Database : MEDLINE
Search on : Myeloproliferative and Disorders [Words]
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[PMID]: 27773925
[Au] Autor:Visconte V; Przychodzen B; Han Y; Nawrocki ST; Thota S; Kelly KR; Patel BJ; Hirsch C; Advani AS; Carraway HE; Sekeres MA; Maciejewski JP; Carew JS
[Ad] Address:Department of Translational Hematology and Oncology Research, Taussig Cancer Institute, Cleveland Clinic, Cleveland, OH, USA.
[Ti] Title:Complete mutational spectrum of the autophagy interactome: a novel class of tumor suppressor genes in myeloid neoplasms.
[So] Source:Leukemia;31(2):505-510, 2017 02.
[Is] ISSN:1476-5551
[Cp] Country of publication:England
[La] Language:eng
[Mh] MeSH terms primary: Autophagy/genetics
Bone Marrow Neoplasms/genetics
Mutation
[Mh] MeSH terms secundary: Genes, Tumor Suppressor
Humans
Myeloproliferative Disorders/genetics
[Pt] Publication type:LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1709
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[Js] Journal subset:IM
[Da] Date of entry for processing:161025
[St] Status:MEDLINE
[do] DOI:10.1038/leu.2016.295

  2 / 7618 MEDLINE  
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[PMID]: 29516275
[Au] Autor:Spivak JL
[Ad] Address:Hematology Division, Department of Medicine, Johns Hopkins University School of Medicine, Traylor 924, 720 Rutland Avenue, Baltimore, MD, 21205, USA. jlspivak@jhmi.edu.
[Ti] Title:Polycythemia Vera.
[So] Source:Curr Treat Options Oncol;19(2):12, 2018 Mar 07.
[Is] ISSN:1534-6277
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OPINION STATEMENT: Polycythemia vera (PV) is the most common myeloproliferative neoplasm (MPN), the ultimate phenotype of the JAK2 V1617F mutation, the MPN with the highest incidence of thromboembolic complications, which usually occur early in the course of the disease, and the only MPN in which erythrocytosis occurs. The classical presentation of PV is characterized by erythrocytosis, leukocytosis, and thrombocytosis, often with splenomegaly and occasionally with myelofibrosis, but it can also present as isolated erythrocytosis with or without splenomegaly, isolated thrombocytosis or isolated leukocytosis, or any combination of these. When PV is present, the peripheral blood hematocrit (or hemoglobin) determination will not accurately represent the actual volume of red cells in the body, because in PV, in contrast to other disorders causing erythrocytosis, when the red cell mass increases, the plasma volume usually increases. In fact, unless the hematocrit is greater than 59%, true erythrocytosis cannot be distinguished from pseudoerythrocytosis due to plasma volume contraction. Usually, the presence of splenomegaly or leukocytosis or thrombocytosis establishes the diagnosis. However, when a patient presents with isolated thrombocytosis and a positive JAK2 V617F assay, particularly a young woman, the possibility of PV must always be considered because of plasma volume expansion. The WHO PV diagnostic guidelines are not helpful in this situation, since the hematocrit is invariably normal and a bone marrow examination will not distinguish ET from PV. Only a direct measurement of both the red cell mass and plasma volume can establish the correct diagnosis. In managing a PV patient, it is important to remember that PV is an indolent disorder in which life span is usually measured in decades, even when myelofibrosis is present, that chemotherapy is futile in eradicating the disease but does increase the incidence of acute leukemia and that hydroxyurea is not safe in this regard nor is it antithrombotic. Phlebotomy to a sex-specific normal hematocrit is the cornerstone of therapy and there now exist safe remedies for controlling leukocytosis, thrombocytosis, and extramedullary hematopoiesis and symptoms due to inflammatory cytokines when this is necessary.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1007/s11864-018-0529-x

