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[PMID]:28960095
[Au] Autor:Kayser S; Levis MJ; Schlenk RF
[Ad] Endereço:a Department of Internal Medicine V , University Hospital of Heidelberg , Heidelberg , Germany.
[Ti] Título:Midostaurin treatment in FLT3-mutated acute myeloid leukemia and systemic mastocytosis.
[So] Source:Expert Rev Clin Pharmacol;10(11):1177-1189, 2017 Nov.
[Is] ISSN:1751-2441
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: A number of tyrosine kinase inhibitors (TKIs) have been developed that inhibit the constitutively activated kinase activity caused by activating tyrosine kinase mutations, such as FLT3 or KIT, thus interrupting signaling pathways. Currently, midostaurin is the only approved TKI as monotherapy for aggressive systemic mastocytosis (SM), SM with associated hematological neoplasm, or mast cell leukemia displaying a KIT mutation as well as in combination with standard intensive chemotherapy for adult patients with newly diagnosed FLT3-mutated acute myeloid leukemia (AML). Areas covered: We provide a concise review of the pharmacology, tolerability and clinical efficacy of midostaurin and emerging new treatment options for ASM and FLT3-mutated AML. Expert commentary: Currently, midostaurin is the only approved TKI in aggressive SM, SM with associated hematological neoplasm, or mast cell leukemia inducing responses including complete remissions. With regard to AML, midostaurin is the first drug to receive regulatory approval in this indication in the molecularly defined subgroup of AML with FLT3 mutations. By introduction of this new standard in AML with FLT3 mutations, the bare has been raised for future approvals of next generation FLT3 inhibitors which will be based increasingly on head to head comparisons with midostaurin.
[Mh] Termos MeSH primário: Leucemia Mieloide Aguda/tratamento farmacológico
Mastocitose Sistêmica/tratamento farmacológico
Estaurosporina/análogos & derivados
[Mh] Termos MeSH secundário: Adulto
Animais
Seres Humanos
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/patologia
Mastocitose Sistêmica/genética
Mastocitose Sistêmica/fisiopatologia
Mutação
Inibidores de Proteínas Quinases/efeitos adversos
Inibidores de Proteínas Quinases/farmacologia
Inibidores de Proteínas Quinases/uso terapêutico
Estaurosporina/efeitos adversos
Estaurosporina/farmacologia
Estaurosporina/uso terapêutico
Tirosina Quinase 3 Semelhante a fms/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); H88EPA0A3N (Staurosporine); ID912S5VON (midostaurin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE
[do] DOI:10.1080/17512433.2017.1387051


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[PMID]:28866309
[Au] Autor:Hermans MAW; Arends NJT; Gerth van Wijk R; van Hagen PM; Kluin-Nelemans HC; Oude Elberink HNG; Pasmans SGMA; van Daele PLA
[Ad] Endereço:Department of Internal Medicine, Section of Allergy, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Internal Medicine, Section of Clinical Immunology, Erasmus University Medical Center, Rotterdam, The Netherlands. Electronic address: m.hermans@erasmusmc.nl.
[Ti] Título:Management around invasive procedures in mastocytosis: An update.
[So] Source:Ann Allergy Asthma Immunol;119(4):304-309, 2017 Oct.
[Is] ISSN:1534-4436
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Mastocytosis is a chronic hematologic disorder that is characterized by the accumulation of aberrant mast cells and typically involves the skin and/or bone marrow. Patients with mastocytosis are at increased risk of anaphylaxis. Based on theoretical assumptions, medical procedures requiring general anesthesia or radiocontrast media are deemed hazardous for patients with mastocytosis. The objective of this article is to provide a comprehensive overview of the actual risk of iatrogenic anaphylaxis and provide recommendations for daily practice. DATA SOURCES: Various scientific search engines were used (eg, PubMed and Medline). STUDY SELECTIONS: Because of the paucity of high-level studies on this topic, all available evidence was considered, including case reports. RESULTS: Reliable data on the incidence of iatrogenic anaphylaxis in mastocytosis are lacking. However, although the incidence as reported in (retrospective) cohort studies is higher than in the general population, it is still lower than commonly anticipated, with an incidence of 5.4% in 1 study. Adequate premedication and avoidance of certain physical stimuli can further decrease this risk by 10-fold. The role of drugs as elicitors of anaphylaxis is perhaps overestimated, and physical stimuli are at least as important in inducing release of mast cell mediators. CONCLUSION: This article provides practical recommendations for the management of invasive procedures in patients with mastocytosis based on current knowledge of this topic.
