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[PMID]:29385210
[Au] Autor:Eadie LN; Dang P; Goyne JM; Hughes TP; White DL
[Ad] Endereço:Cancer Theme, South Australian Health and Medical Research Institute (SAHMRI), Adelaide, South Australia.
[Ti] Título:ABCC6 plays a significant role in the transport of nilotinib and dasatinib, and contributes to TKI resistance in vitro, in both cell lines and primary patient mononuclear cells.
[So] Source:PLoS One;13(1):e0192180, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ATP Binding Cassette family efflux proteins ABCB1 and ABCG2 have previously been demonstrated to interact with Tyrosine Kinase Inhibitors (TKIs); however, evidence for the interaction of other potentially relevant drug transporters with TKIs is lacking. Through Taqman transporter array technology we assessed the impact of nilotinib on mRNA expression of ABC transporters, with ABCC6 identified as a transporter of interest. Additionally, increased expression of ABCC6 mRNA was observed during in vitro development of nilotinib resistance in BCR-ABL1-expressing cell lines. K562 cells exposed to gradually increasing concentrations of nilotinib (to 2 µM) expressed up to 57-fold higher levels of ABCC6 mRNA when compared with control cells (p = 0.002). Analogous results were observed in nilotinib resistant K562-Dox cells (up to 33-fold higher levels of ABCC6, p = 0.002). IC50 experiments were conducted on patient mononuclear cells in the absence and presence of three ABCC6 inhibitors: indomethacin, probenecid and pantoprazole. Results demonstrated that all three inhibitors significantly reduced nilotinib IC50 (p<0.001) indicating ABCC6 is likely involved in nilotinib transport. Cell line data confirmed these findings. Similar results were obtained for dasatinib, but not imatinib. Combined, these studies suggest that nilotinib and dasatinib are likely substrates of ABCC6 and to our knowledge, this is the first report of ABCC6 involvement in TKI transport. In addition, ABCC6 overexpression may also contribute to nilotinib and dasatinib resistance in vitro. With nilotinib and dasatinib now front line therapy options in the treatment of CML, concomitant administration of ABCC6 inhibitors may present an attractive option to enhance TKI efficacy.
[Mh] Termos MeSH primário: Dasatinibe/farmacologia
Leucócitos Mononucleares/efeitos dos fármacos
Proteínas Associadas à Resistência a Múltiplos Medicamentos/fisiologia
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular
Dasatinibe/farmacocinética
Resistência a Medicamentos Antineoplásicos
Proteínas de Fusão bcr-abl/metabolismo
Seres Humanos
Proteínas Associadas à Resistência a Múltiplos Medicamentos/genética
Inibidores de Proteínas Quinases/farmacocinética
Pirimidinas/farmacocinética
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide); 0 (ABCC6 protein, human); 0 (Multidrug Resistance-Associated Proteins); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (RNA, Messenger); EC 2.7.10.2 (Fusion Proteins, bcr-abl); RBZ1571X5H (Dasatinib)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0192180


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[PMID]:29390324
[Au] Autor:Harada Y; Nishiwaki S; Sugimoto T; Onodera K; Goto T; Sato T; Kamoshita S; Kawashima N; Seto A; Okuno S; Yamamoto S; Iwasaki T; Ozawa Y; Miyamura K; Akatsuka Y; Sugiura I
[Ad] Endereço:Division of Hematology and Oncology, Toyohashi Municipal Hospital.
[Ti] Título:Successful treatment with allogeneic stem cell transplantation followed by DLI and TKIs for e6a2 BCR-ABL-positive acute myeloid leukaemia: A case report and literature review.
[So] Source:Medicine (Baltimore);96(50):e9160, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Patients with the e6a2 BCR-ABL transcript, 1 of the atypical transcripts, have been reported to have a poor prognosis, and allogeneic stem cell transplantation (ASCT) can be considered as additional therapy. However, long-term survival after ASCT for this disease is rare. PATIENT CONCERNS: This report concerns a 55-year-old female patient with e6a2 BCR-ABL-positive acute myeloid leukemia including the outcome of ASCT followed by donor lymphocyte infusion (DLI). DIAGNOSES: The breakpoint was confirmed by direct sequencing. Her minimal residual disease could be detected by nested reverse-transcription polymerase chain reaction using primers for the minor BCR-ABL (e1a2) transcript. INTERVENTIONS: Treatment with tyrosine kinase inhibitors (TKIs) and ASCT followed by DLI. OUTCOMES: Despite multiple cytogenetic and molecular relapses after ASCT, she remains in molecular remission at 46 months after ASCT. LESSONS: This case indicates the efficacy of the combination of the graft-versus-leukemia effect and TKIs for e6a2 BCR-ABL-positive acute leukemia. When the Philadelphia chromosome with an unusual chromosomal breakpoint is suggested, we should clarify the breakpoint because that information can aid molecular assessments and decisions to provide an additional or alternative therapy.
