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[PMID]:29072953
[Au] Autor:Charles NJ; Boyer DF
[Ad] Endereço:From the Department of Pathology, The University of Michigan, Ann Arbor.
[Ti] Título:Mixed-Phenotype Acute Leukemia: Diagnostic Criteria and Pitfalls.
[So] Source:Arch Pathol Lab Med;141(11):1462-1468, 2017 Nov.
[Is] ISSN:1543-2165
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mixed-phenotype acute leukemia (MPAL) is a heterogeneous category in the World Health Organization classification that comprises acute leukemias with discrete admixed populations of myeloid and lymphoid blasts ("bilineal") or with extensive coexpression of lymphoid and myeloid markers in a single blast population ("biphenotypic"). Flow cytometric findings suggestive of MPAL are often met with consternation by pathologists and oncologists alike, owing to unfamiliarity with the disease and uncertainty about how MPAL fits into established paradigms for treatment of acute leukemia. The purpose of this review is to explain the diagnostic criteria for MPAL, summarize its biological and clinical features, and address common diagnostic pitfalls of these unusual leukemias.
[Mh] Termos MeSH primário: Leucemia Aguda Bifenotípica/diagnóstico
Guias de Prática Clínica como Assunto
[Mh] Termos MeSH secundário: Biomarcadores Tumorais/sangue
Biomarcadores Tumorais/metabolismo
Diagnóstico Diferencial
Proteínas de Fusão bcr-abl/sangue
Proteínas de Fusão bcr-abl/genética
Proteínas de Fusão bcr-abl/metabolismo
Histona-Lisina N-Metiltransferase/sangue
Histona-Lisina N-Metiltransferase/genética
Histona-Lisina N-Metiltransferase/metabolismo
Seres Humanos
Imuno-Histoquímica/tendências
Imunofenotipagem/tendências
Leucemia Aguda Bifenotípica/genética
Leucemia Aguda Bifenotípica/metabolismo
Leucemia Aguda Bifenotípica/terapia
Proteína de Leucina Linfoide-Mieloide/sangue
Proteína de Leucina Linfoide-Mieloide/genética
Proteína de Leucina Linfoide-Mieloide/metabolismo
Prognóstico
Translocação Genética
Organização Mundial da Saúde
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (MLL protein, human); 149025-06-9 (Myeloid-Lymphoid Leukemia Protein); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171027
[St] Status:MEDLINE
[do] DOI:10.5858/arpa.2017-0218-RA


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[PMID]:28527401
[Au] Autor:Tan J; Wang Y; Yu SJ; Ma YY; Lei HY; Liu QF
[Ad] Endereço:Department of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China; Department of Hematology, Jingzhou First People's Hospital, Yangtze University, Jingzhou, Hubei, China.
[Ti] Título:Prognostic factors on graft-versus-host disease-free and relapse-free survival after allogeneic hematopoietic stem cell transplantation for adults with acute leukemia.
[So] Source:Leuk Res;59:1-7, 2017 Aug.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The cure of acute leukemia by allogeneic hematopoietic stem cell transplantation (allo-HSCT) is closely linked to major complications leading to adverse outcomes, including graft-versus-host disease (GVHD), disease relapse and death. This study retrospectively investigated a consecutive series of 312 adult patients with acute leukemia receiving allo-HSCT by using a novel concept of GVHD-free/relapse-free survival (GRFS), and further evaluated the impact of clinical factors on GRFS. Results indicated that the 1- and 2-year GRFS were 54.8% and 51.5%, respectively. In multivariable analysis, recipient age >35years (HR 1.676; p=0.006), diagnosis of acute lymphoblastic leukemia (HR 1.653; p=0.027) and acute biphenotypic leukemia (HR 2.175; p=0.010), advanced disease (HR 2.702; p<0.001), and donor age >35 years (HR 1.622; p=0.008) were significantly associated with inferior GRFS post-HSCT. GRFS of haploidentical-related donor transplant was comparable to that of matched sibling donor or matched unrelated donor transplant. Furthermore, prophylactic donor lymphocyte infusion (DLI) had an overall beneficial effect on GRFS (HR 0.645, p=0.044). Collectively, with a better understanding of these significant prognostic factors which impacted on GRFS, we can effectively evaluate the risk and probability of real recovery after allo-HSCT, further optimizing the therapeutic avenues for acute leukemia.
