Bibliografias temáticas / Acute Leukaemia - Treatment

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Literatura científica selecionada sobre o tema "Acute Leukaemia - Treatment"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 25 de janeiro de 2023

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Artigos de revistas sobre o assunto "Acute Leukaemia - Treatment"

Kuzmits, Rudolf, Paul Aiginger, Matthias M. Müller, Günter Steurer e Werner Linkesch. "Assessment of the sensitivity of leukaemic cells to cytotoxic drugs by bioluminescence measurement of ATP in cultured cells". Clinical Science 71, n.º 1 (1 de julho de 1986): 81–88. http://dx.doi.org/10.1042/cs0710081.

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1. A short-term test in vitro is described, which can be used to detect resistance to cytostatic agents in leukaemic cells. Leukaemic cell suspensions were incubated with cytostatic agents and the resulting intracellular ATP concentrations were measured by a bioluminescence ATP assay. 2. There was a clear dose-effect relationship in acute leukaemia and chronic lymphocytic leukaemia cells for drugs used in the treatment of leukaemias. A good correlation was found between the ATP content of leukaemic cells and cell viability as determined by the trypan blue dye exclusion test. 3. Preliminary individual clinical correlations suggest a correlation between the chemosensitivity in vitro and the response patterns in vivo in leukaemia patients. This simple, fast and sensitive method may have application for determination of drug-induced cytotoxicity in leukaemic cells in vitro.

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Ivanovic, Mirjana, Olivera Jovicic, Jelena Mandic, Dusko Bogetic e Marcello Maddalone. "Oral manifestations of acute leukaemia". Srpski arhiv za celokupno lekarstvo 139, n.º 1-2 (2011): 103–6. http://dx.doi.org/10.2298/sarh1102103i.

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Acute leukaemia is the most common form of chilhood cancer. The aim of this paper was to underline the importance of oral manifestations in children with acute leukaemia. The disease and its treatment can directly or indirectly affect oral health. Oral manifestations are gingival inflammation and enlargement. Leukaemic cells are capable of infiltrating the gingiva and the deeper periodontal tissues which leads to ulceration and infection of oral tissues. Gingival bleeding is a common sign in patients with leukaemia. Symptoms include local lymphadenopathy, mucous membrane Petechiae and ecchymoses. Cytotoxic drugs have direct effects like mucositis, involving atrophy, desquamation and ulceration of the mucosa, with increasing the risk for local and systemic infections. Leukaemia can directly influence dental care and dental treatment, while oral lesions may have life-threatening consequences. Knowledge and skills among dentists may also not be adequate to treat children with acute leukaemia. It is therefore imperative that all stomatologists be aware of dental problems that occur in leukaemia in order to be able to effectively carry out appropriate measures to mitigate these problems.

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Skarsgård, Lisa Stenman, Mattias K. Andersson, Marta Persson, Ann-Cathrine Larsen, Sarah E. Coupland, Göran Stenman e Steffen Heegaard. "Clinical and genomic features of adult and paediatric acute leukaemias with ophthalmic manifestations". BMJ Open Ophthalmology 4, n.º 1 (outubro de 2019): e000362. http://dx.doi.org/10.1136/bmjophth-2019-000362.