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[PMID]: 29378171
[Au] Autor:Kim SY; Park Y; Kim H; Kim J; Kwon GC; Koo SH
[Ad] Address:Department of Laboratory Medicine, Chungnam National University School of Medicine, Chungnam National University Hospital, Daejeon, Republic of Korea; Cancer Research Institute, Chungnam National University School of Medicine, Daejeon, Republic of Korea. Electronic address: ksuny55@cnu.ac.kr.
[Ti] Title:Discriminating myelodysplastic syndrome and other myeloid malignancies from non-clonal disorders by multiparametric analysis of automated cell data.
[So] Source:Clin Chim Acta;480:56-64, 2018 Jan 31.
[Is] ISSN:1873-3492
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: We investigated the usefulness of novel complete blood count (CBC) data for discriminating myeloid malignancies from non-clonal CBC abnormalities. METHODS: Data were obtained during routine CBC tests of 119 samples from 37 myelodysplastic syndrome (MDS) patients, 92 samples from 45 myeloproliferative neoplasm (MPN) patients, and 15 samples from 11 chronic myelogenous leukemia (CML) patients using a DxH800 (Beckman Coulter). Data obtained from patients with hypocellular bone marrow and from those with other non-clonal diseases with CBC abnormalities were included in the comparisons. RESULTS: For cell population data of neutrophils, the means of median, upper median, lower median, and low angle light scatters were significantly lower in MDS patients than in patients without hematological malignancies. Low hemoglobin density (LHD) did not significantly differ between the MDS and non-clonal cytopenia patients, but it was significantly higher in the MPN and CML patients. We selected 13 parameters and scored the MDS diagnosis using cut-off values obtained from receiver operating characteristic (ROC) curve analysis. Using a score > 9, MDS was distinguished from non-clonal cytopenia with a sensitivity of 92.4% and a specificity of 85.4%. CONCLUSIONS: Multiparametric analyses of new automated parameters are useful for discriminating MDS from non-clonal cytopenia.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher

  4 / 7618 MEDLINE  
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[PMID]: 29486661
[Au] Autor:Umino K; Fujiwara SI; Ikeda T; Toda Y; Ito S; Mashima K; Minakata D; Nakano H; Yamasaki R; Kawasaki Y; Sugimoto M; Yamamoto C; Ashizawa M; Hatano K; Sato K; Oh I; Ohmine K; Muroi K; Kanda Y
[Ad] Address:a Division of Hematology, Department of Medicine , Jichi Medical University , Tochigi , Japan.
[Ti] Title:Clinical outcomes of myeloid/lymphoid neoplasms with fibroblast growth factor receptor-1 (FGFR1) rearrangement.
[So] Source:Hematology;:1-8, 2018 Feb 28.
[Is] ISSN:1607-8454
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Myeloid/lymphoid neoplasms with fibroblast growth factor receptor-1 (FGFR1) rearrangement are hematopoietic stem cell disorders with a poor prognosis, but no established standard therapy. METHODS: We experienced a patient with T-lymphoblastic lymphoma (LBL) associated with FGFR1 rearrangement who underwent cord blood transplantation, but died of pulmonary complication. We collected the clinical data of patients with FGFR1 rearrangement from the medical literature and analyzed 45 patients, including our patient. RESULTS: The primary diagnoses were myeloproliferative neoplasm (MPN) or myelodysplastic syndromes (MDS) in 14 and acute leukemia or LBL in 31. In MPN and MDS patients, the cumulative incidence of transformation to blast phase (BP) at 12 months was 46.2%. The 1-year overall survival (OS) from diagnosis in all cases was 43.1%. With regard to the impact of treatment response on survival, the achievement of complete response with a landmark at 2 months after diagnosis of BP was associated with a superior OS (40.0% vs. 26.0% P = 0.011 for 1-year OS from BP). Allogeneic hematopoietic stem cell transplantation (HSCT) was performed in 13 patients, and the 1-year OS from allogeneic HSCT was 61.5%. The hazard ratio for mortality was 0.34 (95% CI, 0.08-1.51, P = 0.15) for allogeneic HSCT treated as a time-dependent covariate, which suggests that allogeneic HSCT may confer a clinical benefit. CONCLUSION: The further accumulation of clinical data is needed to determine the optimal therapeutic approach for these neoplasms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180228
[Lr] Last revision date:180228
[St] Status:Publisher
[do] DOI:10.1080/10245332.2018.1446279

