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Chronic myeloproliferative neoplasm

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https://www.readbyqxmd.com/read/29239838/mediator-kinase-phosphorylation-of-stat1-s727-promotes-growth-of-neoplasms-with-jak-stat-activation
#1
Ioana I Nitulescu, Sara C Meyer, Qiang Jeremy Wen, John D Crispino, Madeleine E Lemieux, Ross L Levine, Henry E Pelish, Matthew D Shair
Constitutive JAK-STAT signaling drives the proliferation of most myeloproliferative neoplasms (MPN) and a subset of acute myeloid leukemia (AML), but persistence emerges with chronic exposure to JAK inhibitors. MPN and post-MPN AML are dependent on tyrosine phosphorylation of STATs, but the role of serine STAT1 phosphorylation remains unclear. We previously demonstrated that Mediator kinase inhibitor cortistatin A (CA) reduced proliferation of JAK2-mutant AML in vitro and in vivo and also suppressed CDK8-dependent phosphorylation of STAT1 at serine 727...
November 21, 2017: EBioMedicine
https://www.readbyqxmd.com/read/29228125/myeloid-neoplasms-following-solid-organ-transplantation-clinicopathologic-studies-of-23-cases
#2
Bin Wu, Kimberly Ingersoll, Rachel Jug, Lian-He Yang, Catherine Luedke, Amanda Lo, Pu Su, Xin Liu, Catherine Rehder, Jerald Gong, Chuanyi Mark Lu, Endi Wang
Objectives: Myeloid neoplasms (MNs) after solid organ transplant are rare, and their clinicopathologic features have not been well characterized. Methods: We retrospectively analyzed 23 such cases. Results: The ages ranged from 2 to 76 years, with a median of 59 years at the diagnosis. The median interval between the transplant and diagnosis was 56 months (range, 8-384 months). The transplanted organs included liver in five, kidney in six, lung in five, heart in six, and heart/lung in one case(s)...
December 7, 2017: American Journal of Clinical Pathology
https://www.readbyqxmd.com/read/29225884/setbp1-mutations-as-a-biomarker-for-myelodysplasia-myeloproliferative-neoplasm-overlap-syndrome
#3
REVIEW
Katherine Linder, Chaitanya Iragavarapu, Delong Liu
Myelodysplasia (MDS) /myeloproliferative neoplasm (MPN) overlap syndrome has been described since the 2001 WHO classification as disorders that have both proliferative and dysplastic changes simultaneously. Specific disorders include chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JMML), BCR-ABL negative atypical chronic myeloid leukemia (aCML) and unclassifiable MDS/MPN (MPN/MDS-U). Recurrent gene mutations in these conditions have been described. Among them, SETBP1 mutations have been identified in up to 32% of aCML, 24% of JMML, 18% of CMML and 10% of MDS/MPN-U patients...
2017: Biomarker Research
https://www.readbyqxmd.com/read/29225675/pregnancy-and-myeloproliferative-neoplasms-a-retrospective-monocentric-cohort
#4
Mathieu Puyade, Emilie Cayssials, Fabrice Pierre, Olivier Pourrat
Background: The most frequent myeloproliferative neoplasms are essential thrombocythemia and chronic myelogenous leukemia, which usually manifests with thrombocytosis. Only essential thrombocythemia is associated with morbidity during pregnancy (recurrent miscarriages, intrauterine fetal death, small for gestational age and preeclampsia). The aim of this paper is to describe outcomes of pregnancy in women with myeloproliferative neoplasms seen at a single academic institution. Methods: Data were collected retrospectively from 2002 to 2015...
December 2017: Obstetric Medicine
https://www.readbyqxmd.com/read/29222296/what-are-the-current-treatment-approaches-for-patients-with-polycythemia-vera-and-essential-thrombocythemia
#5
REVIEW
Alessandro M Vannucchi, Paola Guglielmelli
Polycythemia vera (PV) and essential thrombocythemia (ET) are chronic myeloproliferative neoplasms that are characterized by thrombohemorrhagic complications, symptom burden, and impaired survival mainly due to thrombosis, progression to myelofibrosis, and transformation to acute leukemia. In this manuscript, we will review the most recent changes in diagnostic criteria, the improvements in risk stratification, and the "state of the art" in the daily management of these disorders. The role of conventional therapies and novel agents, interferon α and the JAK2 inhibitor ruxolitinib, is critically discussed based on the results of a few basic randomized clinical studies...