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ObjectiveTo describe the clinicopathological and genomic features of nine patients with primary and secondary orbital/ocular manifestations of leukaemia.MethodsAll orbital/ocular leukaemic specimens from 1980 to 2009 were collected from the Danish Register of Pathology. In six cases, medical records and formalin-fixed, paraffin-embedded blocks were available. Three cases from the Department of Pathology, Royal Liverpool University Hospital, were also included. Immunophenotypes and MYB oncoprotein expression were ascertained by immunohistochemistry. Genomic imbalances were analysed with comparative genomic hybridisation arrays and oncogene rearrangements with fluorescence in situ hybridisation.ResultsFour patients had B-cell precursor acute lymphoblastic leukaemia (BCP-ALL) and five had acute myeloid leukaemia (AML). Two patients with BCP-ALL and one with AML had primary orbital manifestations of leukaemia. Common symptoms were proptosis, displacement of the eye, and reduced eye mobility in patients with orbital leukaemias and pain, and reduced visual acuity in patients with ocular leukaemias. All patients with primary orbital lesions were alive up to 18 years after diagnosis. All but one patient with secondary ophthalmic manifestations died of relapse/disseminated disease. ETV6 and RUNX1 were rearranged in BCP-ALL, and RUNX1 and KMT2A in AML. Genomic profiling revealed quiet genomes (0–7 aberrations/case). The MYB oncoprotein was overexpressed in the majority of cases.ConclusionsLeukaemias with and without ophthalmic manifestations have similar immunophenotypes, translocations/gene fusions and copy number alterations. Awareness of the clinical spectrum of leukaemic lesions of the eye or ocular region is important to quickly establish the correct diagnosis and commence prompt treatment.

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Arruda, Walter Oleschko, María Belén Montú, Marcelo de Souza R. de Oliveira e Ricardo Ramina. "Acute myeloid leukaemia induced by mitoxantrone: case report". Arquivos de Neuro-Psiquiatria 63, n.º 2a (junho de 2005): 327–29. http://dx.doi.org/10.1590/s0004-282x2005000200024.

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Mitoxantrone (MX) is an immunosupressant drug used in secondarily progressive multiple sclerosis (SPMS) and in relapsing-remitting multiple sclerosis (RRMS). It has a leukemogenesis potential induced by cytogenetic abnormalities, though with a low incidence. Promyelocitic leukaemia (type M3) and other forms of acute myeloblastic leukaemias (M4 and M5) have been described in a few MS patients who received MX during their treatment. We describe a white female patient, 47 year-old, with SPMS (EDSS = 4) with 14 years of disease. She received MX during her disease and developed acute promyelocytic leukaemia (M3), with severe thrombocytopenia 30 months later. She ultimately died due to intracerebral hemorrhage. Other cases of treatment related to AML are reviewed and discussed.

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Bhalla, Amit. "Clofarabine: a next-generation deoxyadenosine analogue". International Journal of Basic & Clinical Pharmacology 7, n.º 5 (23 de abril de 2018): 1048. http://dx.doi.org/10.18203/2319-2003.ijbcp20181660.

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Acute lymphoblastic leukaemia (ALL) is the most common of the paediatric leukaemias. It is estimated that the use of modern combination chemotherapy results in long-term remission in nearly 80% of children diagnosed with ALL. Despite therapy advances, approximately 20% of children with ALL, experience leukaemia relapse. Clofarabine (2-chloro-2’-fluoro-2’-deoxy-9-β-D-arabinofuranosyladenine) is a second-generation nucleoside analogue and is structurally related to fludarabine and cladribine which are widely used in the treatment of lymphoproliferative disorders. Clofarabine exhibits greater affinity to deoxycytidine kinase (dCyd kinase) and prolonged retention in leukaemic blasts compared to fludarabine and cladribine. Clofarabine inhibits both DNA polymerases and ribonucleotide reductase (RNR). This results in impaired DNA synthesis through inhibition of DNA elongation as well as depletion of deoxyribonucleotides. Accumulation of clofarabine triphosphate, in the blasts of patients with refractory leukemia has been demonstrated. Prolonged intracellular half-life of 24 hours for clofarabine triphosphate. Clofarabine is indicated for the treatment of pediatric patients 1 to 21 years old with relapsed or refractory acute lymphoblastic leukemia after at least two prior regimens.

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Burnett, Alan K. "Treatment of acute myeloid leukaemia". Clinical Medicine 13, Suppl 6 (dezembro de 2013): s58—s61. http://dx.doi.org/10.7861/clinmedicine.13-6-s58.

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Apostolidou, Effrosyni, Ronan Swords, Yesid Alvarado e Francis J. Giles. "Treatment of Acute Lymphoblastic Leukaemia". Drugs 67, n.º 15 (2007): 2153–71. http://dx.doi.org/10.2165/00003495-200767150-00004.