[Mh] Termos MeSH primário: Doença Enxerto-Hospedeiro/mortalidade
Transplante de Células-Tronco Hematopoéticas/efeitos adversos
Leucemia/diagnóstico
Prognóstico
[Mh] Termos MeSH secundário: Doença Aguda
Adolescente
Adulto
Fatores Etários
Aloenxertos
Doadores de Sangue
Intervalo Livre de Doença
Feminino
Doença Enxerto-Hospedeiro/etiologia
Transplante de Células-Tronco Hematopoéticas/mortalidade
Seres Humanos
Leucemia/mortalidade
Leucemia/terapia
Leucemia Aguda Bifenotípica/diagnóstico
Leucemia Aguda Bifenotípica/mortalidade
Leucemia Aguda Bifenotípica/terapia
Transfusão de Linfócitos
Masculino
Meia-Idade
Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico
Leucemia-Linfoma Linfoblástico de Células Precursoras/mortalidade
Leucemia-Linfoma Linfoblástico de Células Precursoras/terapia
Estudos Retrospectivos
Medição de Risco
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:170521
[St] Status:MEDLINE


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[PMID]:28436985
[Au] Autor:Vu LP; Prieto C; Amin EM; Chhangawala S; Krivtsov A; Calvo-Vidal MN; Chou T; Chow A; Minuesa G; Park SM; Barlowe TS; Taggart J; Tivnan P; Deering RP; Chu LP; Kwon JA; Meydan C; Perales-Paton J; Arshi A; Gönen M; Famulare C; Patel M; Paietta E; Tallman MS; Lu Y; Glass J; Garret-Bakelman FE; Melnick A; Levine R; Al-Shahrour F; Järås M; Hacohen N; Hwang A; Garippa R; Lengner CJ; Armstrong SA; Cerchietti L; Cowley GS; Root D; Doench J; Leslie C; Ebert BL; Kharas MG
[Ad] Endereço:Molecular Pharmacology Program, Center for Cell Engineering, Center for Stem Cell Biology, and Center for Experimental Therapeutics, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
[Ti] Título:Functional screen of MSI2 interactors identifies an essential role for SYNCRIP in myeloid leukemia stem cells.
[So] Source:Nat Genet;49(6):866-875, 2017 Jun.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The identity of the RNA-binding proteins (RBPs) that govern cancer stem cells remains poorly characterized. The MSI2 RBP is a central regulator of translation of cancer stem cell programs. Through proteomic analysis of the MSI2-interacting RBP network and functional shRNA screening, we identified 24 genes required for in vivo leukemia. Syncrip was the most differentially required gene between normal and myeloid leukemia cells. SYNCRIP depletion increased apoptosis and differentiation while delaying leukemogenesis. Gene expression profiling of SYNCRIP-depleted cells demonstrated a loss of the MLL and HOXA9 leukemia stem cell program. SYNCRIP and MSI2 interact indirectly though shared mRNA targets. SYNCRIP maintains HOXA9 translation, and MSI2 or HOXA9 overexpression rescued the effects of SYNCRIP depletion. Altogether, our data identify SYNCRIP as a new RBP that controls the myeloid leukemia stem cell program. We propose that targeting these RBP complexes might provide a novel therapeutic strategy in leukemia.
[Mh] Termos MeSH primário: Regulação Leucêmica da Expressão Gênica
Ribonucleoproteínas Nucleares Heterogêneas/genética
Leucemia Mieloide/genética
Proteínas de Ligação a RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular
Feminino
Hematopoese/genética
Ribonucleoproteínas Nucleares Heterogêneas/metabolismo
Proteínas de Homeodomínio/genética
Seres Humanos
Leucemia Aguda Bifenotípica/genética
Leucemia Aguda Bifenotípica/patologia
Leucemia Mieloide/patologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Progenitoras Mieloides/metabolismo
Células Progenitoras Mieloides/patologia
RNA Interferente Pequeno
Proteínas de Ligação a RNA/genética
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Heterogeneous-Nuclear Ribonucleoproteins); 0 (Homeodomain Proteins); 0 (MSI2 protein, human); 0 (RNA, Small Interfering); 0 (RNA-Binding Proteins); 0 (SYNCRIP protein, human); 0 (Syncrip protein, mouse); 0 (homeobox protein HOXA9)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170425
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3854


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[PMID]:28195090
[Au] Autor:Pawar RN; Banerjee S; Bramha S; Krishnan S; Bhattacharya A; Saha V; Chakrapani A; Bhave S; Chandy M; Nair R; Parihar M; Arora N; Mishra DK
[Ad] Endereço:Department of Laboratory Haematology and Molecular Genetics, Tata Medical Centre, Kolkata, West Bengal, India.