  5 / 7618 MEDLINE  
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[PMID]: 29400094
[Au] Autor:Ling T; Crispino JD; Zingariello M; Martelli F; Migliaccio AR
[Ad] Address:a Division of Hematology/Oncology , Northwestern University , Chicago , IL , USA.
[Ti] Title:GATA1 insufficiencies in primary myelofibrosis and other hematopoietic disorders: consequences for therapy.
[So] Source:Expert Rev Hematol;11(3):169-184, 2018 Mar.
[Is] ISSN:1747-4094
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:INTRODUCTION: GATA1, the founding member of a family of transcription factors, plays important roles in the development of hematopoietic cells of several lineages. Although loss of GATA1 has been known to impair hematopoiesis in animal models for nearly 25 years, the link between GATA1 defects and human blood diseases has only recently been realized. Areas covered: Here the current understanding of the functions of GATA1 in normal hematopoiesis and how it is altered in disease is reviewed. GATA1 is indispensable mainly for erythroid and megakaryocyte differentiation. In erythroid cells, GATA1 regulates early stages of differentiation, and its deficiency results in apoptosis. In megakaryocytes, GATA1 controls terminal maturation and its deficiency induces proliferation. GATA1 alterations are often found in diseases involving these two lineages, such as congenital erythroid and/or megakaryocyte deficiencies, including Diamond Blackfan Anemia (DBA), and acquired neoplasms, such as acute megakaryocytic leukemia (AMKL) and the myeloproliferative neoplasms (MPNs). Expert commentary: Since the first discovery of GATA1 mutations in AMKL, the number of diseases that are associated with impaired GATA1 function has increased to include DBA and MPNs. With respect to the latter, we are only just now appreciating the link between enhanced JAK/STAT signaling, GATA1 deficiency and disease pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:In-Data-Review
[do] DOI:10.1080/17474086.2018.1436965

  6 / 7618 MEDLINE  
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[PMID]: 29299961
[Au] Autor:Klein-Weigel PF; Volz TS; Richter JG
[Ad] Address:1 Klinik für Angiologie, Helios Klinik Berlin-Buch, Berlin, Germany.
[Ti] Title:Erythromelalgia.
[So] Source:Vasa;47(2):91-97, 2018 Feb.
[Is] ISSN:0301-1526
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Erythromelalgia is a rare syndrome characterized by the intermittent or, less commonly, by the permanent occurrence of extremely painful hyperperfused skin areas mainly located in the distal extremities. Primary erythromelalgia is nowadays considered to be a genetically determined neuropathic disorder affecting SCN9A, SCN10A, and SCN11A coding for NaV1.7, NaV1.8, and NaV1.9 neuronal sodium channels. Secondary forms might be associated with myeloproliferative disorders, connective tissue disease, cancer, infections, and poisoning. Between the pain episodes, the affected skin areas are usually asymptomatic, but there are patients with typical features of acrocyanosis and/or Raynaud's phenomenon preceding or occurring in between the episodes of erythromelalgia. Diagnosis is made by ascertaining the typical clinical features. Thereafter, the differentiation between primary and secondary forms should be made. Genetic testing is recommended, especially in premature cases and in cases of family clustering in specialized genetic institutions after genetic counselling. Multimodal therapeutic intervention aims toward attenuation of pain and improvement of the patient's quality of life. For this purpose, a wide variety of nonpharmacological approaches and pharmacological substances for topical and systemic use have been proposed, which are usually applied individually in a step-by-step approach. Prognosis mainly depends on the underlying condition and the ability of the patients and their relatives to cope with the disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[St] Status:In-Data-Review
[do] DOI:10.1024/0301-1526/a000675