[Mh] Termos MeSH primário: Anafilaxia/prevenção & controle
Meios de Contraste/efeitos adversos
Mastócitos/patologia
Mastocitose Sistêmica/terapia
Radiografia
[Mh] Termos MeSH secundário: Corticosteroides/efeitos adversos
Anafilaxia/etiologia
Anafilaxia/imunologia
Anafilaxia/patologia
Anestesia Geral/efeitos adversos
Medula Óssea/efeitos dos fármacos
Medula Óssea/imunologia
Medula Óssea/patologia
Contraindicações
Feminino
Antagonistas dos Receptores Histamínicos/efeitos adversos
Seres Humanos
Doença Iatrogênica
Masculino
Mastócitos/efeitos dos fármacos
Mastócitos/imunologia
Mastocitose Sistêmica/diagnóstico por imagem
Mastocitose Sistêmica/imunologia
Mastocitose Sistêmica/patologia
Pele/efeitos dos fármacos
Pele/imunologia
Pele/patologia
Estresse Mecânico
Procedimentos Cirúrgicos Operatórios/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Contrast Media); 0 (Histamine Antagonists)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170904
[St] Status:MEDLINE


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[PMID]:28673393
[Au] Autor:Gotlib J
[Ad] Endereço:Division of Hematology, Stanford Cancer Institute/Stanford University School of Medicine, 875 Blake Wilbur Drive, Room 2324, Stanford, CA 94305-5821, USA. Electronic address: jason.gotlib@stanford.edu.
[Ti] Título:Tyrosine Kinase Inhibitors in the Treatment of Eosinophilic Neoplasms and Systemic Mastocytosis.
[So] Source:Hematol Oncol Clin North Am;31(4):643-661, 2017 Aug.
[Is] ISSN:1558-1977
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The World Health Organization's semimolecular classification of eosinophilias emphasizes neoplasms driven by fusion tyrosine kinases. More than 80% of patients with systemic mastocytosis carry the KIT D816V mutation, the primary driver of disease pathogenesis. Genetic annotation of these diseases is critical and affords opportunities for targeted therapy. This article discusses our understanding of the mutated tyrosine kinome of eosinophilic neoplasms and systemic mast cell disease, and the successes and limitations of available therapies. Use of tyrosine kinase inhibitors as a bridge to hematopoietic stem cell transplantation, and development of more selective and potent tyrosine kinase inhibitors is also highlighted.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Mastocitose Sistêmica/tratamento farmacológico
Mastocitose Sistêmica/metabolismo
Inibidores de Proteínas Quinases/uso terapêutico
Proteínas Tirosina Quinases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Algoritmos
Antineoplásicos/farmacologia
Gerenciamento Clínico
Ativação Enzimática
Seres Humanos
Janus Quinases/metabolismo
Mastocitose Sistêmica/diagnóstico
Mutação
Proteínas de Fusão Oncogênicas/antagonistas & inibidores
Proteínas de Fusão Oncogênicas/genética
Proteínas de Fusão Oncogênicas/metabolismo
Inibidores de Proteínas Quinases/farmacologia
Proteínas Tirosina Quinases/genética
Proteínas Tirosina Quinases/metabolismo
Fatores de Transcrição STAT/metabolismo
Transdução de Sinais/efeitos dos fármacos
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Oncogene Proteins, Fusion); 0 (Protein Kinase Inhibitors); 0 (STAT Transcription Factors); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170705
[St] Status:MEDLINE


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[PMID]:28612232
[Au] Autor:Kim ES
[Ad] Endereço:Springer, Private Bag 65901, Mairangi Bay, 0754, Auckland, New Zealand. dru@adis.com.
[Ti] Título:Midostaurin: First Global Approval.