[Ti] Título:Mixed-phenotypic acute leukemia series from tertiary care center.
[So] Source:Indian J Pathol Microbiol;60(1):43-49, 2017 Jan-Mar.
[Is] ISSN:0974-5130
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Mixed-phenotype acute leukemias (MPALs) are a heterogeneous group of rare leukemias constituting approximately 2%-5% of all leukemias, in which assigning a single lineage of origin is not possible. They are diagnosed by either the presence of antigens of more than one lineage or by the presence of dual population of blasts belonging to two or more lineages. We highlight the clinicopathological, immunophenotype, and genetic data of a cohort (n = 14) of patients diagnosed and treated at our center. MATERIALS AND METHODS: We retrospectively analyzed consecutive cases of MPAL diagnosed in our flow cytometry laboratory from May 2012 to August 2015. These cases were diagnosed based on immunophenotyping of peripheral blood/bone marrow aspirates and morphology/genetics wherever available as per the World Health Organization (WHO) 2008 guideline. RESULTS: Among 628 consecutive acute leukemia (AL) cases diagnosed and evaluated during this period, we identified 14 (2.2%) patients with MPAL fulfilling WHO 2008/EGIL criteria for immunological characterizing of AL criteria. Majority of these were males (n = 8, male:female ratio 1.3:1) and adults (n = 11, 78.5%). The median age of this cohort was 41 years (range 2-80). These cases were further classified as: B/myeloid (n = 9), T/myeloid (n = 4), and B/T MPAL (n = 1). Cytogenetics was available in 12 out of 14 cases, out of which, three cases had normal karyotype, three with t(9;22)(q34;q11), and two cases with complex karyotype. We also came across a rare case of B + T lymphoid MPAL who had mixed-lineage leukemia gene t(v; 11q23) rearrangement. CONCLUSION: MPAL is a complex entity with heterogeneous clinical, immunophenotypic, cytogenetic, and molecular features. Multiparametric flowcytometry by using comprehensive antibody panels is a valuable tool for diagnosis. Subsequent cytogenetic and molecular analysis for further prognostic stratification and treatment modalities are important.
[Mh] Termos MeSH primário: Leucemia Aguda Bifenotípica/diagnóstico
Leucemia Aguda Bifenotípica/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Células Sanguíneas
Medula Óssea/patologia
Criança
Pré-Escolar
Feminino
Citometria de Fluxo
Seres Humanos
Imunofenotipagem
Masculino
Meia-Idade
Estudos Retrospectivos
Centros de Atenção Terciária
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.4103/0377-4929.200057


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[PMID]:28099272
[Au] Autor:Wolach O; Stone RM
[Ad] Endereço:aLeukemia Service, Davidoff Cancer Center, Rabin Medical Center, Petah-Tikva, Israel bDepartment of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, USA.
[Ti] Título:Mixed-phenotype acute leukemia: current challenges in diagnosis and therapy.
[So] Source:Curr Opin Hematol;24(2):139-145, 2017 Mar.
[Is] ISSN:1531-7048
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Mixed-phenotype acute leukemia (MPAL) is a rare disease that poses many diagnostic and therapeutic challenges. Patients with MPAL are considered to have poor outcomes. The difficulties in classifying this leukemia, the lack of prospectively collected data concerning therapeutic outcomes, and rare incidence result in much uncertainty as to the best approach for patients with MPAL. RECENT FINDINGS: Recent studies demonstrated that most MPALs are associated with cytogenetic abnormalities; genetic sequencing studies disclose a high frequency of somatic mutations in genes encoding epigenetic regulators, tumor suppressors, and transcription factors. The limited available data suggest that higher remission rates are achieved with acute lymphoblastic leukemia-like induction regimens compared with acute myeloid leukemia-type approaches. Allogeneic transplantation in first remission may be associated with improved survival compared with consolidation chemotherapy. SUMMARY: Advances in understanding the genetic landscape of MPAL may allow a more biologically driven classification of this heterogeneous group of leukemias in the future that will lead to optimized therapies for individual patients. Most data that inform therapy are based on retrospective, uncontrolled studies; prospective trials that incorporate targeted approaches based on genetics and immunophenotype are needed.