  7 / 7618 MEDLINE  
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[PMID]: 29454474
[Au] Autor:Medeiros BC; Possick J; Fradley M
[Ad] Address:Stanford University School of Medicine, 875 Blake Wilbur Drive, Stanford, CA, USA. Electronic address: brunom@stanford.edu.
[Ti] Title:Cardiovascular, pulmonary, and metabolic toxicities complicating tyrosine kinase inhibitor therapy in chronic myeloid leukemia: Strategies for monitoring, detecting, and managing.
[So] Source:Blood Rev;, 2018 Feb 03.
[Is] ISSN:1532-1681
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm, the incidence of which increases with age. Tyrosine kinase inhibitors (TKIs) are the mainstay of CML treatment, including imatinib, nilotinib, dasatinib, bosutinib, and ponatinib. Beyond matching patient disease profiles with TKI specificity, differences in the efficacy and toxicity profiles and a patient's comorbid risk factors should be considered when selecting the most appropriate agent. Our objectives are to review the incidence and severity of cardiovascular, metabolic, and pulmonary disorders associated with these TKIs, highlighting differences in adverse event profiles, suggested risk-mitigation strategies, and guidance for TKI selection in different settings. Patients receiving TKI agents for CML should be monitored for signs and symptoms of toxicity throughout therapy. Preemptive assessment, early toxicity recognition, and prompt management of cardiovascular, metabolic, and pulmonary toxicities can minimize treatment-limiting complications and improve outcomes in patients with CML.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1802
[Cu] Class update date: 180218
[Lr] Last revision date:180218
[St] Status:Publisher

  8 / 7618 MEDLINE  
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[PMID]: 29447639
[Au] Autor:Neill B; Ryser T; Neill J; Aires D; Rajpara A
[Ti] Title:A patient case highlighting the myriad of cutaneous adverse effects of prolonged use of hydroxyurea.
[So] Source:Dermatol Online J;23(11), 2017 Nov 15.
[Is] ISSN:1087-2108
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Hydroxyurea is an antimetabolite primarily used to treat myeloproliferative disorders, and chronic treatment is associated with many cutaneous adverse effects ranging in severity from ichthyosis to aggressive nonmelanoma skin cancer. CASE PRESENTATION: We report a 67-year-oldman with a history of polycythemia vera who was referred for management of progressively worsening dorsal hand lesions. The patient presented withhyperpigmentation, ichthyosis, plantar keratoderma, dermatomyositis-like eruptions, two squamous cell carcinomas, and actinic keratoses. The adversereactions observed were acknowledged to be related to chronic hydroxyurea use. The patient underwent Mohs excision of the squamous cell carcinomas and thehydroxyurea was promptly discontinued; subsequent cutaneous improvement of the dermatomyositislike lesions ensued. Another clinically suspicious aggressive squamous cell carcinoma was suspected and the patient was referred to the plastic surgery department for complete excision because of the size of the lesion. The patient remains on periodic dermatology follow up. CONCLUSIONS: We report a case that exemplifies the cutaneous adverse effects of chronic hydroxyurea therapy. Although many cases improve after drug discontinuation, strict photoprotection and ongoing surveillance are indicated given the recently proposed premalignant potential of dermatomyositis-like eruptions and the aggressive nature of hydroxyurea-induced nonmelanoma skin cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[St] Status:In-Process

