Overview of Myeloproliferative Neoplasms

Myeloproliferative disorders are a group of diseases morphologically linked by terminal myeloid cell expansion that frequently evolve from one clinical phenotype to another and eventually progress to acute myeloid leukemia. Diagnostic criteria for the Philadelphia chromosome –negative myeloproliferative neoplasms (MPNs) have been established by the World Health Organization and they are recognized as blood cancers. MPNs have a complex and incompletely understood pathogenesis that includes systemic inflammation, clonal hematopoiesis, and constitutive activation of the JAK-STAT pathway. Complications, such as thrombosis and progression to overt forms of myelofibrosis and acute leukemia, contribute significantly to morbidity and mortality of patients with MPN.
Source: Hematology/Oncology Clinics of North America - Category: Cancer & Oncology Authors: Source Type: research

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We analyzed the clinical characteristics, laboratory characteristics, cytogenetics, thromboembolism status, disease progression, and overall survival of 1537 Chinese MPN patients with the JAK2V617F mutation. The multivariate analysis indicated that age ≥60 years old, HCT ≥48%, at least one cardiovascular risk factor, history of thrombosis, and JAK2V617F allele burden (V617F%) ≥50% are risk factors for thrombosis of JAK2V617F‐mutated MPN. Our study suggested that for elderly patients with JAK2V617F‐mutated MPN and a history of thrombosis, reducingV617F%, controlling HCT, and mitigating cardiovascular risk ...
Source: Cancer Medicine - Category: Cancer & Oncology Authors: Tags: ORIGINAL RESEARCH Source Type: research
Conclusions The discovery of JAK2V617F mutation in BCR-ABL1-negative MPNs by four different international cooperative groups in 2005 (2–5) led to significant insights on the pathogenesis of these disorders. In fact, this mutation results in a gain-of-function with activation of cytokine and growth factor receptors, and thus of the downstream JAK-STAT pathway (79, 95–98). The JAK2 point mutation in exon 12, present in a small percentage of patients with PV, is able to induce the MPN phenotype through the same pathogenic mechanism (6, 7). In 2006 the MPLW515L/K was reported in ET and PMF patients (44, 45) and d...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research
This article reviews existing data on cytoreduction, evaluating hydroxyurea, interferons, and ruxolitinib in ET and PV. This review evaluates whether evidence supports a more liberal strategy of cytoreduction for all patients with ET and PV. PMID: 30545998 [PubMed - in process]
Source: Journal of the National Comprehensive Cancer Network : JNCCN - Category: Cancer & Oncology Tags: J Natl Compr Canc Netw Source Type: research
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