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myeloprolifeative 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/29236390/serum-glycomarkers-of-endoplasmic-reticulum-and-lysosomal-endosomal-system-stress-in-human-healthy-aging-and-diseases
#2
I U Pismenetskaya, T D Butters
To verify the idea that extracellular free oligosaccharides might be able to reflect the functional status of the endoplasmic reticulum (ER) and lysosomal-endosomal system, HPLC-profiles of serum-derived free oligosaccharides (FOS) in human healthy aging, acute myeloproliferative neoplasms, and cardiovascular pathologies were compared with intracellular glycans. After plasma deproteinization and FOS purification the oligosaccharides were labelled with anthranilic acid, separated into the neutral and charged with QAE Sephadex (Q25-120) chromatography and analysed using high-performance liquid chromatography (HPLC)...
January 2017: Ukrainian Biochemical Journal
https://www.readbyqxmd.com/read/29235894/pacritinib-and-its-use-in-the-treatment-of-patients-with-myelofibrosis-who-have-thrombocytopenia
#3
Adolfo Enrique Diaz, Ruben A Mesa
The treatment landscape for myelofibrosis (MF) has reached the molecular era by targeting different pathways that are implied in this myeloproliferative neoplasm. A few years ago, the first-in-class JAK1/JAK2 inhibitor ruxolitinib, demonstrated reductions in both constitutional symptoms and splenomegaly, leading to the US FDA approval. The development or worsening of cytopenias in patients receiving ruxolitinib uncovered an unmet need that has been addressed by alternative approaches. Pacritinib, a dual JAK2 and FLT3 inhibitor which also inhibits IRAK1, has demonstrated the ability to favorably impact MF-associated splenomegaly and symptom burden, while having limited myelosuppression with manageable gastrointestinal toxicity...
December 13, 2017: Future Oncology
https://www.readbyqxmd.com/read/29228564/inhibitors-of-the-pi3k-mtor-pathway-prevent-stat5-phosphorylation-in-jak2v617f-mutated-cells-through-pp2a-cip2a-axis
#4
Niccolò Bartalucci, Laura Calabresi, Manjola Balliu, Serena Martinelli, Maria Caterina Rossi, Jean Luc Villeval, Francesco Annunziato, Paola Guglielmelli, Alessandro M Vannucchi
Inhibition of the constitutively activated JAK/STAT pathway in JAK2V617F mutated cells by the JAK1/JAK2 inhibitor ruxolitinib resulted in clinical benefits in patients with myeloproliferative neoplasms. However, evidence of disease-modifying effects remains scanty; furthermore, some patients do not respond adequately to ruxolitinib, or have transient responses, thus novel treatment strategies are needed. Here we demonstrate that ruxolitinib causes incomplete inhibition of STAT5 in JAK2V617F mutated cells due to persistence of phosphorylated serine residues of STAT5b, that conversely are targeted by PI3K and mTORC1 inhibitors...
November 14, 2017: Oncotarget
https://www.readbyqxmd.com/read/29228125/myeloid-neoplasms-following-solid-organ-transplantation-clinicopathologic-studies-of-23-cases
#5
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
#6
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
#7
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/29223988/prevalence-of-physical-problems-detected-by-the-distress-thermometer-and-problem-list-in-patients-with-myeloproliferative-disorders
#8
Daniel C McFarland, Kelly M Shaffer, Heather Polizzi, John Mascarenhas, Marina Kremyanskaya, Jimmie Holland, Ronald Hoffman
Background: Patients with myeloproliferative neoplasms (MPNs) can have a severe physical symptom burden over an extended disease trajectory that contributes to decreased quality of life. Few studies, however, have characterized which patients most frequently consider physical symptoms a problem. This study describes the physical symptoms of patients with MPNs and the relationship of these symptoms to patient characteristics. Methods: Patients with MPNs (N=117) completed questionnaires in a dedicated academic medical center MPN clinic...