[Mh] Termos MeSH primário: Transplante de Células-Tronco Hematopoéticas
Leucemia Mieloide Aguda/terapia
[Mh] Termos MeSH secundário: Feminino
Proteínas de Fusão bcr-abl
Efeito Enxerto vs Leucemia
Seres Humanos
Transfusão de Linfócitos
Meia-Idade
Neoplasia Residual
Cromossomo Filadélfia
Proteínas Tirosina Quinases/antagonistas & inibidores
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009160


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[PMID]:28457753
[Au] Autor:Sadovnik I; Herrmann H; Eisenwort G; Blatt K; Hoermann G; Mueller N; Sperr WR; Valent P
[Ad] Endereço:Department of Internal Medicine I, Division of Hematology & Hemostaseology, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Expression of CD25 on leukemic stem cells in BCR-ABL1 CML: Potential diagnostic value and functional implications.
[So] Source:Exp Hematol;51:17-24, 2017 07.
[Is] ISSN:1873-2399
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Chronic myeloid leukemia (CML) is a stem cell-derived leukemia in which neoplastic cells exhibit the Philadelphia chromosome and the related oncoprotein BCR-ABL1. The disease is characterized by an accumulation of myeloid precursor cells in the peripheral blood and bone marrow (BM). A small fraction of neoplastic cells in the CML clone supposedly exhibits self-renewal and thus long-term disease-propagating ability. However, so far, little is known about the phenotype, function, and target expression profiles of these leukemic stem cells (LSCs). Recent data suggest that CML LSCs aberrantly express the interleukin-2 receptor alpha chain CD25. Whereas normal CD34 /CD38 BM stem cells display only low amounts of CD25 or lack CD25 altogether, CD34 /CD38 LSCs express CD25 strongly in more than 90% of all patients with untreated CML. As a result, CD25 can be used to identify and quantify CML LSCs. In addition, it has been shown that CD25 serves as a negative growth regulator of CML LSCs. Here, we review the value of CD25 as a novel marker and potential drug target in CML LSCs.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/biossíntese
Proteínas de Fusão bcr-abl/metabolismo
Regulação Leucêmica da Expressão Gênica
Subunidade alfa de Receptor de Interleucina-2/biossíntese
Leucemia Mielogênica Crônica BCR-ABL Positiva/diagnóstico
Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo
Proteínas de Neoplasias/metabolismo
Células-Tronco Neoplásicas/metabolismo
[Mh] Termos MeSH secundário: ADP-Ribosil Ciclase 1/metabolismo
Antígenos CD34/metabolismo
Células da Medula Óssea/metabolismo
Seres Humanos
Glicoproteínas de Membrana/metabolismo
Células-Tronco Neoplásicas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD34); 0 (BCR-ABL1 fusion protein, human); 0 (Biomarkers, Tumor); 0 (IL2RA protein, human); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Membrane Glycoproteins); 0 (Neoplasm Proteins); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.2.2.5 (CD38 protein, human); EC 3.2.2.6 (ADP-ribosyl Cyclase 1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29265184
[Au] Autor:Cony-Makhoul P; Gardembas M; Coiteux V; Carpentier N; Pommier C; Violet I; Quittet P; Berger MG; TARGET-RMC Investigators
[Ad] Endereço:Centre Hospitalier Annecy Genevois, Pringy, France.
[Ti] Título:Nilotinib after imatinib first-line: a real-life longitudinal cohort of patients with chronic myeloid leukaemia in chronic phase.