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LÖWENBERG, B. "Treatment of acute myelogenous leukaemia". Journal of Internal Medicine 242 (julho de 1997): 17–22. http://dx.doi.org/10.1111/joim.1997.242.s740.17.

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Omura, GeorgeA. ""MAINTENANCE TREATMENT" FOR ACUTE LEUKAEMIA". Lancet 328, n.º 8516 (novembro de 1986): 1154. http://dx.doi.org/10.1016/s0140-6736(86)90553-2.

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Burnett, AK, e OB Eden. "The treatment of acute leukaemia". Lancet 349, n.º 9047 (janeiro de 1997): 270–75. http://dx.doi.org/10.1016/s0140-6736(96)08086-5.

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Mais fontes

Teses / dissertações sobre o assunto "Acute Leukaemia - Treatment"

Thornton, Nadia. "L-alanosine : selective treatment in relapsed childhood acute lymphoblastic leukaemia". Thesis, University of Newcastle Upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.440588.

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Johnson, Peter R. E. "The biology and treatment of acute myeloid leukaemia in elderly patients". Thesis, University of Aberdeen, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306856.

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Acute myeloid leukaemia (AML) is predominantly a disease of the elderly; the median age is 64 years and almost 60% of cases are over 60 years old. Unfortunately however, the treatment of AML in elderly patients is generally unsatisfactory with significantly poorer remission rates and overall survival than in younger patients. We have designed a novel treatment regimen consisting of Mitozantrone and Cytosine Arabinoside specifically for elderly patients and have evaluated the regimen in 104 patients over 60 years old in the North West region. The complete remission rate was 58%, the median duration of remission was 11 months and the median survival was 9 months. These results compare very favourably with previous reports in elderly patients. The regimen was associated with tolerable toxicity and a gratifying improvement in the performance status of responders. Extensive univariate and mutivariate analysis of data arising from the study has been performed, and models to predict outcome of therapy and overall survival have been performed. The latter model may be particularly useful in assisting the identification of elderly patients who would benefit from intensive chemotherapy. The biology of AML in elderly patients has been studied with particular emphasis on morphology, cytogenetic abnormalities and in-vitro culture patterns. Compared with younger patients, cases of AML in the elderly have a high incidence of clinical and morphological myelodysplasia, frequently have prognostically adverse chromosomal abnormalities and have reduced in-vitro cloning efficiency. Thus intrinsic differences in the biology of AML in the elderly have been demonstrated which may, in part, account for the adverse prognosis of AML in elderly patients. The impact of new technologies upon the treatment of AML in the elderly is discussed with particular emphasis on the haemopoietic growth factors and new techniques for studying leukaemia biology.

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Lehtinen, S. (Satu). "Neurotoxicity in children after treatment for acute lymphoblastic leukaemia and methotrexate neurotoxicity in a controlled animal model". Doctoral thesis, University of Oulu, 2003. http://urn.fi/urn:isbn:9514270339.