December 2017: Journal of the National Comprehensive Cancer Network: JNCCN
https://www.readbyqxmd.com/read/29222296/what-are-the-current-treatment-approaches-for-patients-with-polycythemia-vera-and-essential-thrombocythemia
#9
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/29222295/myeloproliferative-neoplasms-from-origins-to-outcomes
#10
REVIEW
Jyoti Nangalia, Anthony R Green
Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations in JAK2 over a decade ago heralded a new age for patient care as a consequence of improved diagnosis and the development of therapeutic JAK inhibitors. The more recent identification of mutations in calreticulin brought with it a sense of completeness, with most patients with myeloproliferative neoplasm now having a biological basis for their excessive myeloproliferation...
December 8, 2017: Hematology—the Education Program of the American Society of Hematology
https://www.readbyqxmd.com/read/29217833/calr-mutational-status-identifies-different-disease-subtypes-of-essential-thrombocythemia-showing-distinct-expression-profiles
#11
Roberta Zini, Paola Guglielmelli, Daniela Pietra, Elisa Rumi, Chiara Rossi, Sebastiano Rontauroli, Elena Genovese, Tiziana Fanelli, Laura Calabresi, Elisa Bianchi, Simona Salati, Mario Cazzola, Enrico Tagliafico, Alessandro M Vannucchi, Rossella Manfredini
Polycythemia vera (PV) and essential thrombocythemia (ET) are Philadelphia-negative myeloproliferative neoplasms (MPNs) characterized by erythrocytosis and thrombocytosis, respectively. Approximately 95% of PV and 50-70% of ET patients harbor the V617F mutation in the exon 14 of JAK2 gene, while about 20-30% of ET patients carry CALRins5 or CALRdel52 mutations. These ET CALR-mutated subjects show higher platelet count and lower thrombotic risk compared to JAK2-mutated patients. Here, we showed that CALR-mutated and JAK2V617F-positive CD34+ cells display different gene and miRNA expression profiles...
December 8, 2017: Blood Cancer Journal
https://www.readbyqxmd.com/read/29217781/benefits-and-pitfalls-of-peg-interferon-%C3%AE-2a-therapy-in-patients-with-myeloproliferative-neoplasm-associated-myelofibrosis-a-french-intergroup-of-myeloproliferative-neoplasms-fim-study
#12
Jean-Christophe Ianotto, Aurélie Chauveau, Françoise Boyer-Perrard, Emmanuel Gyan, Kamel Laribi, Pascale Cony-Makhoul, Jean-Loup Demory, Benoit de Renzis, Christine Dosquet, Jerome Rey, Lydia Roy, Brigitte Dupriez, Laurent Knoops, Laurence Legros, Mohamed Malou, Pascal Hutin, Dana Ranta, Omar Benbrahim, Valérie Ugo, Eric Lippert, Jean-Jacques Kiladjian
We have previously described the safety and efficacy of pegylated interferon-α2a therapy in a cohort of sixty-two patients with myeloproliferative neoplasm-associated myelofibrosis followed in centers affiliated to the French Intergroup of Myeloproliferative neoplasms. In this study, we report their long-term outcomes and correlations with mutational patterns of driver and non-driver mutations analyzed by targeted next generation sequencing. The median age at diagnosis was 66 years-old, the median follow-up since pegylated interferon initiation was 58 months...
December 7, 2017: Haematologica
https://www.readbyqxmd.com/read/29214759/clinical-implications-of-quantitative-jak2-v617f-analysis-using-droplet-digital-pcr-in-myeloproliferative-neoplasms
#13
Eunyoung Lee, Kyoung Joo Lee, Hyein Park, Jin Young Chung, Mi Na Lee, Myung Hee Chang, Jongha Yoo, Hyewon Lee, Sun Young Kong, Hyeon Seok Eom
BACKGROUND: JAK2 V617F is the most common mutation in myeloproliferative neoplasms (MPNs) and is a major diagnostic criterion. Mutation quantification is useful for classifying patients with MPN into subgroups and for prognostic prediction. Droplet digital PCR (ddPCR) can provide accurate and reproducible quantitative analysis of DNA. This study was designed to verify the correlation of ddPCR with pyrosequencing results in the diagnosis of MPN and to investigate clinical implications of the mutational burden...