December 8, 2017: Hematology—the Education Program of the American Society of Hematology
https://www.readbyqxmd.com/read/29194068/polycythemia-vera-and-essential-thrombocythemia-algorithmic-approach
#6
Alessandro M Vannucchi, Paola Guglielmelli, Ayalew Tefferi
PURPOSE OF REVIEW: To describe an algorithm-based approach, whenever available, to the diagnosis, the risk stratification criteria informing therapy and the current management of polycythemia vera and essential thrombocythemia. RECENT FINDINGS: Description of recurrent genetic abnormalities in driver genes, including Janus Kinase 2 (JAK2), myeloproliferative leukemia and calreticulin, a better appreciation of the key diagnostic role of bone marrow features, results of large epidemiologic studies and a few but landmark controlled clinical trials produced in the last decade, all resulted in a reappraisal of the approach to polycythemia vera and essential thrombocythemia...
November 30, 2017: Current Opinion in Hematology
https://www.readbyqxmd.com/read/29192651/myeloid-neoplasms-with-features-intermediate-between-primary-myelofibrosis-and-chronic-myelomonocytic-leukemia
#7
Jennifer Chapman, Julia T Geyer, Mahsa Khanlari, Adrienne Moul, Carmen Casas, Scot T Connor, Yao-Shan Fan, Justin M Watts, Ronan T Swords, Francisco Vega, Attilio Orazi
Monocytosis can develop during disease course in primary myelofibrosis simulating that seen in chronic myelomonocytic leukemia, and should not lead to disease reclassification. In contrast, at presentation, rare cases have clinical, morphologic, and molecular genetic features truly intermediate between primary myelofibrosis and chronic myelomonocytic leukemia. The taxonomy and natural history of these diseases are unclear. We identified cases which either: (1) fulfilled the 2008 World Health Organization criteria for primary myelofibrosis but had absolute monocytosis and, when available, chronic myelomonocytic leukemia-related mutations (ASXL1, SRSF2, TET2) or (2) fulfilled criteria of chronic myelomonocytic leukemia but had megakaryocytic proliferation and atypia, marrow fibrosis, and myeloproliferative-type driver mutations (JAK2, MPL, CALR)...
December 1, 2017: Modern Pathology: An Official Journal of the United States and Canadian Academy of Pathology, Inc
https://www.readbyqxmd.com/read/29185819/reversal-of-glanzmann-thrombasthenia-platelet-phenotype-after-imatinib-treatment-in-a-pediatric-chronic-myeloid-leukemia-patient
#8
Richa Chauhan, Sudha Sazawal, Kanwaljeet Singh, R Ragesh R Nair, Sunita Chhikara, Roopam Deka, Rekha Chaubey, Karthika Kundil Veetil, Prasad Dange, Manoranjan Mahapatra, Renu Saxena
Chronic Myelogenous Leukemia (CML) is a myeloproliferative neoplasm characterized by proliferation of Philadelphia positive clonal pluripotent hematopoietic cells. Bleeding is a rare presentation of CML that can occur due to platelet dysfunction. Both pre-treatment and post-treatment platelet function abnormalities in CML have been described in the literature. We describe a rare case of childhood CML who presented with mucocutateous bleeding manifestations. On laboratory workup, a Glanzmann Thrombasthenia (GT) like platelet phenotype was demonstrated along with confirmation of diagnosis of CML in chronic phase...
November 29, 2017: Platelets
https://www.readbyqxmd.com/read/29181334/inflammatory-signaling-pathways-in-preleukemic-and-leukemic-stem-cells
#9
REVIEW
Shayda Hemmati, Tamanna Haque, Kira Gritsman
Hematopoietic stem cells (HSCs) are a rare subset of bone marrow cells that usually exist in a quiescent state, only entering the cell cycle to replenish the blood compartment, thereby limiting the potential for errors in replication. Inflammatory signals that are released in response to environmental stressors, such as infection, trigger active cycling of HSCs. These inflammatory signals can also directly induce HSCs to release cytokines into the bone marrow environment, promoting myeloid differentiation. After stress myelopoiesis is triggered, HSCs require intracellular signaling programs to deactivate this response and return to steady state...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/29169164/a-novel-pcm1-pdgfrb-fusion-in-a-patient-with-a-chronic-myeloproliferative-neoplasm-and-an-ins-8-5
#10
Muna Ghazzawi, Varun Mehra, Marcin Knut, Loretta Brown, William Tapper, Andrew Chase, Hugues de Lavallade, Nicholas C P Cross
No abstract text is available yet for this article.
