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JAK2 in Myeloproliferative Neoplasms: Still a Protagonist [PDF]
Pharmaceuticals, 2022 The discovery of the activating V617F mutation in Janus kinase 2 (JAK2) has been decisive for the understanding of myeloproliferative neoplasms (MPN).
Sara C Meyer
exaly +3 more sources
Blood, 2010 The JAK2 V617F mutation is found in most patients with a myeloproliferative neoplasm and is sufficient to produce a myeloproliferative phenotype in murine retroviral transplantation or transgenic models.
Wendy Erber +2 more
exaly +2 more sources
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Medicina Clínica (English Edition), 2016
Pharmacological inhibition of the kinase activity of JAK proteins can interfere with the signaling of immunomodulatory cytokines and block the constitutive activation of the JAK-STAT pathway that characterizes certain malignancies, including chronic myeloproliferative neoplasms.
Juan Carlos, Hernández Boluda +2 more
openaire +4 more sources
Pharmacological inhibition of the kinase activity of JAK proteins can interfere with the signaling of immunomodulatory cytokines and block the constitutive activation of the JAK-STAT pathway that characterizes certain malignancies, including chronic myeloproliferative neoplasms.
Juan Carlos, Hernández Boluda +2 more
openaire +4 more sources
Mechanisms of Resistance to JAK2 Inhibitors in Myeloproliferative Neoplasms [PDF]
Hematology/Oncology Clinics of North America, 2017 Myeloproliferative neoplasms are driven by activated JAK2 signaling due to somatic mutations in JAK2, the thrombopoietin receptor MPL or the chaperone calreticulin in hematopoietic stem/progenitor cells.
Sara C Meyer
exaly +2 more sources
JAK2-mediated Intracellular Signaling
Current Molecular Medicine, 2021Janus kinase-2 (JAK2) is a non-receptor tyrosine kinase that serves key roles as the intracellular signaling effector of the cytokine receptor, such as mediating effects of leptin, erythropoietin, interferon, and growth hormone. A lot of molecular underlying mechanisms of JAK2 participation are known, however, additional signaling mechanisms of its ...
Mentor Sopjani +2 more
exaly +3 more sources
2021
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell (HSC) disorders with overproduction of mature myeloid blood cells, including essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF). In 2005, several groups identified a single gain-of-function point mutation JAK2V617F in the majority of MPN patients.
openaire +2 more sources
Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell (HSC) disorders with overproduction of mature myeloid blood cells, including essential thrombocythemia (ET), polycythemia vera (PV), and primary myelofibrosis (PMF). In 2005, several groups identified a single gain-of-function point mutation JAK2V617F in the majority of MPN patients.
openaire +2 more sources
Blood, 2013
Abstract Approximately 50% of myeloproliferative neoplasms (MPNs) harbor the JAK2 V617F mutation while approximately 50% of B-cell acute lymphoblastic leukemias (B-ALLs) with CRLF2 rearrangements harbor JAK2 exon 16 mutations that primarily involve R683.
Nadja Kopp +7 more
openaire +1 more source
Abstract Approximately 50% of myeloproliferative neoplasms (MPNs) harbor the JAK2 V617F mutation while approximately 50% of B-cell acute lymphoblastic leukemias (B-ALLs) with CRLF2 rearrangements harbor JAK2 exon 16 mutations that primarily involve R683.
Nadja Kopp +7 more
openaire +1 more source
JAK2 Inhibitors: A Reality? A Hope?
Clinical Lymphoma and Myeloma, 2009Myelofibrosis (MF; primary or post-polycythemia vera/essential thrombocythemia) carries the worst prognosis among BCR-ABL-negative myeloproliferative neoplasms (MPNs). Stem cell transplantation is the only curative approach but is hampered by significant nonrelapse mortality. Thus, effective, targeted therapies are needed.
Effrosyni, Apostolidou +2 more
openaire +2 more sources