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Abstract In the Nordic countries, event-free survival (EFS) exceeds 80% in certain groups of children treated for acute lymphoblastic leukaemia (ALL). With the improved cure rates, however, there are more children suffering from neurological late effects, especially due to therapy directed at the central nervous system (CNS). The aim of this study is to examine the changes taking place in the nervous system after leukemia treatment and to evaluate the role of treatment in these changes in patients and in an animal model. Twenty-seven ALL survivors and healthy controls were examined by means of motor evoked potentials (MEPs). ALL survivors were also examined clinically. The children with ALL continued to show decreased motor nerve conduction in the peripheral nerves, but not within the CNS, five years after the cessation of treatment. Clinical neurological findings were obtained in 33% of the cases. The MEP results indicated reversibility of the motor injury due to CNS effects. Nineteen patients underwent perfusion magnetic resonance imaging (MRI) at the cessation of treatment or 4-8 years after the treatment. Seventeen of them also underwent single-photon emission computed tomography (SPECT). The studies showed small perfusion defects in SPECT, which were not visible by perfusion MRI. Methotrexate (Mtx) neurotoxicity was studied in a swine model using functional MRI, brain perfusion SPECT, iodine-123 labelled 2β-carbomethoxy-3β-(4-iodophenyl) tropane ([123I]β-CIT) SPECT and whole-hemisphere autoradiography with [125I]β-CIT in ten Mtx-treated animals and five control animals. Mtx-related changes in the brain could be detected as reduced or negative blood-oxygen-level-dependent (BOLD) responses to somatosensory activation in BOLD contrast MRI, which indicates changes in flow metabolism coupling. Perfusion defects in brain SPECT were seen in the Mtx group and the control group, which suggests that the perfusion defects seen in brain SPECT are probably multifactorial. The change in dopamine transporter (DAT) density in the Mtx group was not different from that in the controls. The abnormalities in nerve conduction after treatment in survivors of ALL were partly reversible years after the treatment. The patients had perfusion defects in SPECT imaging which were not seen in perfusion MRI. The clinical significance of these defects remains obscure. The animal model suggested perfusion defects to be multifactorial.

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Hallböök, Helene. "Acute lymphoblastic leukaemia in adult patients : studies of prognostic factors, treatment results and in vitro cellular drug resistance /". Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5768.

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Hallböök, Helene. "Acute Lymphoblastic Leukaemia in Adult Patients : Studies of Prognostic Factors, Treatment Results and in vitro Cellular Drug Resistance". Doctoral thesis, Uppsala University, Department of Medical Sciences, 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5768.

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Treatment results and clinical characteristics in adult acute lymphoblastic leukaemia (ALL) were evaluated regarding three issues: a new treatment with cytarabine up-front, stem cell transplantation and a comparison between adult and paediatric treatment protocols. All studies were conducted on a national basis. Furthermore, activity of imatinib was investigated by in vitro cytotoxicity assay.

The national protocol was evaluated in 153 adult ALL patients. A high complete remission rate, 86%, was achieved with 29% overall survival at 3-years. Favourable outcome was identified in patients < 40 years with precursor B phenotype and continuous complete remission was higher for precursor B compared to T-ALL.

Stem cell transplantation was evaluated in 187 patients. No differences in outcome between allogeneic and autologous transplantation were found, with the exception of Philadelphia-positive ALL, in which allogeneic transplantation was preferable. Limited chronic graft-versus-host disease (compared to none) resulted in superior disease free survival.

The paediatric NOPHO-92 and the Adult protocols were evaluated for 243 ALL-patients. Superior remission rate and survival were achieved for 10-18 year-olds treated according to the Paediatric protocol compared to both 15-25 and 25-40 year-olds treated according to the Adult protocol. Treatment protocol was a significant prognostic factor for patients aged 15-20 years.

Fluorometric Microculture Cytotoxicity Assey was used to analyze 15 tumour cell samples from ALL patients. High concordance was determined between in vitro sensitivity to imatinib and presence of BCR-ABL. Daunorubicin, prednisolone and cytarabine had the greatest benefit from a combination with imatinib.

The national adult treatment protocol’s results were consistent with international trials regarding precursor B ALL but may be under performing for T-ALL. Adolescents may benefit from treatment according to the Paediatric protocol. No difference in outcome between allogeneic and autologous stem cell transplantation was determined except for Philadelphia-positive patients, despite the indication of a graft-versus-leukaemia effect.

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Krishnan, Shekhar. "In vitro evaluation of asparagine endopeptidase as a candidate biomarker of treatment failure in childhood acute lymphoblastic leukaemia". Thesis, Queen Mary, University of London, 2011. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1294.