[So] Source:Drugs;77(11):1251-1259, 2017 Jul.
[Is] ISSN:1179-1950
[Cp] País de publicação:New Zealand
[La] Idioma:eng
[Ab] Resumo:Midostaurin (Rydapt ) is a multikinase inhibitor being developed by Novartis Pharmaceuticals. In April 2017, midostaurin was approved in the USA for the treatment of adult patients with newly diagnosed, FMS-like tyrosine kinase 3 (FLT3) mutation-positive acute myeloid leukaemia (AML) [in combination with standard cytarabine and daunorubicin induction, and cytarabine consolidation], or aggressive systemic mastocytosis (ASM), systemic mastocytosis with associated haematological neoplasm (SM-AHN) or mast cell leukaemia (MCL) [collectively known as advanced SM]. The article summarizes the milestones in the development of midostaurin leading to this first global approval.
[Mh] Termos MeSH primário: Leucemia de Mastócitos/tratamento farmacológico
Leucemia Mieloide Aguda/tratamento farmacológico
Mastocitose Sistêmica/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
Estaurosporina/análogos & derivados
[Mh] Termos MeSH secundário: Adolescente
Adulto
Ensaios Clínicos como Assunto
Aprovação de Drogas
Seres Humanos
Meia-Idade
Estaurosporina/administração & dosagem
Estaurosporina/efeitos adversos
Estaurosporina/farmacocinética
Estaurosporina/uso terapêutico
Estados Unidos
United States Food and Drug Administration
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Protein Kinase Inhibitors); H88EPA0A3N (Staurosporine); ID912S5VON (midostaurin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170615
[St] Status:MEDLINE
[do] DOI:10.1007/s40265-017-0779-0


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[PMID]:28599188
[Au] Autor:Jain P; Wang S; Patel KP; Sarwari N; Cortes J; Kantarjian H; Verstovsek S
[Ad] Endereço:Department of Leukemia, The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
[Ti] Título:Mast cell leukemia (MCL): Clinico-pathologic and molecular features and survival outcome.
[So] Source:Leuk Res;59:105-109, 2017 Aug.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mast cell leukemia (MCL) is a very rare subtype of systemic mastocytosis (SM). We have identified 13 such patients (5.9%) among 218 patients with SM seen at our institution between 1994 and 2016. Patients with MCL had poor survival (median 31.6 months); response to various therapies was rare and not durable. Clinical course may be affected by concurrent associated hematologic neoplasm and different genetic profiles. More research is required to decipher this rare and enigmatic SM subtype.
[Mh] Termos MeSH primário: Leucemia de Mastócitos/mortalidade
Leucemia de Mastócitos/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Medula Óssea/patologia
Feminino
Neoplasias Hematológicas/complicações
Neoplasias Hematológicas/mortalidade
Neoplasias Hematológicas/patologia
Seres Humanos
Leucemia de Mastócitos/complicações
Masculino
Mastocitose Sistêmica
Meia-Idade
Estudos Retrospectivos
Taxa de Sobrevida
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE


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[PMID]:28486845
[Au] Autor:de Mol CL; Hermans MAW; Gerth van Wijk R; van Hagen PM; van Daele PLA
[Ad] Endereço:a Department of Internal Medicine, Section of Clinical Immunology , Erasmus University Medical Centre , Rotterdam , Netherlands.
[Ti] Título:Routine abdominal ultrasonography has limited value in the care for patients with indolent systemic mastocytosis.
[So] Source:Hematology;22(9):544-547, 2017 Oct.
[Is] ISSN:1607-8454
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Systemic mastocytosis (SM) is a myeloproliferative disease characterized by the accumulation of aberrant mast cells. Since advanced subtypes of SM can lead to organ dysfunction and shortened survival, timely recognition of progressive disease is important for the adequate treatment of SM patients. METHODS: Here, we report the results of our cohort study on the value of routine abdominal ultrasonography for the detection of progression of indolent systemic mastocytosis (ISM). RESULTS: We included 88 patients with ISM, of whom 9 developed new hepatosplenomegaly during follow-up. In this group, the median serum tryptase level increased by 11.60 µg/l, compared with a decrease of -0.20 µg/l in the 79 patients with unchanged ultrasonography results (p = 0.016). A change in liver and/or spleen size never led to a change in clinical classification, nor management. DISCUSSION: Based on the finding that a change in ultrasonography findings did not correlate to disease progression in general, it appears that isolated hepatosplenomegaly does not have prognostic implications in patients with ISM. CONCLUSIONS: Routine abdominal ultrasonography is redundant in the follow-up of patients with ISM. A combination of physical examination with serum tryptase levels can be used to screen for hepatosplenomegaly.