November 24, 2017: Acta Haematologica
https://www.readbyqxmd.com/read/29147619/the-jak2v617f-and-calr-exon-9-mutations-are-shared-immunogenic-neoantigens-in-hematological-malignancy
#11
Morten Orebo Holmström, Hans Carl Hasselbalch, Mads Hald Andersen
Approximately 90% of patients with the hematological malignancies termed the chronic myeloproliferative neoplasms harbor either the JAK2V617F-mutation or CALR exon 9 mutation. Both of these are recognized by T-cells, which make the mutations ideal targets for cancer immune therapy as they are shared antigens.
2017: Oncoimmunology
https://www.readbyqxmd.com/read/29124948/tasigna-nilotinib-in-chronic-myeloid-leukemia%C3%A2-treatment-free-remission-after-nearly-2%C3%A2-years-an-interview-with-adam-mead
#12
Adam Mead
Dr Mead earned his medical degree from the University of Oxford and trained in hematology at St Bartholomew's Hospital and University College London. In 2007, he earned his PhD at UCL, which focused on the analysis of FLT3 mutations in acute myeloid leukemia. He is now Associate Professor of Hematology and MRC Senior Clinical Fellow at the WIMM, University of Oxford. His research group focuses on myeloid diseases and normal blood stem-cell biology. Dr Mead is the lead clinician for myeloproliferative neoplasms (MPN) and chronic myeloid leukemia in the Thames Valley Strategic Clinical Network and is the chief investigator for several chronic myeloid leukemia and MPN clinical trials...
November 10, 2017: Future Oncology
https://www.readbyqxmd.com/read/29107666/jak2-mutated-langerhans-cell-histiocytosis-associated-with-primary-myelofibrosis-treated-with-ruxolitinib
#13
Arturo Bonometti, Filippo Bagnoli, Daniele Fanoni, Luigia Venegoni, Laura Corti, Paola Bianchi, Elena Maria Elli, Giuseppe Isimbaldi, Vincenzo L'Imperio, Gianluca Nazzaro, Emanuela Passoni, Emilio Berti
The pathogenesis and cellular origin of Langerhans cell histiocytosis (LCH) are debated. Recently, mutations on MAPK and PI3K pathways have been linked to disrupted cell proliferation in LCH. Janus Kinase 2 (JAK2) mutations play the same role in Philadelphia-negative chronic myeloproliferative neoplasms. We describe the case of a patient affected by JAK2-positive Primary Myelofibrosis (PMF) who developed a clonally related LCH while in treatment with Ruxolitinib. JAK-inhibitors are well known to affect function and differentiation of different hematological lineages, including mononuclear phagocytes precursors...
October 28, 2017: Human Pathology
https://www.readbyqxmd.com/read/29104287/risk-of-developing-chronic-myeloid-neoplasms-in-well-differentiated-thyroid-cancer-patients-treated-with-radioactive-iodine
#14
R J Molenaar, C Pleyer, T Radivoyevitch, S Sidana, A Godley, A S Advani, A T Gerds, H E Carraway, M Kalaycio, A Nazha, D Adelstein, C Nasr, D Angelini, J P Maciejewski, N Majhail, M A Sekeres, S Mukherjee
Exposure to ionizing radiation increases the risk of myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN), but such risks are not known in well-differentiated thyroid cancer (WDTC) patients treated with radioactive iodine (RAI). A total of 148 215 WDTC patients were identified from Surveillance Epidemiology and End Results (SEER) registries between 1973 and 2014, of whom 54% underwent definitive thyroidectomy and 46% received adjuvant RAI. With a median follow-up of 6.6 years, 77 and 66 WDTC patients developed MDS and MPN, respectively...
