Results 21 to 30 of about 44,548 (260)
Genetics of Myeloproliferative Neoplasms
Hematology/Oncology Clinics of North America, 2021 Myeloproliferative neoplasms are hematopoietic stem cell disorders based on somatic mutations in JAK2, calreticulin, or MPL activating JAK-STAT signaling. Modern sequencing efforts have revealed the genomic landscape of myeloproliferative neoplasms with additional genetic alterations mainly in epigenetic modifiers and splicing factors.
Jakub, Szybinski, Sara C, Meyer
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Epigenetics in Myeloproliferative Neoplasms [PDF]
Journal of Cellular and Molecular Medicine, 2017 AbstractA decade on from the description of JAK2 V617F, the MPNs are circumscribed by an increasingly intricate landscape. There is now evidence that they are likely the result of combined genetic dysregulation, with several mutated genes involved in the regulation of epigenetic mechanisms. Epigenetic changes are not due to a change in the DNA sequence
Suzanne McPherson +2 more
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Myelodysplastic/Myeloproliferative Neoplasms [PDF]
American Journal of Clinical Pathology, 2009 AbstractMyelodysplastic/myeloproliferative neoplasms (MDS/MPNs) are rare de novo myeloid neoplasms that exhibit hybrid dysplastic and proliferative features at presentation. This SHP/EAHP Workshop session was uniquely problematic owing to the overlap between MDS/MPNs and both chronic myeloproliferative neoplasms and myelodysplasia.
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The Thrombopoietin Receptor, MPL, Is a Therapeutic Target of Opportunity in the MPN
Frontiers in Oncology, 2021 The myeloproliferative neoplasms, polycythemia vera, essential thrombocytosis and primary myelofibrosis share driver mutations that either activate the thrombopoietin receptor, MPL, or indirectly activate it through mutations in the gene for JAK2, its ...
Jerry L. Spivak, Alison R. Moliterno
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Platelets as mediators of Thromboinflammation in chronic Myeloproliferative Neoplasms [PDF]
, 2019 Chronic myeloproliferative neoplasms (MPN) are stem cell disorders driven by mutations in JAK2, CALR, or MPL genes and characterized by myeloid proliferation and increased blood cell counts.
Heller, Paula Graciela +1 more
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The SMAC mimetic LCL-161 selectively targets JAK2V617F mutant cells. [PDF]
, 2020 Background:Evasion from programmed cell death is a hallmark of cancer and can be achieved in cancer cells by overexpression of inhibitor of apoptosis proteins (IAPs).
Craver, Brianna M +6 more
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Gaucher Disease and Myelofibrosis: A Combined Disease or a Misdiagnosis? [PDF]
, 2018 Background: Gaucher disease (GD) and primary myelofibrosis (PMF) share similar clinical and laboratory features, such as cytopenia, hepatosplenomegaly, and marrow fibrosis, often resulting in a misdiagnosis.
Cardarelli, L +5 more
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Breakthroughs in myeloproliferative neoplasms
Hematology, 2012 The discovery of the JAK2V617F mutation ushered the field of Philadelphia-negative myeloproliferative neoplasms (MPNs) into the era of targeted therapy. Currently, there are several JAK2 inhibitors in clinical trials for patients with MPNs, particularly for patients with myelofibrosis (MF).
Fabio P S, Santos, Srdan, Verstovsek
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Natural history of patients with non cirrhotic portal hypertension: Comparison with patients with compensated cirrhosis [PDF]
, 2018 Background. The knowledge of natural history of patients with portal hypertension (PH) not due to cirrhosis is less well known than that of cirrhotic patients. Aim.
Aprile, Francesca +7 more
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