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Journal articles on the topic 'Chronic myeloid leucemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 February 2022

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1

ArnautovicCustovic, Aida, Samira Hasic, Emina Kopic, Azra Jahic, and Svetlana Jovic. "Myeloprolipherative Disorder Type Chronic Myeloid Leucemia - Eosinophilic Form." Medical Archives 65, no. 3 (2011): 173. http://dx.doi.org/10.5455/medarh.2011.65.173-175.

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2

Cristófalo, Milena Martello, Carina Pita Lottenberg, and Rômulo Negrini. "Parto cesárea como fator de risco de leucemia infantil / C section as a risk fator for leucemias." Arquivos Médicos dos Hospitais e da Faculdade de Ciências Médicas da Santa Casa de São Paulo 64, no. 2 (2019): 84. http://dx.doi.org/10.26432/1809-3019.2019.64.2.084.

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Introdução: As condições de nascimento, em especial o parto cesáreo, impactam a curto e longo prazo a saúde infantil. Nesse estudo, tivemos como objetivo: Associar o parto cesárea a incidência de leucemias em crianças. Métodos: Trata-se de estudo observacional com pacientes dos Ambulatórios da Pediatria Oncológica, entre 0 a 14 anos, nascidos a termo, em tratamento ou acompanhamento por Leucemia Mieloblástica Aguda, Leucemia Linfoblástica Aguda, ou Leucemia Mielóide Crônica. A investigação sobre gestação e parto foi feita por meio de questionário, que aborda, após identificação do paciente, da

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3

Granjeiro, Claudia da Fonseca, Alex Semenoff-Segundo, Alessandra Nogueira Porto, Natalino Francisco da Silva, Álvaro Henrique Borges, and Tereza Aparecida Delle Vedove Semenoff. "Epidemiological Profile of Patients with Hematological Neoplasms in an Oncological Hospital of Mato Grosso." Journal of Health Sciences 20, no. 4 (2018): 232. http://dx.doi.org/10.17921/2447-8938.2018v20n4p232-237.

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O objetivo do estudo foi analisar os aspectos epidemiológicos de pacientes adultos com diagnóstico de neoplasia hematológica, no período de 2004 a 2014, em um Hospital Oncológico em Mato Grosso. A coleta de dados foi realizada através de busca e análise de 590 prontuários. Entre os pacientes, 335 (56,8%) eram do sexo masculino (p<0,05). A maioria possuía mais de 50 anos (p<0,05), com idade média de 53,97±16,55 anos. Quanto ao local de procedência, 257 pacientes eram provenientes da região metropolitana de Cuiabá (43,6%) e 333 (56,4%) de outros locais (p<0,05). A maioria eram pacientes

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4

Valencia, Juan E., and John J. Orozco. "Adaptation to Colombia and Venezuela of the economic model Dasatinib first-line treatment of chronic myeloid leukemia, developed by the York Health Economics Consortium." Medwave 12, no. 04 (2012): e5348-e5348. http://dx.doi.org/10.5867/medwave.2012.04.5348.

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5

Moreira Funke, Vaneuza Araujo, Lucas Gabriel Silva, Ana Lucia Vieira Mion, et al. "Analysis of BCR-ABL Levels As a Predictor of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation (HSCT) in Chronic Myeloid Leucemia (CML) in the Era of Tyrosine Kinase Inhibitors (ITQ)." Transplantation and Cellular Therapy 27, no. 3 (2021): S163—S164. http://dx.doi.org/10.1016/s2666-6367(21)00202-5.

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6

Silva, Adriane Maria B. da, Caroline Aquino Moreira-Nunes, and José Alexandre R. de Lemos. "Expressão do gene ABCA7 como indicador de adesão terapêutica ao Mesilato de Imatinib em pacientes com Leucemia Mieloide Crônica / Expression of the ABCA7 gene as adherence indicator to Imatinib Mesylate in patients with Chronic Myeloid Leukemia." Brazilian Journal of Health Review 4, no. 1 (2021): 1829–40. http://dx.doi.org/10.34119/bjhrv4n1-149.

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7

Ene, Georgiana, Ana Maria Vlădăreanu, Horia Bumbea, and Ion Dumitru. "T lymphocyte subsets studied in a patient with two associated hematologic neoplasias – chronic lymphocytic leukemia B and chronic myeloid leukemia." Romanian Journal of Medical Practice 14, no. 3 (2019): 325–30. http://dx.doi.org/10.37897/rjmp.2019.3.21.