November 6, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/29075489/intravascular-large-b-cell-lymphoma-associated-with-myelofibrosis-a-case-report
#15
Jong Gwon Choi, Hwan Hwi Cho, Sang Rok Kang, Se Min Jang, Eun Hyung Yoo, Hyun Jung Cho, Sun Moon Kim, Do Yeun Cho
Myelofibrosis (MF) is often accompanied by chronic myeloid leukemia, hairy cell leukemia, or certain primary myeloproliferative neoplasms, but is rarely associated with lymphoid neoplasms. We herein describe a case of intravascular large B-cell lymphoma (IVLBCL) with MF. IVLBCL is a rare, aggressive type of extranodal B-cell lymphoma, defined by proliferation of lymphomatous cells within small-to medium-sized vessels. A 60-year-old woman was admitted to the hospital with anemia, thrombocytopenia and fever. Bone marrow biopsy findings included trilineage hematopoiesis, increased numbers of immature cells, markedly abnormal and enlarged megakaryocytes, and diffuse fibrosis in multiple focal areas throughout the entire bone marrow space...
November 2017: Molecular and Clinical Oncology
https://www.readbyqxmd.com/read/29075087/bcr-abl-and-jak2v617f-mutation-co-existence-rare-or-just-unexplored
#16
H S Darling, Rajiv Kumar, Rajan Kapoor, Jasjit Singh, Tarun Verma
Current hematology practice distinguishes chronic myeloid leukemia (CML) and other major chronic myeloproliferative neoplasms as different entities classically characterized by positivity of BCR-ABL fusion gene and JAK2V617F mutations. These are different in clinical presentation, molecular genetics, therapy and response to present treatments. Nevertheless, there have been occasional case reports of detection of both mutations in the same patient. Although some of these had been incidentally detected, most have manifested clinically while being treated for one disease...
December 2017: Indian Journal of Hematology & Blood Transfusion
https://www.readbyqxmd.com/read/29064026/models-of-prognostication-in-chronic-myelomonocytic-leukemia
#17
REVIEW
Francesco Onida
PURPOSE OF REVIEW: Within the group of the myelodysplastic/myeloproliferative overlap neoplasms of the adult age, chronic myelomonocytic leukemia (CMML) is characterized by an extremely variable clinical course. This review aims to cover over the years main advancements in the identification of CMML clinical and biological features associated to survival outcomes and the consequent development of prognostic tools for individual patient treatment decision making. RECENT FINDINGS: According to the last WHO classification of myeloid neoplasms, three subgroups of patients may be recognized on the base of percentage of blasts in marrow and in peripheral blood (CMML-0, CMML-1, and CMML-2), with corresponding decreasing life-expectations...
December 2017: Current Hematologic Malignancy Reports
https://www.readbyqxmd.com/read/29040257/current-challenges-in-the-management-of-essential-thrombocythemia
#18
Ariel Kleman, Arun K Singavi, Laura C Michaelis
Essential thrombocythemia (ET), an uncommon blood cancer, is one of the classic myeloproliferative neoplasms, a category that also includes polycythemia vera and primary myelofibrosis. All 3 diseases are clonal hematopoietic stem cell disorders. Since 2005, when scientists discovered a molecular aberration driving clonal hematopoiesis in polycythemia vera, our understanding of the genomic underpinnings of these conditions has increased rapidly. Over the last decades, primary prevention of thrombotic and hemorrhagic complications has improved the lives of patients with ET, and the ability to characterize the disease by the presence or absence of molecular mutations has lent precision to our prognostic models...
October 2017: Clinical Advances in Hematology & Oncology: H&O
https://www.readbyqxmd.com/read/29027642/familial-mpn-predisposition
#19
REVIEW
Tsewang Tashi, Sabina Swierczek, Josef T Prchal
Chronic myeloproliferative neoplasms (MPN) characteristically arise from a somatic mutation in the pluripotent hematopoietic stem cell, and most common recurring mutations are in the JAK2, CALR, and cMPL genes. However, these mutations are not founder mutations, but mainly drive the disease phenotype and a pre-existing germline predisposition has been long speculated, but has not been clearly defined to date. Genome-wide association studies in family clusters of MPN have identified a number of genetic variants that are associated with increased germline risk for developing clonal MPN...
October 2017: Current Hematologic Malignancy Reports
https://www.readbyqxmd.com/read/29027146/correction-to-jsh-guideline-for-tumors-of-hematopoietic-and-lymphoid-tissues-lukemia-4-chronic-myelogenous-leukemia-cml-myeloproliferative-neoplasms-mpn
#20
Noriko Usui
In the original publication of this article, the "Acknowledgements" was not included and it is given below for your reading.
October 12, 2017: International Journal of Hematology
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