[Mh] Termos MeSH primário: Mastocitose Sistêmica/diagnóstico por imagem
Mastocitose Sistêmica/patologia
[Mh] Termos MeSH secundário: Cavidade Abdominal/diagnóstico por imagem
Cavidade Abdominal/patologia
Idoso
Gerenciamento Clínico
Feminino
Seguimentos
Hepatomegalia
Seres Humanos
Masculino
Meia-Idade
Esplenomegalia
Ultrassonografia
Fluxo de Trabalho
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1080/10245332.2017.1324377


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[PMID]:28424161
[Au] Autor:Jawhar M; Schwaab J; Naumann N; Horny HP; Sotlar K; Haferlach T; Metzgeroth G; Fabarius A; Valent P; Hofmann WK; Cross NCP; Meggendorfer M; Reiter A
[Ad] Endereço:Department of Hematology and Oncology, Mannheim University Medical Center, Mannheim, Germany.
[Ti] Título:Response and progression on midostaurin in advanced systemic mastocytosis: D816V and other molecular markers.
[So] Source:Blood;130(2):137-145, 2017 Jul 13.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In advanced systemic mastocytosis (advSM), disease evolution is often triggered by mutations (D816V in >80% of cases) and by additional mutations (eg, in , , and/or [S/A/R in >60% of cases]). In a recently reported phase 2 study, midostaurin, a multikinase/KIT inhibitor, demonstrated an overall response rate (ORR) of 60% in advSM but biomarkers predictive of response are lacking. We evaluated the impact of molecular markers at baseline and during follow-up in 38 midostaurin-treated advSM patients. The median overall survival (OS) was 30 months (95% confidence interval, 6-54) from start of midostaurin. ORR and OS were significantly different between S/A/R (n = 12) and S/A/R (n = 23) patients (ORR: 75% vs 39%, = .04; OS: = .01, HR 4.5 [1.3-16.2]). Depending on the relative reduction of the D816V expressed allele burden (EAB) at month 6, patients were classified as responders (≥25%, n = 17) or nonresponders (<25%, n = 11). In univariate analyses at month 6, reduction of D816V EAB ≥25%, tryptase ≥50%, and alkaline phosphatase ≥50% were significantly associated with improved OS. In multivariate analysis, only D816V EAB reduction ≥25% remained an independent on-treatment marker for improved OS ( = .004, HR 6.8 [1.8-25.3]). Serial next-generation sequencing analysis of 28 genes in 16 patients revealed acquisition of additional mutations or increasing variant allele frequency in / , , , or associated with progression in 7 patients. In midostaurin-treated advSM patients, the complexity and dynamics of mutational profiles significantly affect response, progression, and prognosis.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Biomarcadores Tumorais/genética
Mastocitose Sistêmica/tratamento farmacológico
Inibidores de Proteínas Quinases/uso terapêutico
Proteínas Proto-Oncogênicas c-kit/genética
Estaurosporina/análogos & derivados
[Mh] Termos MeSH secundário: Idoso
Alelos
Biomarcadores Tumorais/metabolismo
Subunidade alfa 2 de Fator de Ligação ao Core/genética
Subunidade alfa 2 de Fator de Ligação ao Core/metabolismo
Progressão da Doença
Feminino
Expressão Gênica
Seres Humanos
Isocitrato Desidrogenase/genética
Isocitrato Desidrogenase/metabolismo
Masculino
Mastocitose Sistêmica/diagnóstico
Mastocitose Sistêmica/genética
Mastocitose Sistêmica/mortalidade
Meia-Idade
Mutação
Proteínas Nucleares/genética
Proteínas Nucleares/metabolismo
Prognóstico
Proteínas Proto-Oncogênicas c-kit/metabolismo
Proteínas Proto-Oncogênicas p21(ras)/genética
Proteínas Proto-Oncogênicas p21(ras)/metabolismo
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Fatores de Processamento de Serina-Arginina/genética
Fatores de Processamento de Serina-Arginina/metabolismo