  9 / 7618 MEDLINE  
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[PMID]: 29356090
[Au] Autor:Gupta M; Chauhan K; Singhvi T; Kumari M; Grover RK
[Ad] Address:Department of Oncopathology, Delhi State Cancer Institute, Delhi, India.
[Ti] Title:Useful information provided by graphic displays of automated cell counter in hematological malignancies.
[So] Source:J Clin Lab Anal;, 2018 Jan 21.
[Is] ISSN:1098-2825
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Automated cell counters have become more and more sophisticated with passing years. The numerical and graphic data both provide useful clues for suspecting a diagnosis especially when the workload is very high. AIM: We present our experience of useful information provided by graphic displays of an automated cell counter in hematological malignancies in a cancer hospital where a large number of complete blood count (CBC) requests are received either before or during chemotherapy. This study was conducted to assess the usefulness of hematology cell counter, viz. WBC-Diff (WBC differential), WBC/BASO (WBC basophil) and IMI (immature myeloid information) channel scatter plots, and the flaggings generated in various hematological malignancies. MATERIAL & METHODS: The graphic displays have been compiled over a period of 1 year (October 2015-September 2016) from blood samples of various solid and hematological malignancies (approximately 400 per day) received for routine CBC in the laboratory. Approximately 50 000 scattergrams have been analyzed during the study period. The findings were confirmed by peripheral blood smear examination. RESULTS: The scattergram analysis on XE-2100 is very sensitive as well as specific for diagnosing acute leukemia, viz. acute myeloid leukemia, acute lymphoblastic leukemia; chronic myeloproliferative disorders, viz. chronic myeloid leukemia; and chronic lymphoproliferative disorder especially chronic lymphocytic leukemia. CONCLUSION: It is suggested that the laboratories using the hematology analyzers be aware of graphic display patterns in addition to flaggings generated which provide additional information and give clue toward the diagnosis even before peripheral smear examination.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[St] Status:Publisher
[do] DOI:10.1002/jcla.22392

  10 / 7618 MEDLINE  
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[PMID]: 29439183
[Au] Autor:Schneeweiss M; Peter B; Bibi S; Eisenwort G; Smiljkovic D; Blatt K; Jawhar M; Berger D; Stefanzl G; Herndlhofer S; Greiner G; Hoermann G; Hadzijusufovic E; Gleixner KV; Bettelheim P; Geissler K; Sperr WR; Reiter A; Arock M; Valent P
[Ad] Address:Ludwig Boltzmann Cluster Oncology, Medical University of Vienna, Austria.
[Ti] Title:The KIT and PDGFRA switch-control inhibitor DCC-2618 blocks growth and survival of multiple neoplastic cell types in advanced mastocytosis.
[So] Source:Haematologica;, 2018 Feb 08.
[Is] ISSN:1592-8721
[Cp] Country of publication:Italy
[La] Language:eng
[Ab] Abstract:Systemic mastocytosis is a complex disease defined by abnormal growth and accumulation of neoplastic mast cells in various organs. Most patients exhibit a D816V-mutated variant of KIT, which confers resistance against imatinib. Clinical problems in systemic mastocytosis arise from mediator-related symptoms and/or organ destruction caused by malignant expansion of neoplastic mast cells and/or other myeloid cells in various organ systems. DCC-2618 is a spectrum-selective pan KIT and PDGFRA inhibitor which blocks KIT D816V and multiple other kinase-targets relevant to systemic mastocytosis. We found that DCC-2618 inhibits the proliferation and survival of various human mast cell lines (HMC-1, ROSA, MCPV-1) as well as primary neoplastic mast cells obtained from patients with advanced systemic mastocytosis (IC50 <1 mM). Moreover, DCC-2618 decreased growth and survival of primary neoplastic eosinophils obtained from patients with systemic mastocytosis or eosinophilic leukemia, leukemic monocytes obtained from patients with chronic myelomonocytic leukemia including systemic mastocytosis with chronic myelomonocytic leukemia, and blast cells obtained from patients with acute myeloid leukemia. Furthermore, DCC-2618 was found to suppress the proliferation of endothelial cells, suggesting additional drug effects on systemic mastocytosis-related angiogenesis. Finally, DCC-2618 was found to downregulate IgE-mediated histamine release in basophils and tryptase release in mast cells. Together, DCC-2618 inhibits growth, survival and activation of multiple cell types relevant to advanced systemic mastocytosis. Whether DCC-2618 is effective in vivo in patients with advanced systemic mastocytosis is currently under investigation in clinical trials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180213
[Lr] Last revision date:180213
[St] Status:Publisher


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