[So] Source:Br J Haematol;180(3):356-364, 2018 02.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This prospective, observational study enrolled 150 adult patients with chronic myeloid leukaemia (CML) in chronic phase (CP) treated with nilotinib as second-line after imatinib, in a real life setting in France. Two-thirds of patients switched to nilotinib treatment due to lack of imatinib efficacy. Of 146 evaluable patients, 16 (11·0%) (95% confidence interval: 6·4-17·2%) achieved uMR , defined as undetectable molecular disease in cDNA with MR sensitivity (≥10 000 ABL1 transcripts) at 18 months and confirmed at 24 months (primary endpoint). Among patients without major molecular response (MMR) or deep molecular response (DMR) at study entry, 66·3% achieved MMR and 44·2% DMR within a median of 5·7 and 6·24 months, respectively. Fifty-three patients (36·3%) have prematurely terminated the study before 24 months of follow-up, primarily due to nilotinib treatment discontinuation (n = 43; 29·5%), mainly motivated by treatment intolerance (n = 27; 18·5%) and inefficacy (n = 10; 6·8%). The most frequent extra-haematological adverse events (AEs) reported as related to treatment with nilotinib were pruritus (16·4%), asthenia (13·7%) and dry skin (13·0%). Ischaemic cardiovascular AEs were reported in 18 patients (12·3%). This French nationwide large cohort adds valuable information to the body of evidence on the efficiency and safety of nilotinib in the treatment of patients with CP-CML.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Leucemia Mieloide de Fase Crônica/tratamento farmacológico
Leucemia Mieloide de Fase Crônica/patologia
Inibidores de Proteínas Quinases/uso terapêutico
Pirimidinas/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Antineoplásicos/administração & dosagem
Antineoplásicos/efeitos adversos
Estudos de Coortes
Resistência a Medicamentos Antineoplásicos
Feminino
Proteínas de Fusão bcr-abl/genética
Seres Humanos
Mesilato de Imatinib/administração & dosagem
Mesilato de Imatinib/efeitos adversos
Mesilato de Imatinib/uso terapêutico
Leucemia Mieloide de Fase Crônica/genética
Leucemia Mieloide de Fase Crônica/mortalidade
Estudos Longitudinais
Masculino
Meia-Idade
Inibidores de Proteínas Quinases/administração & dosagem
Inibidores de Proteínas Quinases/efeitos adversos
Pirimidinas/administração & dosagem
Pirimidinas/efeitos adversos
Retratamento
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (4-methyl-N-(3-(4-methylimidazol-1-yl)-5-(trifluoromethyl)phenyl)-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)benzamide); 0 (Antineoplastic Agents); 0 (BCR-ABL1 fusion protein, human); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 8A1O1M485B (Imatinib Mesylate); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.15042


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[PMID]:28452984
[Au] Autor:Togasaki E; Takeda J; Yoshida K; Shiozawa Y; Takeuchi M; Oshima M; Saraya A; Iwama A; Yokote K; Sakaida E; Hirase C; Takeshita A; Imai K; Okumura H; Morishita Y; Usui N; Takahashi N; Fujisawa S; Shiraishi Y; Chiba K; Tanaka H; Kiyoi H; Ohnishi K; Ohtake S; Asou N; Kobayashi Y; Miyazaki Y; Miyano S; Ogawa S; Matsumura I; Nakaseko C; Naoe T
[Ad] Endereço:Department of Hematology, Chiba University Hospital, Chiba, Japan.
[Ti] Título:Frequent somatic mutations in epigenetic regulators in newly diagnosed chronic myeloid leukemia.
[So] Source:Blood Cancer J;7(4):e559, 2017 Apr 28.