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Background Although cure rates in childhood acute lymphoblastic leukaemia (ALL) approach 90%, relapses, particularly central nervous system (CNS) relapses, pose a significant therapeutic challenge. Prevention of relapses requires better predictive biomarkers. Towards this end, global gene-expression microarray screens of primary ALL samples were performed. Overexpression of the lysosomal cysteine protease, asparagine endopeptidase (AEP) was identified in adverse-risk progenitor-B ALL genotypes. AEP overexpression in adult human epithelial cancers has been linked to metastasis and adverse prognosis. Hypothesis AEP overexpression promotes leukaemic cell infiltration of the CNS and other extramedullary sites. AEP degrades the bacterial protein, E. coli L-asparaginase (ASNase) and potentially mediates lymphoblast resistance to this key antileukaemic drug. Summary of findings Quantitative AEP transcript estimation validated microarray findings in the discovery cohort. Sample availability precluded conclusive demonstration of protein overexpression. Intracellular expression in SD1 cells, a model AEPoverepressing ALL cell line, was strikingly heterogeneous and included aberrant peripheral localisation in endolysosomal macrovesicles. Similar findings were observed anecdotally in primary lymphoblasts. In SD1 cells, precursor AEP protein was shed in microvesicles. AEP’s role in cell motility was examined in human embryonic kidney (HEK293) cells. Contrary to published reports, ectopic AEP overexpression in HEK293 cells was not associated with enhanced motility. ASNase was consistently degraded when incubated with ALL cell lysates. In overexpressing disease, ASNase degradation is potentially accelerated by AEP, resulting in inadequate drug activity during early treatment. AEP-cleaved ASNase Synopsis fragments retain known sensitising epitopes, suggesting that AEP cleavage could also potentiate formation of neutralising ASNase antibodies, compounding ASNase treatment failure. Sole substitution at an AEP cleavage site generated an AEP-resistant ASNase variant. Computational protein modelling enabled identification of an appropriate substituting amino acid that best retains drug activity. Conclusions AEP is a candidate marker of poor treatment response in childhood ALL and is presently the subject of a prospective nationwide clinical biomarker study. Its postulated role in cell motility appears to be cell-specific and dependent on the concomitant upstream expression of additional candidate pro-motility molecules. The protease also appears to be a marker of aberrant lymphoblast vesicle phenotype, an observation that is currently the focus of further studies.

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Liem, Natalia Women's &amp Children's Health Faculty of Medicine UNSW. "The development of an in vivo model to study the biology and treatment of childhood acute lymphoblastic leukaemia (ALL)". Awarded by:University of New South Wales. Women's & Children's Health, 2007. http://handle.unsw.edu.au/1959.4/40537.

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Relapsed ALL remams one of the most common causes of death from disease in children. Broad-range drug resistance is often associated with relapse, although its underlying molecular mechanisms remained poorly understood. The aim of this thesis was to establish an in vivo model using the non-obese diabetic/severe combined immunodeficient (NOD/SCID) mouse strain, to facilitate the engraftment, expansion and characterisation of childhood ALL cells, obtained from patients at diagnosis or relapse. Mice were inoculated with leukaemia cells from patients' biopsies and engraftment was monitored by the proportion of human CD45+ cells in the blood. Successful leukaemia engraftment was achieved for 20/20 patient biopsies. Continuous passaging of ten xenografts has also been achieved. Immunophenotypic analysis showed only minor changes in cell surface markers after passage in mice. Leukaemia dissemination in murine bone marrow, liver, spleen and blood was consistent with the human disease. The in vivo responses of ten continuous xenografts to dexamethasone and vincristine, but not methotrexate, significantly correlated with patient outcome (p<0.05). Xenograft sub-lines resistant to vincristine, dexamethasone, methotrexate and cytosine arabinoside were also selected by in vivo drug treatments, although these sublines were not found to be cross resistant to structurally unrelated drugs. Resistance to vincristine, either in in vivo selected sub-lines or inherently resistant xenografts, was not associated with increased activity of drug efflux pumps such as P-gp or MRPl. Class I ?? tubulin levels remained unchanged when compared between vincristine resistant sublines and their parental xenografts. Decreased expression of stathmin and increased polymerised tubulin were observed in vincristine resistant sub-lines, suggesting a possible mechanism of counteracting the depolymerising effects of vincristine. In summary, this study has shown that primary ALL cells engraft efficiently into NOD/SCID mice, and indicates that their response to vincristine and dexamethasone mimics the clinical situation. This model appears to be highly relevant for the study of childhood ALL and will provide the foundation to delineate clinically relevant mechanisms of drug resistance.

