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<https://discovery.ucl.ac.uk/id/eprint/1333965> <http://purl.org/dc/terms/title> "Genetic determinants of sepsis in haematological malignancy"^^<http://www.w3.org/2001/XMLSchema#string> .
<https://discovery.ucl.ac.uk/id/eprint/1333965> <http://purl.org/ontology/bibo/abstract> "Background:\r\nSepsis is a systemic illness caused by microbial invasion of normally sterile parts\r\nof the body. In haematological malignancies, patients are more prone to\r\ndeveloping infections due to defects in the neutrophil count and function which\r\noccur as a part of the neoplastic process or due to chemotherapy. The presence of\r\nneutropenia calls for other means of defence including the innate immune system.\r\nGenetic studies have attempted to examine the relationship between particular\r\ngenes involved in innate immunity and susceptibility to infections. Genes involved\r\nin the host defence mechanism such as pathogen presentation, recognition and\r\nphagocytosis result in the initiation of a cascade of events ending in the innate\r\nimmune system activation. Chitotriosidase and nucleotide oligmerization domain\r\n(NOD2) are two genes suggested to have a possible role in the innate immune\r\nresponse against bacterial and fungal infections. Studies of acute lymphoblastic\r\nleukaemia (ALL) and NOD2 mutations have been conducted in allogenic transplant\r\npatients in order to examine any association with the incidence of relapse, survival\r\nand graft versus host disease. The occurrence of NOD2 variants are also\r\nimplicated in the onset or progression of different malignancies via its effect on\r\nimmune system. Purpose gene:\r\nThe aim of our study was to explore the effect of mutations in genes involved in the\r\ninnate immune system in relation to incidence and outcome of sepsis, prevalence\r\nof particular microorganism, and depth and duration of neutropenia in patients with\r\nhaematological malignancies. The study aimed to identify mutations in\r\nchitotriosidase and NOD2, individually, and then looked at the synergetic effect of both mutations, given previous evidence of molecular interaction between the gene\r\nproducts. We also looked at NOD2 mutation in non-transplanted ALL patients so\r\nas to evaluate the effect of this mutation on outcome and prognosis.\r\nMethods:\r\nThe study was carried out in the RFH in patients diagnosed with haematological\r\nmalignancies. Blood was collected and DNA extracted. Genotyping identified\r\nchitotriosidase mutations while NOD2 missense mutations (SNP8 and SNP12)\r\nwere determined by pyrosequencing.\r\nIn the study of NOD2 mutations and ALL outcome, samples were collected as a\r\npart of UKALL-12 trial-MRD study in patients with the diagnosis of ALL. The NOD2\r\nmutations (SNP8, SNP12 and SNP13) were identified by genescanning.\r\nResults:\r\nThe incidence of febrile events with positive (p=0.031) or negative growth for any\r\norganism cultures (p=0.029) was increased in patients with chitotriosidase\r\nmutations. These results were most significant during periods of neutropenia;\r\nfebrile events with bacterial isolates (p=0.015) and without (p=0.007).\r\nDuring periods of normal neutrophil count the incidence of fevers with positive\r\nbacterial cultures was also increased in patients with NOD2 mutation,(p=0.017).\r\nThe incidence of fevers without positive cultures was decreased (p=0.029). There\r\nwere no significant differences in CR, incidence of relapse or OS in ALL patients\r\nwith NOD2 mutations. Conclusions:\r\nThis study suggests an association between chitotriosidase mutations and the\r\nincidence of febrile events (with or without positive bacterial cultures) in\r\nneutropenic patients. The NOD2 mutation was found in association with an\r\nincreased incidence of fevers with bacterial organisms identified and a decreased\r\nincidence of fever of unknown origin in non-neutropenic patients."^^<http://www.w3.org/2001/XMLSchema#string> .
<https://discovery.ucl.ac.uk/id/eprint/1333965> <http://purl.org/dc/terms/date> "2011-10-28" .
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