[Mh] Termos MeSH primário: Leucemia Aguda Bifenotípica/diagnóstico
Leucemia Aguda Bifenotípica/terapia
[Mh] Termos MeSH secundário: Biomarcadores Tumorais
Terapia Combinada
Variação Genética
Transplante de Células-Tronco Hematopoéticas
Seres Humanos
Imunofenotipagem
Leucemia Aguda Bifenotípica/genética
Leucemia Aguda Bifenotípica/metabolismo
Indução de Remissão
Transplante Homólogo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers, Tumor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170119
[St] Status:MEDLINE
[do] DOI:10.1097/MOH.0000000000000322


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[PMID]:28068328
[Au] Autor:Ugale A; Säwén P; Dudenhöffer-Pfeifer M; Wahlestedt M; Norddahl GL; Bryder D
[Ad] Endereço:Molecular Hematology, Institution for Laboratory Medicine, Lund University, Lund, Sweden.
[Ti] Título:MLL-ENL-mediated leukemia initiation at the interface of lymphoid commitment.
[So] Source:Oncogene;36(22):3207-3212, 2017 Jun 01.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Translocations involving the mixed lineage leukemia-1 are recurrent events in acute leukemia and associate with lymphoid (ALL), myeloid (AML) or mixed lineage (MLL) subtypes. Despite an association with ALL in humans, murine MLL fusion models are persistently restricted to AML. We here explored this issue using an inducible mixed lineage leukemia-eleven nineteen leukemia (MLL-ENL) mouse model. Although multiple progenitor cell types with myeloid potential are potent AML leukemia-initiating cells, also the earliest lymphoid progenitors were capable of initiating AML. This ability to evoke a latent myeloid potential in the earliest lymphoid progenitors was lost upon further lymphoid commitment. At the same time, more downstream/committed lymphoid precursors also failed to initiate lymphoid leukemia. Co-expression of MLL-ENL with a constitutively active RAS allele, the most common co-mutation in MLL fusion leukemias, could influence on both disease latency and lineage assignment of developing leukemia in what appears to be a mutation-order-dependent manner. Finally, CEBPB-mediated transdifferentation of committed and otherwise leukemia-incompetent B-cell progenitors imbued these cells with leukemic competence for AML. Therefore, apart from providing detailed insight into the differential responsiveness of candidate target cells to a first-hit MLL fusion event, our data warrants caution to therapeutic approaches based on the concept of transdifferentiation.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Histona-Lisina N-Metiltransferase/genética
Leucemia Aguda Bifenotípica/genética
Proteína de Leucina Linfoide-Mieloide/genética
Proteínas de Fusão Oncogênicas/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Animais
Transformação Celular Neoplásica
Proteínas de Ligação a DNA/metabolismo
Modelos Animais de Doenças
Histona-Lisina N-Metiltransferase/metabolismo
Leucemia Aguda Bifenotípica/metabolismo
Leucemia Aguda Bifenotípica/patologia
Camundongos
Proteína de Leucina Linfoide-Mieloide/metabolismo
Proteínas de Fusão Oncogênicas/metabolismo
Fatores de Transcrição/metabolismo
Translocação Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA-Binding Proteins); 0 (Mllt1 protein, mouse); 0 (Oncogene Proteins, Fusion); 0 (Transcription Factors); 149025-06-9 (Myeloid-Lymphoid Leukemia Protein); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (Mll protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2016.470


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[PMID]:28065413
[Au] Autor:Liang K; Volk AG; Haug JS; Marshall SA; Woodfin AR; Bartom ET; Gilmore JM; Florens L; Washburn MP; Sullivan KD; Espinosa JM; Cannova J; Zhang J; Smith ER; Crispino JD; Shilatifard A
[Ad] Endereço:Department of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, 320 E. Superior St., Chicago, IL 60611, USA; Stowers Institute for Medical Research, 1000 E. 50th St., Kansas City, MO 64110, USA.
[Ti] Título:Therapeutic Targeting of MLL Degradation Pathways in MLL-Rearranged Leukemia.