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Fordham, Sarah Elizabeth. "DNA mismatch repair and cellular response to cytarabine : implications for the pathogenesis and treatment of therapy-related acute myeloid leukaemia". Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1366.

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The DNA mismatch repair (MMR) pathway is responsible for correction of replicative errors, hence is a key factor in maintenance of genomic stability. Paradoxically, functional DNA MMR also mediates the cytotoxicity of certain chemotherapeutic DNA damaging agents. Poor treatment response in therapy-related acute myeloid leukaemia (t-AML) is influenced by a number of factors, one of which might be chemoresistance due to acquired defects in DNA MMR. Using a range of paired MMR proficient and deficient cell lines, investigations herein demonstrate that DNA MMR status mediates response to nucleoside analogues such as cytarabine (Ara-C) used in t-AML chemotherapy. Interestingly, defects of specific MMR components had different and opposing effects on the cytotoxicity of these agents. These findings implicate defects of MMR components as potential prognostic factors in t-AML and suggest assessment of DNA MMR status may be warranted in individual patients when selecting treatment. Cytarabine was mutagenic to DNA at the TK and HPRT loci. Furthermore, the frequency of Ara-C-induced mutation was increased in an MMR-deficient cell line, supporting a role for MMR components in the cellular response to nucleoside analogues, and also suggesting that use of these agents themselves could contribute to the risk of t-AML development. Defective DNA MMR might also contribute to development of relapsed AML, given that genomic instability is demonstrated in some patients at relapse. Genome-wide analysis of DNA copy number aberrations and loss of heterozygosity in a small cohort of matched presentation and relapsed AML samples demonstrated a potential MMR defect in one patient, and also provided some important insights into the clonal origins of relapsed AML. The findings of these investigations together highlight several important considerations for the use of nucleoside analogues in the treatment of t-AML, as well as in other cancers in which dysfunction of the DNA MMR system is implicated.

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Burrett, Julie Ann. "Identification of randomized trials for inclusion in meta-analyses of treatments for childhood acute lymphoblastic leukaemia, and investigation of factors leading to publication bias". Thesis, Open University, 2003. http://oro.open.ac.uk/22376/.

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Purpose: Some randomized trials are reported widely, while others remain unpublished. It is essential to systematic reviewers and meta-analysts that factors leading to publication bias in the form of delayed or non-publication of an eligible study are identified. This thesis is an attempt to do this.

Data: The set of randomized trials identified by the Childhood Acute Lymphoblastic Leukaemia (ALL) Collaborative Group was used. This consists of 149 trials comprising 243 randomized comparisons (randomizations), starting prior to 1 January 1988, reported in 257 articles, published prior to 1 January 2000. Each mention of a randomization in an article (irrespective of whether results are given) generates a publication record, of which there are 610.

Methods: The main focus is on identifying which trial characteristics lead to a delay in publication of a randomization. Time to the first mention of a randomization in an article (irrespective of whether any results are given) and to the first reporting of its results are both modelled using ordinary linear regression (the independence model). However, when these analyses are extended to include all mentions and all reportings of results respectively, non-independence necessitates the use of techniques for dealing with repeated measures. In such cases the independence model is the starting point, the residuals from which are used to form the covariance matrix, which in turn is used to suggest plausible correlation structures for repeated measures models. Generalised estimating equation (GEE) analysis is used to select an appropriate correlation structure, and a linear mixed effects model serves to confirm this. The conclusions are then discussed in the context of other studies identified. Finally logistic regression is used to identify trial characteristics associated with a randomization remaining unpublished, and Poisson and negative binomial models to identify those affecting frequency of reporting.