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8

Ribeiro, Ana Claudia de Almeida, Juliana Elena Silveira Pratti, Thaisa Amorim Nogueira, and Benedito Carlos Cordeiro. "Acompanhamento Farmacoterpêutico e a Detecção de Reações Adversas a Inibidores de Tirosinoquinase utilizados no Tratamento da Leucemia Mielóide Crônica / Pharmacotherapeutic Follow-up and Detection of Adverse Reactions to Tyrosinokinase Inhibitors used in the Treatment of Chronic Myeloid Leukemia." Brazilian Journal of Health Review 3, no. 6 (2020): 19438–54. http://dx.doi.org/10.34119/bjhrv3n6-323.

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9

Ribeiro, Ana Claudia de Almeida, Juliana Elena Silveira Pratti, Thaisa Amorim Nogueira, and Benedito Carlos Cordeiro. "Acompanhamento Farmacoterpêutico e a Detecção de Reações Adversas a Inibidores de Tirosinoquinase utilizados no Tratamento da Leucemia Mielóide Crônica / Pharmacotherapeutic Follow-up and Detection of Adverse Reactions to Tyrosinokinase Inhibitors used in the Treatment of Chronic Myeloid Leukemia." Brazilian Journal of Health Review 3, no. 6 (2020): 19438–54. http://dx.doi.org/10.34119/bjhrv3n6-323.

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10

Mancini, Manuela, Sara De Santis, Cecilia Monaldi, et al. "Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Induces Genetic Instability and Can be Therapeutically Targeted." Blood 132, Supplement 1 (2018): 1726. http://dx.doi.org/10.1182/blood-2018-99-112908.

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Abstract The SETD2 protein is a histone methyltransferase that specifically catalyzes the trimethylation of Lysine 36 on histone H3 (H3K36me3). SETD2/H3K36me3 are implicated in transcript elongation and splicing, DNA repair, chromosome segregation. SETD2 gene deletions and/or mutations (mostly frameshift or nonsense) have been reported in solid tumors (clear cell renal cell carcinoma, bladder cancer, lung cancer, melanoma, endometrial cancer) and in acute leukemias. Using a Western Blotting (WB) approach to screen for SETD2 protein expression and for H3K36me3 levels in a relatively large cohor

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11

Mancini, Manuela, Sara De Santis, Cecilia Monaldi, et al. "Aurora Kinase a/MDM2-Mediated SETD2 Loss of Function in Chronic Myeloid Leukemia Patients in Blast Crisis Can be Therapeutically Targeted Inducing Apoptotic Cell Death in a Caspase-Dependent Way." Blood 134, Supplement_1 (2019): 4142. http://dx.doi.org/10.1182/blood-2019-126500.

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One of the hallmarks of chronic myeloid leukemia (CML) is genomic instability, that fosters the acquisition of tyrosine kinase inhibitor (TKI)-resistant BCR-ABL1 mutations and/or of additional chromosomal aberrations leading to progression to blast crisis (BC). Inactivating mutations in the SETD2 tumor suppressor occur in solid tumors and acute leukemias. SETD2 trimethylates histone H3 Lysine 36 (H3K36Me3) playing a key role in maintaining DNA integrity. We have recently demonstrated that, in CML, SETD2 loss of function may occur at the post-translational level. Reduced or null SETD2 and H3K36

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12

Cîrstea, Mihaela, Adriana Coliță, Bogdan Ionescu, et al. "Chronic myelomonocytic leukemia “myelodysplastic type’’ in transformation to acute myeloid leukemia – diagnostic and therapeutic options: case report and literature review / Leucemie mielomonocitară cronică forma mielodisplazică în transformare spre leucemie acută mieloidă – diagnostic și opțiuni terapeutice: prezentare de caz și revizuirea literaturii." Revista Romana de Medicina de Laborator 24, no. 3 (2016): 263–77. http://dx.doi.org/10.1515/rrlm-2016-0033.

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Abstract Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell disorder that is characterized by the presence of an absolute monocytosis (1 × 10^ 9/l) in the peripheral blood, the overlap of myelodisplastic aspects and myeloproliferative aspects in the bone marrow and tendency to transform into acute myeloid leukemia. CMML is considered to be the most aggressive chronic myeloid leukemia. We present the case of a 48 years old woman who was hospitalized in March 2013 in the Center of Hematology and Bone Marrow Transplantation for anemia related symptoms. Initial investigatio

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13

Rea, Delphine, Gabriel Etienne, Franck Emmanuel Nicolini, et al. "Front-Line Imatinib Mesylate (IM) in Patients with Newly Diagnosed Accelerated Phase (AP)-Chronic Myeloid Leukemia (CML), a Study From the FILMC Group (France Intergroupe Leucemie Myeloide Chronique)." Blood 114, no. 22 (2009): 3288. http://dx.doi.org/10.1182/blood.v114.22.3288.3288.