[Is] ISSN:2044-5385
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Although tyrosine kinase inhibitors (TKIs) have significantly improved the prognosis of chronic myeloid leukemia (CML), the ability of TKIs to eradicate CML remains uncertain and patients must continue TKI therapy for indefinite periods. In this study, we performed whole-exome sequencing to identify somatic mutations in 24 patients with newly diagnosed chronic phase CML who were registered in the JALSG CML212 study. We identified 191 somatic mutations other than the BCR-ABL1 fusion gene (median 8, range 1-17). Age, hemoglobin concentration and white blood cell counts were correlated with the number of mutations. Patients with mutations ⩾6 showed higher rate of achieving major molecular response than those<6 (P=0.0381). Mutations in epigenetic regulator, ASXL1, TET2, TET3, KDM1A and MSH6 were found in 25% of patients. TET2 or TET3, AKT1 and RUNX1 were mutated in one patient each. ASXL1 was mutated within exon 12 in three cases. Mutated genes were significantly enriched with cell signaling and cell division pathways. Furthermore, DNA copy number analysis showed that 2 of 24 patients had uniparental disomy of chromosome 1p or 3q, which disappeared major molecular response was achieved. These mutations may play significant roles in CML pathogenesis in addition to the strong driver mutation BCR-ABL1.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/genética
Dioxigenases/genética
Histona Desmetilases/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Proteínas Proto-Oncogênicas/genética
Proteínas Repressoras/genética
[Mh] Termos MeSH secundário: Fatores Etários
Variações do Número de Cópias de DNA/genética
Resistência a Medicamentos Antineoplásicos/genética
Epigênese Genética/genética
Feminino
Proteínas de Fusão bcr-abl/genética
Seres Humanos
Leucemia Mielogênica Crônica BCR-ABL Positiva/sangue
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
Contagem de Leucócitos
Masculino
Mutação
Inibidores de Proteínas Quinases/administração & dosagem
Transdução de Sinais
Sequenciamento Completo do Exoma
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ASXL1 protein, human); 0 (DNA-Binding Proteins); 0 (G-T mismatch-binding protein); 0 (Protein Kinase Inhibitors); 0 (Proto-Oncogene Proteins); 0 (Repressor Proteins); 0 (TET2 protein, human); EC 1.- (TET3 protein, human); EC 1.13.11.- (Dioxygenases); EC 1.14.11.- (Histone Demethylases); EC 1.5.- (KDM1A protein, human); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1038/bcj.2017.36


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[PMID]:28467002
[Au] Autor:Kayastha GK; Ranjitkar N; Gurung R; Kc RK; Karki S; Shrestha R; Rajbhandari P; Thapa RK; Poudyal B; Acharya P; Roberts DJ; Hayes B; Zimmerman M; Basnyat B
[Ad] Endereço:Patan Academy of Health Science, Patan Hospital, Kathmandu, Nepal.
[Ti] Título:The use of Imatinib resistance mutation analysis to direct therapy in Philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukaemia patients failing Imatinib treatment, in Patan Hospital, Nepal.
[So] Source:Br J Haematol;177(6):1000-1007, 2017 06.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Philadelphia chromosome/BCR-ABL1 positive chronic myeloid leukaemia (CML) can be successfully treated with Glivec (Imatinib), which is available free of cost through the Glivec International Patient Assistance programme (GIPAP) to patients with proven CML without means to pay for the drug. We review the acquired mutations in the tyrosine kinase encoded by the BCR-ABL1 gene underlying Glivec failure or resistance in a cohort of 388 imatinib-treated CML patients (149 Female and 239 male) registered between February 2003 and June 2016 in Nepal. Forty-five patients (11 female 34 male) were studied; 18 different BCR-ABL1 mutations were seen in 33 patients. P-loop mutation, Kinase domain and A-loop mutations were seen in 9, 16 and 4 patients respectively. Other mutations were seen in five patients. A T315I mutation was the most common mutation, followed by F359V and M244V. Sixteen mutations showed intermediate activity to complete resistance to Glivec. Among the 45 patients evaluated for BCR-ABL1 mutations, 4 were lost to follow-up, 14 died and 27 are still alive. Among the surviving patients, 16 are receiving Nilotinib, 5 Dasatinib and 3 Ponatinib, while 3 patients were referred to India, one of who received allogenic bone marrow transplantation. Understanding the spectrum of further acquired mutations in BCR-ABL1 may help to choose more specific targeted tyrosine kinase inhibitors that can be provided by GIPAP.
[Mh] Termos MeSH primário: Antineoplásicos/uso terapêutico
Resistência a Medicamentos Antineoplásicos/genética
Proteínas de Fusão bcr-abl/genética
Mesilato de Imatinib/uso terapêutico
Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico
Mutação
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Masculino
Proteínas Tirosina Quinases/genética
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BCR-ABL1 fusion protein, human); 8A1O1M485B (Imatinib Mesylate); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14683


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[PMID]:28450577
[Au] Autor:Parilla M; Venkataraman G
[Ad] Endereço:University of Chicago.
[Ti] Título:The thin line between CML and CMML.