Estaurosporina/uso terapêutico
Análise de Sobrevida
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ASXL1 protein, human); 0 (Antineoplastic Agents); 0 (Biomarkers, Tumor); 0 (Core Binding Factor Alpha 2 Subunit); 0 (KRAS protein, human); 0 (Nuclear Proteins); 0 (Protein Kinase Inhibitors); 0 (RUNX1 protein, human); 0 (Repressor Proteins); 117896-08-9 (nucleophosmin); 147153-65-9 (SRSF2 protein, human); 170974-22-8 (Serine-Arginine Splicing Factors); EC 1.1.1.41 (Isocitrate Dehydrogenase); EC 1.1.1.41 (isocitrate dehydrogenase 2, human); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.6.5.2 (Proto-Oncogene Proteins p21(ras)); H88EPA0A3N (Staurosporine); ID912S5VON (midostaurin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170815
[Lr] Data última revisão:
170815
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-01-764423


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[PMID]:28262030
[Au] Autor:Van den Poel B; Kochuyt AM; Del Biondo E; Dewaele B; Lierman E; Tousseyn T; de Hertogh G; Vandenberghe P; Boeckx N
[Ad] Endereço:a Department of Laboratory Medicine , University Hospitals Leuven , Leuven , Belgium.
[Ti] Título:Highly sensitive assays are mandatory for the differential diagnosis of patients presenting with symptoms of mast cell activation: diagnostic work-up of 38 patients.
[So] Source:Acta Clin Belg;72(2):123-129, 2017 Apr.
[Is] ISSN:2295-3337
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mastocytosis is a heterogeneous disease caused by excessive mast cell (MC) proliferation. Diagnosis of systemic mastocytosis (SM) is based on the presence of major and minor criteria defined by the World Health Organization. Symptoms of MC activation can also occur in patients without SM or without allergic or inflammatory disease. These MC activation syndromes (MCAS) can be divided into primary (monoclonal) MCAS (MMAS) vs. secondary and idiopathic MCAS. In this single center study, the diagnostic work-up of 38 patients with a clinical suspicion of SM and/or with elevated basic tryptase levels is presented. Clinical symptoms, biochemical parameters, results of bone marrow investigation, flow cytometric immunophenotyping, and molecular analysis were retrospectively reviewed. Twenty-three patients were found to have a monoclonal MC disorder of which 19 were diagnosed with SM and 4 with MMAS. In 13/19 SM patients, multifocal MC infiltrates in the bone marrow were found (major criterion), while in 6 the diagnosis was based on the presence of ≥3 minor criteria. Flow cytometric analysis of bone marrow showed CD25 expression of MCs in all patients with SM and MMAS (range: 0.002-0.3% of cells). In bone marrow, the KIT D816V mutation was detected in all SM patients but in only 2 patients with MMAS (range: 0.007-9% mutated cells). Basic tryptase elevation was demonstrated in 16/19 patients with SM but also in 9/19 patients without SM. Our study reveals the heterogeneity of primary MC disorders and the importance of sensitive assays in patients suspected of having SM.
[Mh] Termos MeSH primário: Mastocitose Sistêmica/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Criança
Diagnóstico Diferencial
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170307
[St] Status:MEDLINE
[do] DOI:10.1080/17843286.2017.1293312


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[PMID]:28246420
[Au] Autor:Woldemeskel M; Merrill A; Brown C
[Ad] Endereço:University of Georgia, College of Veterinary Medicine, Veterinary Diagnostic and Investigational Laboratory, 43 Brighton Road, Tifton, Georgia 31793 (Woldemeskel, Merrill); Plantation Center Animal Hospital, 6411 Peake Road, Macon, Georgia 31210, USA (Brown).