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Abstract Abstract 3288 Poster Board III-1 IM is approved for the treatment of AP-CML at 600mg daily. Clinical trials in which IM was evaluated in this setting have mainly enrolled patients (pts) who have failed prior therapies and the efficacy of the drug in newly diagnosed AP-CML has never been specifically studied. We collected data from 43 de novo pts with disease acceleration at diagnosis and treated with first-line IM. Thirty-three showed hematological acceleration (HEMAP) according to WHO 2002 or ELN 2006 criteria and 10 had cytogenetic acceleration only (CYAP), defined as the presence o

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14

Treiber, G., T. Wex, S. Eberhard, C. Hosius, and P. Malfertheiner. "Imatinib for hepatocellular cancer (HCC)—Focus on PK/PD modelling and liver function." Journal of Clinical Oncology 24, no. 18_suppl (2006): 13088. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.13088.

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13088 Background: Imatinib represents standard medical care for treatment of gastrointestinal stroma tumors (GIST) and chronic myeloic leucemia (CML). Indications for other malignancies are evolving, especially in the context of antiangiogenesis, mediated by the inhibition of platelet-derived growth factor (PDGF). Liver metastasis occurs often in GIST patients, usually not affecting liver function. No reliable data about imatinib metabolisation under conditions of true hepatic impairment are available. Methods: Phase-II trial, involving 10 patients with hepatocellular cancer (HCC) as a model d

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15

Monne, Maria, Giovanna Piras, Antonella Uras, et al. "Analysis of BCL11A gene Variants in Hematological Malignancies." Blood 114, no. 22 (2009): 2956. http://dx.doi.org/10.1182/blood.v114.22.2956.2956.

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Abstract Abstract 2956 Poster Board II-932 Background. The B-cell leukemia 11A gene (BCL11A/Evi9/CTIP1) is essential for normal lymphoid development and genetic association studies have shown its potential regulator effect in blood related phenotypes. BCL11A encodes a Krüppel-like zinc-finger protein and functions as a transcriptional repressor through its interaction with several proteins including BCL6. The corresponding mouse gene is a common site of retroviral integration in myeloid leukemia, and may function as a leukemia oncogene. It is down-regulated during hematopoietic cell different

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16

Guilhot, Francois, Francoise Rigal-Huguet, Joelle Guilhot та ін. "Long Term Outcome of Chronic Phase Chronic Myeloid Leukemia (CP CML) Patients (pts) from the French Spirit Study Comparing Imatinib (IM) 400 Mg to Higher Dose Imatinib or Combination with Peg-interferonα2a (PegIFN) or Cytarabine (Ara-C) : A Trial of the FI LMC (France intergroupe de la leucemie myéloïde chronique)". Blood 124, № 21 (2014): 1793. http://dx.doi.org/10.1182/blood.v124.21.1793.1793.

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Abstract Although they produce high rate of molecular response second generation tyrosine kinase inhibitors or imatinib cannot eradicate CML primitive progenitors. Interferon has been shown to modulate gene expression, inhibits leukemic cell growth and induces an immunomodulatory response. In vitro studies support the use of combination of IM plus interferon. We designed a phase III randomised multicenter open-label prospective trial comparing IM 400 mg/d (n=223) with 3 experimental arms: IM 600 mg/d (n=171), IM 400 mg/d combined to s/c Peg-IFN2a (90 µg/wk) (n=221) and IM 400 mg/d combined to

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17

Popescu, Roxana, Angela Dăscălescu, Cătălin Dănăilă та ін. "Co-expression of the CBFβ-MYH11 and BCR-ABL fusion genes in chronic myeloid leukaemia / Coexistenţa genelor de fuziune CBFβ-MYH11 şi BCR-ABL în leucemia mieloidă cronică". Romanian Review of Laboratory Medicine 23, № 2 (2015). http://dx.doi.org/10.1515/rrlm-2015-0013.

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AbstractThe coexistence of t(9;22) and inv(16) has been described in a very limited number of cases of CML, de novo or therapy-related AML. We report a patient with CML who presented both inversion of chromosome 16 and Philadelphia chromosome and evolved towards the blast phase under treatment with Imatinib. Laboratory diagnosis and monitoring was made by flow cytometry, conventional cytogenetics and molecular genetics techniques. The inv(16), detected by karyotyping in the Philadelphia chromosome positive clone at the moment of the blast transformation, was retrospectively assessed by means o

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