[So] Source:Blood;129(17):2456, 2017 04 27.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Proteínas de Fusão bcr-abl
Leucemia Mielogênica Crônica BCR-ABL Positiva
Leucemia Mielomonocítica Crônica
[Mh] Termos MeSH secundário: Feminino
Proteínas de Fusão bcr-abl/sangue
Proteínas de Fusão bcr-abl/genética
Seres Humanos
Leucemia Mielogênica Crônica BCR-ABL Positiva/sangue
Leucemia Mielogênica Crônica BCR-ABL Positiva/diagnóstico
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
Leucemia Mielomonocítica Crônica/sangue
Leucemia Mielomonocítica Crônica/diagnóstico
Leucemia Mielomonocítica Crônica/genética
Leucemia Mielomonocítica Crônica/patologia
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180117
[Lr] Data última revisão:
180117
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-01-763565


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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]:29023488
[Au] Autor:Askmyr M; von Palffy S; Hansen N; Landberg N; Högberg C; Rissler M; Ågerstam H; Fioretos T
[Ad] Endereço:Department of Clinical Genetics, Lund University, Lund, Sweden.
[Ti] Título:Transgenic expression of human cytokines in immunodeficient mice does not facilitate myeloid expansion of BCR-ABL1 transduced human cord blood cells.
[So] Source:PLoS One;12(10):e0186035, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Several attempts have been made to model chronic myeloid leukemia (CML) in a xenograft setting but expansion of human myeloid cells in immunodeficient mice has proven difficult to achieve. Lack of cross-reacting cytokines in the microenvironment of the mice has been proposed as a potential reason. In this study we have used NOD/SCID IL2-receptor gamma deficient mice expressing human SCF, IL-3 and GM-CSF (NSGS mice), that should be superior in supporting human, and particularly, myeloid cell engraftment, to expand BCR-ABL1 expressing human cells in order to model CML. NSGS mice transplanted with BCR-ABL1 expressing cells became anemic and had to be sacrificed due to illness, however, this was not accompanied by an expansion of human myeloid cells but rather we observed a massive expansion of human T-cells and macrophages/histiocytes. Importantly, control human cells without BCR-ABL1 expression elicited a similar reaction, although with a slight delay of disease induction, suggesting that while BCR-ABL1 contributes to the inflammatory reaction, the presence of normal human hematopoietic cells is detrimental for NSGS mice.
[Mh] Termos MeSH primário: Citocinas/genética
Sangue Fetal/citologia
Proteínas de Fusão bcr-abl/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Feminino
Sangue Fetal/transplante
Expressão Gênica
Fator Estimulador de Colônias de Granulócitos e Macrófagos/genética
Seres Humanos
Interleucina-3/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Masculino
Camundongos Endogâmicos NOD
Camundongos SCID
Camundongos Transgênicos
Transdução Genética
Transplante Heterólogo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BCR-ABL1 fusion protein, human); 0 (Cytokines); 0 (IL3 protein, human); 0 (Interleukin-3); 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186035


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[PMID]:28986256
[Au] Autor:Jiang MJ; Dai JJ; Gu DN; Huang Q; Tian L
[Ad] Endereço:Institute of Translational Medicine, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China; Shanghai Key Laboratory of Pancreatic Diseases, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 201620, China.
[Ti] Título:MicroRNA-7 inhibits cell proliferation of chronic myeloid leukemia and sensitizes it to imatinib in vitro.
[So] Source:Biochem Biophys Res Commun;494(1-2):372-378, 2017 Dec 09.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNA is a large class of non-coding small RNA that exerts critical roles in many physiological processes including cell proliferation. MicroRNA-7 (miR-7) has been considered as a tumor suppressor in most malignant tumors versus a tumor promoter in some other ones. However, its role in chronic myeloid leukemia remains unknown. Herein, we found that K562 cell proliferation was largely suppressed when it was stably transfected with miR-7. In accordance with that, apoptosis was also significantly upregulated in miR-7 stably-transfected K562 cells. Moreover, we found that miR-7-overexpressed K562 cells were far more sensitive to imatinib than controls. Further investigations showed that the ABL1 was a direct target of miR-7. Expression level of BCR-ABL and the activity of its downstream PI3K/AKT pathway were significantly reduced in miR-7-transfected cells. Taken together, our results showed that miR-7 inhibited proliferation and promoted apoptosis in K562 cells, and miR-7 might help to sensitize them to imatinib through BCR-ABL/PI3K/AKT signaling in chronic myeloid leukemia.
[Mh] Termos MeSH primário: Proteínas de Fusão bcr-abl/genética
MicroRNAs/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Proteínas de Fusão bcr-abl/metabolismo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Mesilato de Imatinib/farmacologia
Células K562
MicroRNAs/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (BCR-ABL1 fusion protein, human); 0 (MIRN7 microRNA, human); 0 (MicroRNAs); 8A1O1M485B (Imatinib Mesylate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[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:171008
[St] Status:MEDLINE



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