[So] Source:Cell;168(1-2):59-72.e13, 2017 Jan 12.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chromosomal translocations of the mixed-lineage leukemia (MLL) gene with various partner genes result in aggressive leukemia with dismal outcomes. Despite similar expression at the mRNA level from the wild-type and chimeric MLL alleles, the chimeric protein is more stable. We report that UBE2O functions in regulating the stability of wild-type MLL in response to interleukin-1 signaling. Targeting wild-type MLL degradation impedes MLL leukemia cell proliferation, and it downregulates a specific group of target genes of the MLL chimeras and their oncogenic cofactor, the super elongation complex. Pharmacologically inhibiting this pathway substantially delays progression, and it improves survival of murine leukemia through stabilizing wild-type MLL protein, which displaces the MLL chimera from some of its target genes and, therefore, relieves the cellular oncogenic addiction to MLL chimeras. Stabilization of MLL provides us with a paradigm in the development of therapies for aggressive MLL leukemia and perhaps for other cancers caused by translocations.
[Mh] Termos MeSH primário: Leucemia Aguda Bifenotípica/tratamento farmacológico
Leucemia Aguda Bifenotípica/metabolismo
Proteólise/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Histona-Lisina N-Metiltransferase/metabolismo
Seres Humanos
Interleucina-1/metabolismo
Quinases Associadas a Receptores de Interleucina-1/antagonistas & inibidores
Quinases Associadas a Receptores de Interleucina-1/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Proteína de Leucina Linfoide-Mieloide/metabolismo
Enzimas de Conjugação de Ubiquitina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-1); 149025-06-9 (Myeloid-Lymphoid Leukemia Protein); EC 2.1.1.43 (Histone-Lysine N-Methyltransferase); EC 2.1.1.43 (Mll protein, mouse); EC 2.3.2.23 (Ubiquitin-Conjugating Enzymes); EC 2.3.2.24 (UBE2O protein, human); EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170110
[St] Status:MEDLINE


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[PMID]:27696204
[Au] Autor:Vogt N; Heß K; Bialek R; Buerke B; Brüggemann M; Topp MS; Groth C; Berdel WE; Lenz G; Stelljes M
[Ad] Endereço:Department of Medicine A/Hematology and Oncology, University of Muenster, Albert-Schweitzer-Campus 1, D-48149, Muenster, Germany.
[Ti] Título:Epileptic seizures and rhinocerebral mucormycosis during blinatumomab treatment in a patient with biphenotypic acute leukemia.
[So] Source:Ann Hematol;96(1):151-153, 2017 Jan.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Anticorpos Biespecíficos/efeitos adversos
Antineoplásicos/efeitos adversos
Encefalopatias/induzido quimicamente
Epilepsia/induzido quimicamente
Leucemia Aguda Bifenotípica/tratamento farmacológico
Mucormicose/induzido quimicamente
[Mh] Termos MeSH secundário: Encefalopatias/complicações
Encefalopatias/diagnóstico por imagem
Epilepsia/complicações
Epilepsia/diagnóstico por imagem
Evolução Fatal
Feminino
Seres Humanos
Leucemia Aguda Bifenotípica/complicações
Leucemia Aguda Bifenotípica/diagnóstico por imagem
Mucormicose/complicações
Mucormicose/diagnóstico por imagem
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Antibodies, Bispecific); 0 (Antineoplastic Agents); 4FR53SIF3A (blinatumomab)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170201
[Lr] Data última revisão:
170201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-016-2837-1


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[PMID]:28134942
[Au] Autor:Rodríguez-Rodríguez S; Pomerantz A; Demichelis-Gómez R; Barrera-Lumbreras G; Barrales-Benítez OV; Lopez-Karpovitch X; Aguayo Á
[Ad] Endereço:Department of Hematology and Oncology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico.
[Ti] Título:Impact of Aberrant Antigens in the Outcome of Patients with Acute Leukemia at a Referral Institution in Mexico City.
[So] Source:Rev Invest Clin;68(6):305-313, 2016 Nov-Dec.
[Is] ISSN:0034-8376
[Cp] País de publicação:Mexico
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Patients with acute leukemia can express aberrant markers, defined as antigens that are normally restricted to a different lineage. The reported significance and frequency of these markers is inconclusive. We assessed the frequency and impact of aberrant markers in patients with acute leukemia in a referral institution in Mexico City. METHODS: We included 433 patients, diagnosed and treated between 2005 and 2015 in our institution. RESULTS: Aberrant markers were expressed in 128 patients (29.6%); CD13 and CD33 were the most frequent aberrant markers in patients with acute lymphoblastic leukemia, while CD7 and CD19 were the most frequent in patients with acute myeloid leukemia. In the univariate analysis, the group with aberrant markers had a lower disease-free survival when compared with the aberrant-free group (8 vs. 13 months) (p = 0.03). Aberrant expression of CD10, CD20, and CD33 correlated with a worse outcome in a statistically significant manner. In the multivariate analysis, male gender, lymphoid lineage, secondary leukemia, high risk at diagnosis, and the presence of aberrant markers had a significantly negative impact on disease-free survival. CONCLUSION: The use of more aggressive treatment strategies could be considered in patients with acute leukemia and an aberrant expression of CD10, CD20, and CD33.