March 2018: Annals of Laboratory Medicine
https://www.readbyqxmd.com/read/29212804/myeloproliferative-neoplasms-from-origins-to-outcomes
#14
REVIEW
Jyoti Nangalia, Anthony R Green
Substantial progress has been made in our understanding of the pathogenetic basis of myeloproliferative neoplasms. The discovery of mutations in JAK2 over a decade ago heralded a new age for patient care as a consequence of improved diagnosis and the development of therapeutic JAK inhibitors. The more recent identification of mutations in calreticulin brought with it a sense of completeness, with most patients with myeloproliferative neoplasm now having a biological basis for their excessive myeloproliferation...
December 7, 2017: Blood
https://www.readbyqxmd.com/read/29202466/loss-of-pleckstrin-2-reverts-lethality-and-vascular-occlusions-in-jak2v617f-positive-myeloproliferative-neoplasms
#15
Baobing Zhao, Yang Mei, Lan Cao, Jingxin Zhang, Ronen Sumagin, Jing Yang, Juehua Gao, Matthew J Schipma, Yanfeng Wang, Chelsea Thorsheim, Liang Zhao, Timothy Stalker, Brady Stein, Qiang Jeremy Wen, John D Crispino, Charles S Abrams, Peng Ji
V617F driver mutation of JAK2 is the leading cause of the Philadelphia-chromosome-negative myeloproliferative neoplasms (MPNs). Although thrombosis is a leading cause of mortality and morbidity in MPNs, the mechanisms underlying their pathogenesis are unclear. Here, we identified pleckstrin-2 (Plek2) as a downstream target of the JAK2/STAT5 pathway in erythroid and myeloid cells, and showed that it is upregulated in a JAK2V617F-positive MPN mouse model and in patients with MPNs. Loss of Plek2 ameliorated JAK2V617F-induced myeloproliferative phenotypes including erythrocytosis, neutrophilia, thrombocytosis, and splenomegaly, thereby reverting the widespread vascular occlusions and lethality in JAK2V617F-knockin mice...
November 20, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/29202299/repression-of-interferon-%C3%AE-regulated-cytokines-by-the-jak1-2-inhibitor-ruxolitinib-in-inflammatory-human-macrophages
#16
Marie Febvre-James, Valérie Lecureur, Yu Augagneur, Abdullah Mayati, Olivier Fardel
Ruxolitinib is a Janus kinase (JAK) 1/2 inhibitor, currently used in the treatment of myeloproliferative neoplasms. It exerts potent anti-inflammatory activity, but the involved molecular and cellular mechanisms remain poorly understood. In order to gain insights about this point, ruxolitinib effects towards expression of main inflammatory cytokines were studied in human macrophages, which constitute a key-cell type implicated in inflammation. Analysis of mRNA expression of cytokines (n=84) by PCR array indicated that, among those induced by the pro-inflammatory stimulus lipopolysaccharide (LPS) (n=44), 61...
December 1, 2017: International Immunopharmacology
https://www.readbyqxmd.com/read/29199511/clonogenic-versus-morphogenic-mutations-in-myeloid-neoplasms-chronologic-observations-in-a-u2af1-tet2-csf3r-and-jak2-co-mutated-myeloproliferative-neoplasm-suggest-a-hierarchical-order-of-mutations-and-potential-predictive-value-for-kinase-inhibitor-treatment
#17
Magdalena M Gerlach, Pontus Lundberg, Joerg Halter, Christian Arranto, Friedel Wenzel, Stefan Dirnhofer, Alexandar Tzankov
No abstract text is available yet for this article.
December 3, 2017: Leukemia & Lymphoma
https://www.readbyqxmd.com/read/29194068/polycythemia-vera-and-essential-thrombocythemia-algorithmic-approach
#18
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
#19
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
#20
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
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