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Molecular characterization of C-KIT proto-oncogene in Hong Kong leukemia patients : 'culprit or bystander' /Chui, Chung-hin. January 1998 (has links)
Thesis (Ph. D.)--University of Hong Kong, 1998. / Includes bibliographical references (leaves 132-144).
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The interaction between two MLL fusion partner genes, AF4 and AF9 /Erfurth, Frank. January 2001 (has links)
Thesis (Ph. D.)--University of Chicago, Dept. of Pathaology, 2002. / Includes bibliographical references. Also available on the Internet.
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Structural and functional characterization of EEN/EndophilinA2, a fusion partner in acute leukemia /Cheung, Ngai. January 2005 (has links)
Thesis (Ph. D.)--University of Hong Kong, 2005.
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Ras signalling pathway and MLL-rearranged leukaemiasNg, Ming-him. January 2006 (has links)
Thesis (M. Phil.)--University of Hong Kong, 2006. / Title proper from title frame. Also available in printed format.
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Structural and functional characterization of EEN/EndophilinA2, a fusion partner in acute leukemiaCheung, Ngai., 張毅. January 2005 (has links)
published_or_final_version / Pathology / Doctoral / Doctor of Philosophy
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Molecular characterization of C-KIT proto-oncogene in Hong Kong leukemia patients: 'culprit or bystander'Chui, Chung-hin., 徐宗憲. January 1998 (has links)
published_or_final_version / Pathology / Doctoral / Doctor of Philosophy
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The molecular characterisation of childhood acute lymphoblastic leukaemia : gene expression profiles to elucidate leukaemogenesis /Boag, Joanne. January 2006 (has links)
Thesis (Ph.D.)--University of Western Australia, 2007.
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Clonal rearrangement of T-cell receptor delta gene in hematological malignancies and applications in detection of minimal residual disease /Chan, Wai. January 1995 (has links)
Thesis (M. Phil.)--University of Hong Kong, 1996. / Includes bibliographical references (leaf 121-133).
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Ras signalling pathway and MLL-rearranged leukaemias /Ng, Ming-him. January 2006 (has links)
Thesis (M. Phil.)--University of Hong Kong, 200. / Also available online.
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Polimorfismos dos genes MBL2, IL-10 e TNFα em pacientes com leucemia aguda na infância / Analyse of MBL2, IL-10 and TNFα polymorphisms genes in patients with acute leukemia childhoodBRITTO, Lidiane Regia Pereira Braga de 13 June 2014 (has links)
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Previous issue date: 2014-06-13 / The chemotherapy used in the treatment of acute leukemias (AL) in pediatric immune system, promoting the morbidity and mortality from infection during the induction phase of treatment, the first 50 days. However, questions remain about why some of these children develop severe and fatal infections. The occurrence of polymorphisms (SNPs) in regions associated with regulation of immune system components may be associated with proteins that indicate the recognition of pathogens, such as the mannose-binding lectin (MBL) and cytokine tumor necrosis factor alpha (TNFα) and interleukin 10 (IL-10). The aim of this study was to evaluate the association between susceptibility to infection of pediatric patients and the following polymorphisms: -550 promoter regions (alleles H / L), -221 (alleles X / Y) and structural exon 1 (alleles A / O) MBL2 gene, the promoter region -1082 (allele G / A), -819/-592 (allele C / T) of the IL-10 gene region and -308 (allele G / A) gene TNFα. The 225 patients were evaluated in the CEONHPE / HUOC-UPE. Of these, 84% (n = 189) were diagnosed with acute lymphoblastic leukemia (ALL). Overall group (AL), there was no association between the three polymorphic regions studied with febrile neutropenia (-550 H/L, p=0.912; -221 X/Y, p=0.471; exon 1 A/O, p=0.138), number of infectious events (-550 H/L, p=0.912; exon 1 A/O, p=0.741) and the risk of relapse (-550 H/L, p=0.588; exon 1 A/O, p=0.882). However, an association was observed between age and genotype AO of exon 1 in patients younger than 10 years in AL (p=0.027) and ALL (p=0.038). In conclusion, we can suggest that the pediatric patients younger than 10 years, carriers of the MBL2 genotype AO, that determine low oligomerization and compromised biological function of the protein may have immune response deficiency. / A quimioterapia utilizada no tratamento de leucemias agudas (LA) pediátricas deprime o sistema imune, favorecendo a morbidade e mortalidade por infecções durante a fase de indução do tratamento, ou seja, os primeiros 50 dias. Entretanto, permanecem duvidas sobre o porquê de algumas dessas crianças desenvolverem infecções severas e fatais. A ocorrência de polimorfismos (SNPs) em regiões promotoras e estruturais de genes de componentes do sistema imune pode estar associada ao padrão de reconhecimento de patógenos, a exemplo da Lectina Ligadora de Manose (MBL) e das citocinas Fator de Necrose Tumoral alfa (TNFα) e interleucina 10 (IL-10). O objetivo deste trabalho foi verificar uma possível associação entre a susceptibilidade à infecção nos pacientes pediátricos com os polimorfismos nas regiões promotoras -550 (alelos H/L), -221 (alelos X/Y) e estrutural éxon 1 (alelos A/O) do gene MBL2, das regiões promotoras -1082 (alelos G/A), -819/-592 (alelos C/T) do gene IL-10 e região -308 (alelos G/A) do gene TNFα. Foram avaliados 225 pacientes com LA em tratamento no CEONHPE/HUOC-UPE. Destes, 84%(n=189) tiveram o diagnóstico de Leucemia Linfoblástica Aguda (LLA). No grupo geral (LA), houve ausência de associação entre as três regiões polimórficas estudadas do gene MBL2 com a neutropenia febril (-550 H/L, p=0,912; -221 X/Y, p=0,471; éxon 1 A/O, p=0,138), número de eventos infecciosos (-550 H/L, p=0,912; éxon 1 A/O, p=0.741) e o risco de recaída (-550 H/L, p=0,588; éxon 1 A/O, p=0,882). Entretanto, observou-se que o genótipo AO do gene MBL2 foi associado aos pacientes pediátricos com LA (p=0,027) e LLA (p=0,038) que apresentavam idade abaixo de 10 anos. Com relação aos polimorfismos dos genes IL-10 e TNFα não foi observada associação com as mesmas situações clínicas anteriormente referidas e nem com a idade dos pacientes. Em conclusão, podemos sugerir que os pacientes pediátricos com idade abaixo de 10 anos e portadores do genótipo AO do gene MBL, que determina baixa oligomerização e função biológica comprometida da proteína podem apresentar deficiência na resposta imune.
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