the malfunction of the hematopoiesis process and have as a particular attribute the increased proliferation of myeloid lineage. Among these, chronic neutrophilic leukemia (CNL) is distinguished, caused by the T618I mutation of the CSF3R gene, a trait that generates ligand-independent receptor activation and downstream JAK2/STAT signaling. Previous studies reported that mutations in BCR::ABL1 and JAK2V617F increased the exp...
Source: Blood Cells, Molecules and Diseases - October 15, 2023 Category: Hematology Authors: Nat ália Sudan Parducci Anali Del Milagro Bernabe Garnique Keli Lima Jorge Antonio Elias Godoy Carlos Natasha Peixoto Fonseca L ívia Bassani Lins de Miranda Bruna Oliveira de Almeida Eduardo Magalh ães Rego Fabiola Traina Jo ão Agostinho Machado-Neto Source Type: research

First report of a patient with homozygous hemoglobin Ernz: Evidence to support a non-pathogenic variant
Blood Cells Mol Dis. 2023 Sep 29;104:102797. doi: 10.1016/j.bcmd.2023.102797. Online ahead of print.ABSTRACTHemoglobin Ernz (Hb Ernz) is a missense variant in β-globin caused by a Threonine to Asparagine substitution at the 123rd amino acid position and HBB c.371C > A in gene level. Hb Ernz has been classified as Uncertain Significance (VUS) by ACMG due to limited reports and the absence of any homozygote genotypes. In our study, we found eight cases of Hb Ernz by DNA sequencing of the β-globin gene during >20 years of Thalassemia Screening in individuals with borderline hematological parameters who were possible c...
Source: Blood Cells, Molecules and Diseases - October 12, 2023 Category: Hematology Authors: Zohreh Shojaei Maryam Abiri Fatemeh Zafarghandi Motlagh Masoume Amini Samira Dabbagh Bagheri Sadaf Asnavandi Sedighe Asadi Hamideh Bagherian Sirous Zeinali Source Type: research

First report of a patient with homozygous hemoglobin Ernz: Evidence to support a non-pathogenic variant
Blood Cells Mol Dis. 2023 Sep 29;104:102797. doi: 10.1016/j.bcmd.2023.102797. Online ahead of print.ABSTRACTHemoglobin Ernz (Hb Ernz) is a missense variant in β-globin caused by a Threonine to Asparagine substitution at the 123rd amino acid position and HBB c.371C > A in gene level. Hb Ernz has been classified as Uncertain Significance (VUS) by ACMG due to limited reports and the absence of any homozygote genotypes. In our study, we found eight cases of Hb Ernz by DNA sequencing of the β-globin gene during >20 years of Thalassemia Screening in individuals with borderline hematological parameters who were possible c...
Source: Blood Cells, Molecules and Diseases - October 12, 2023 Category: Hematology Authors: Zohreh Shojaei Maryam Abiri Fatemeh Zafarghandi Motlagh Masoume Amini Samira Dabbagh Bagheri Sadaf Asnavandi Sedighe Asadi Hamideh Bagherian Sirous Zeinali Source Type: research