[Mh] Termos MeSH primário: Antígenos CD/sangue
Antígenos de Neoplasias/sangue
Leucemia Mieloide Aguda/sangue
Leucemia-Linfoma Linfoblástico de Células Precursoras/sangue
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Biomarcadores Tumorais/sangue
Intervalo Livre de Doença
Feminino
Seguimentos
Seres Humanos
Leucemia Aguda Bifenotípica/sangue
Masculino
México
Meia-Idade
Análise Multivariada
Estudos Retrospectivos
Fatores de Risco
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Antigens, Neoplasm); 0 (Biomarkers, Tumor)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170131
[St] Status:MEDLINE


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Fotocópia
[PMID]:27607436
[Au] Autor:Yamamoto K; Kawamoto S; Mizutani Y; Yakushijin K; Yamashita T; Nakamachi Y; Kawano S; Hayashi Y; Matsuoka H; Minami H
[Ad] Endereço:Division of Medical Oncology/Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe, Japan.
[Ti] Título:Mixed Phenotype Acute Leukemia with t(12;17)(p13;q21)/TAF15-ZNF384 and Other Chromosome Abnormalities.
[So] Source:Cytogenet Genome Res;149(3):165-170, 2016.
[Is] ISSN:1424-859X
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The t(12;17)(p13;q11∼21) translocation is a very rare but recurrent cytogenetic aberration observed predominantly in early pre-B acute lymphoblastic leukemia (ALL) with CD19+CD10-CD33+ phenotype. This translocation was shown to form a fusion gene between TAF15 at 17q12 and ZNF384 at 12p13. On the other hand, der(1;18)(q10;q10) has been detected as a rare unbalanced whole-arm translocation leading to trisomy 1q in myeloid malignancies. We describe here the first case of mixed phenotype acute leukemia (MPAL) with a t(12;17)(p13;q21)/TAF15-ZNF384, which also had der(1;18)(q10;q10) as an additional abnormality. A 74-year-old woman was diagnosed with MPAL, B/myeloid, because bone marrow blasts were positive for myeloperoxidase, CD19, and CD22. Chromosome analysis showed 46,XX, +1,der(1;18)(q10;q10),t(2;16)(q13;q13),t(12;17)(p13;q21). Expression of the TAF15-ZNF384 fusion transcript was confirmed: TAF15 exon 6 was fused in-frame to ZNF384 exon 3. This type of fusion gene has been reported in 1 acute myeloid leukemia case and 3 ALL cases. Thus, at present, it is difficult to find a specific association between the structure of the TAF15-ZNF384 fusion gene and the leukemia phenotype. The TAF15-ZNF384 fusion may occur in early common progenitor cells that could differentiate into both the myeloid and lymphoid lineages. Furthermore, der(1;18)(q10;q10) might play some role in the appearance of an additional myeloid phenotype.
[Mh] Termos MeSH primário: Aberrações Cromossômicas
Cromossomos Humanos Par 12/genética
Cromossomos Humanos Par 17/genética
Leucemia Aguda Bifenotípica/genética
Fatores Associados à Proteína de Ligação a TATA/genética
Transativadores/genética
Translocação Genética/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Sequência de Bases
Criança
Pré-Escolar
Bandeamento Cromossômico
Éxons/genética
Feminino
Seres Humanos
Cariótipo
Masculino
Proteínas de Fusão Oncogênicas/genética
Fenótipo
Leucemia-Linfoma Linfoblástico de Células Precursoras B/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Trissomia/genética
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Oncogene Proteins, Fusion); 0 (TAF15 protein, human); 0 (TATA-Binding Protein Associated Factors); 0 (Trans-Activators); 0 (ZNF384 protein, human)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170116
[Lr] Data última revisão:
170116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160909
[St] Status:MEDLINE



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