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SOHO state-of-the-art update and next questions: MPN

The discovery of the activating JAK2V617F mutation in 2005 in the majority of patients with the classic Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) spurred intense interest in research into these disorders, culminating in the identification of activating mutations in MPL in 2006 and indels in CALR in 2013, thus providing additional mechanistic explanations for the universal activation of Janus kinase-signal transducer and activator of transcription (JAK-STAT) observed in these conditions, and the success of the JAK1/2 inhibitor ruxolitinib, which first received regulatory approval in 2011.
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Tags: Review Article Source Type: research

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Publication date: Available online 2 December 2017 Source:Clinical Lymphoma Myeloma and Leukemia Author(s): Prithviraj Bose, Jason Gotlib, Claire N. Harrison, Srdan Verstovsek The discovery of the activating JAK2 V617F mutation in 2005 in the majority of patients with the classic Philadelphia chromosome-negative myeloproliferative neoplasms (MPN) spurred intense interest in research into these disorders, culminating in the identification of activating mutations in MPL in 2006 and indels in CALR in 2013, thus providing additional mechanistic explanations for the universal activation of Janus kinase-signal transducer and ac...
Source: Clinical Lymphoma Myeloma and Leukemia - Category: Cancer & Oncology Source Type: research
Racial and ethnic disparities in patients with solid malignancies have been well documented. Less is known about these disparities in patients with hematologic malignancies. With the advent of novel chemotherapeutics and targeted molecular, cellular, and immunologic therapies, it is important to identify differences in care that may lead to disparate outcomes. This review provides a critical appraisal of the empirical research on racial and ethnic disparities in incidence, survival, and outcomes in patients with hematologic malignancies. The review focuses on patients with acute myeloid leukemia, acute lymphocytic leukemia...
Source: Blood - Category: Hematology Authors: Tags: Myeloid Neoplasia, Lymphoid Neoplasia, Review Articles, Clinical Trials and Observations Source Type: research
Patients with accelerated phase (AP) myelofibrosis (MF;>10% blasts in bone marrow [BM] or peripheral blood [PB]) have shorter overall survival (OS) than those in the chronic phase (
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Tags: Myeloproliferative Neoplasms Source Type: research
Clinical, cytogenetic, and gene-based studies have been used to inform biology and improve prognostication for patients with acute myeloid leukemia (AML), myelodysplasia (MDS), and myeloproliferative neoplasms (MPN). Most recently, a series of candidate gene and whole genome studies have identified recurrent somatic mutations in AML patients including TET2, ASXL1, DNMT3A, and cohesin complex mutations. Moreover, these mutations can be used to improve risk stratification in AML independent of established clinical parameters.
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
The 2016 multiparameter WHO (World Health Organization) classification for Philadelphia-negative myeloproliferative neoplasms (MPNs) integrates clinical features, morphology and genetic data to diagnose polycythemia vera (PV), essential thrombocythemia (ET) and primary myelofibrosis (PMF), now subgrouped into prefibrotic PMF and overt PMF.1
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
The molecular basis of myeloproliferative neoplasms (MPN) has been defined in almost all cases. In greater than 95% of cases of MPN the mutations that drive the development of an MPN phenotype are accounted for by somatic mutations in three genes: JAK2, CALR or MPL, and notably these mutations occur in a mutually exclusive manner1. Mutations in JAK2 and MPL occur as gain-of-function point mutations (i.e. JAK2V617F and MPLW515L/K respectively), while the mutations in CALR occur as +1 base pair frameshifts in the last coding exon of CALR, which result in the generation of a novel C-terminus1,2.
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
Chronic Myelomonocytic Leukemia (CMML) is a lethal myeloid neoplasm with no therapies that improve its dismal natural history. CMML is characterized by peripheral monocytosis, bone marrow dysplasia, and a propensity for AML transformation. CMML has long been classified as a subtype of the Myelodysplastic Syndromes (MDS) until 2008 when the World Health Organization (WHO) consolidated a group of diseases, including CMML, into a new category known as Myelodysplastic/Myeloproliferative Neoplasms (MDS/MPNs)1.
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
Are the myeloid malignancies leading the way, based on our ability to easily obtain tumor tissue and success in CML, or are they following, given the use of multi-gene panels to treat upfront advanced lung cancer and the remarkable outcomes using check point inhibitors to treat formerly intractable solid tumors? Past achievements in the leukemias have been impressive but incomplete. In chronic phase CML we have essentially curative treatments; in myeloproliferative neoplasms we know the mutations but possess only partially effective therapies; and in myelodysplastic syndrome many mutations have been described but effective...
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
The BCR/ABL-negative myeloproliferative neoplasms (MPNs) include essential thrombocytosis, polycythemia vera, and myelofibrosis. Leukemic transformation (LT) of MPNs carries a particularly dismal prognosis, with a median survival of less than 6 months. Despite outcomes that are much worse than many other subtypes of acute myeloid leukemia (AML), most patients with LT are treated with standard induction chemotherapy with minimal benefit. Given the marked disparities in outcomes with induction chemotherapy between de novo AML and LT, it is critical to understand the biologic and genomic factors which differentiate LT from de...
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
In myeloproliferative neoplasms with myelofibrosis (MPN-MF) transformation to AML (sAML) occurs in up to 20% of patients. Ruxolitinib (R) is a type I, JAK1&2 inhibitor (JAKi) which is effective in the therapy of MPN-MF but not post-MPN sAML.
Source: Clinical Lymphoma, Myeloma and Leukemia - Category: Hematology Authors: Source Type: research
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