[Ti] Título:Significance of cytological smear evaluation in diagnosis of splenic mast cell tumor-associated systemic mastocytosis in a cat .
[So] Source:Can Vet J;58(3):293-295, 2017 Mar.
[Is] ISSN:0008-5286
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:An 8-year-old cat was presented with vomiting and weight loss. Histopathology and cytology revealed systemic mastocytosis, a rare condition and a clinical challenge. This case emphasizes the significance of cytological evaluation of smears in diagnosis of mastocytosis and in confirmation in biopsy specimens.
[Mh] Termos MeSH primário: Doenças do Gato/diagnóstico
Mastocitose Sistêmica/veterinária
Neoplasias Esplênicas/veterinária
[Mh] Termos MeSH secundário: Animais
Doenças do Gato/sangue
Doenças do Gato/patologia
Gatos
Feminino
Mastócitos/patologia
Mastocitose Sistêmica/sangue
Mastocitose Sistêmica/diagnóstico
Neoplasias Esplênicas/sangue
Neoplasias Esplênicas/diagnóstico
Neoplasias Esplênicas/patologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170302
[St] Status:MEDLINE


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[PMID]:28074480
[Au] Autor:Fusco N; Bonometti A; Augello C; Fabris S; Boiocchi L; Fiori S; Morotti D; Fracchiolla N; Berti E; Gianelli U
[Ad] Endereço:Division of Pathology, Fondazione IRCCS Ca' Granda, Ospedale Maggiore Policlinico, Milan, Italy.
[Ti] Título:Clonal reticulohistiocytosis of the skin and bone marrow associated with systemic mastocytosis and acute myeloid leukaemia.
[So] Source:Histopathology;70(6):1000-1008, 2017 May.
[Is] ISSN:1365-2559
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: The aims of this study were to define whether diffuse cutaneous reticulohistiocytosis could be underpinned by somatic genetic alterations and represent a precursor of more aggressive forms of disease. METHODS AND RESULTS: A 59-year-old man with diffuse cutaneous reticulohistiocytosis experienced bone marrow localization of the disease, with associated systemic mastocytosis and acute myeloid leukaemia. Cytogenetic analyses of the bone marrow aspirate revealed the presence of a derivative chromosome giving rise to a partial trisomy of chromosome 1q and a partial monosomy of chromosome 9q. Therefore, we characterized the cutaneous lesions before and after chemotherapy by using an integrative approach combining histopathology, electron microscopy, and fluorescence in-situ hybridization. Histologically, the skin lesions belonged to the spectrum of diffuse cutaneous reticulohistiocytoses, as confirmed by immunohistochemistry and ultrastructural analyses. Fluorescence in-situ hybridization in the skin nodules confirmed the presence of the genetic alterations previously detected in the bone marrow. CONCLUSIONS: Here, we provide circumstantial evidence to suggest that at least a subset of cutaneous reticulohistiocytoses harbour clonal molecular alterations. Furthermore, we confirm that these lesions have the potential to arise in the setting of concurrent haematological disorders. In this hypothesis-generating study, two possible tumorigenesis models are proposed.
[Mh] Termos MeSH primário: Neoplasias da Medula Óssea/complicações
Transtornos Histiocíticos Malignos/complicações
Leucemia Mieloide Aguda/complicações
Mastocitose Sistêmica/complicações
Neoplasias Cutâneas/complicações
[Mh] Termos MeSH secundário: Medula Óssea/patologia
Neoplasias da Medula Óssea/genética
Neoplasias da Medula Óssea/patologia
Células Clonais/patologia
Transtornos Histiocíticos Malignos/genética
Transtornos Histiocíticos Malignos/patologia
Seres Humanos
Hibridização in Situ Fluorescente
Leucemia Mieloide Aguda/genética
Leucemia Mieloide Aguda/patologia
Masculino
Mastocitose Sistêmica/genética
Mastocitose Sistêmica/patologia
Meia-Idade
Neoplasias Cutâneas/genética
Neoplasias Cutâneas/patologia
[Pt] Tipo de publicação:CASE REPORTS
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170112
[St] Status:MEDLINE
[do] DOI:10.1111/his.13166



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