Results: Evidence was found of ‘pipeline bias’ in the reporting of first results since, although direction of effect was not found to be significant, highly statistically significant results are published faster than others. However this is not so for first mentions. Negative results (i.e. those in favour of the standard/control) arm were submitted for first publication faster than all others, although this did not effect time to publication. In addition, geographic location is an important predictor of whether a randomization is ever mentioned in an article, frequency of mentions and of time to first publication and results from single-centre trials are published more frequently than those with multi-centre participation.

Conclusions: Although ‘pipeline bias’ was identified in the analysis of time first reporting of results, it was not present in the analysis of time to first mention, and so not a problem for those wishing only to identify randomized trials for inclusion in meta-analyses. The importance of geographic location suggests that the practice of contacting known trialists is worthwhile in addition to the computerised literature searches and should be continued.

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"Daunorubicin kinetics and drug resistance in leukaemia". Thesis, University of Technology, Sydney. Faculty of Science, 1996. http://hdl.handle.net/10453/20146.

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University of Technology, Sydney. Faculty of Science.
The aims of this thesis were to examine: (1) plasma and cellular pharmacokinetics of daunorubicin and its major metabolite daunorubicinol in patients with acute leukaemia, and the relationships between pharmacokinetics, patient response and the presence of P glycoprotein; (2) actions of the multidrug resistance reversing agents cyclosporin A and trifluoperazine, at clinically achievable concentrations, on daunorubicin accumulation and retention in human leukaemia cell lines and patients with acute leukaemia; and (3) effect of daunorubicin on the cell membrane of both sensitive and resistant cell lines, with and without the multidrug resistance reversing agents. Twenty-seven patients with acute leukaemia received daunorubicin as part of induction therapy. The plasma and cellular levels of daunorubicin and its metabolite daunorubicinol were determined using HPLC. There were no significant differences between patients who went into complete remission (12 out of 23) compared to those who did not respond for any of the plasma pharmacokinetic parameters. There was a significant difference in the cellular daunorubicin and daunorubicinol area under the concentration-time curve between responders and non responders (p less than 0.02), as well as in cellular Cmax, cellular clearance and cellular volume of distribution. Eleven patients were P glycoprotein positive and 10 P glycoprotein negative (no sample available for 2 patients). There was no correlation between patient response and the presence of P glycoprotein; nor a correlation between the cellular concentration of daunorubicin or daunorubicinol and P glycoprotein. Patients responding to chemotherapy had higher cellular daunorubicin and daunorubicinol compared to non responders. In contrast to in vitro studies, overexpression of P glycoprotein was not the reason for the lower cellular daunorubicin levels. Cyclosporin A was capable of increasing both cellular accumulation and retention in the drug resistant CEM/VLB and HL 60/ADR cell lines, but not in the drug sensitive CEM and HL 60 cell lines. Trifluoperazine had no effect in any of the four cell lines. In contrast to the cell line findings, only the combination of cyclosporin A and trifluoperazine were able to increase both accumulation and retention in the blast cells of patients at initial presentation. The multidrug resistant reversing agents alone had no effect in increasing accumulation or retention in the blast cells of P glycoprotein positive patients, nor patients in relapse. The cell line studies show that at clinically relevant concentrations only cyclosporin A is capable of increasing daunorubicin accumulation in both the drug resistant P glycoprotein positive (VLB) and P glycoprotein negative (ADR) cell lines. Thus, cyclosporin A does not work only by inhibiting the actions of P glycoprotein. Trifluoperazine was unable to reverse drug resistance at clinically relevant concentrations in either cell lines or patient blast cells. However, the combination of cyclosporin A and trifluoperazine increased accumulation in patient blast cells at initial presentation, suggesting that these agents may be more useful in patients at initial presentation than relapse. Daunorubicin was immobilised by linking it to poly vinyl alcohol and the effect of immobilised-daunorubicin was studied on the four cell lines above. The immobilised-daunorubicin was able to decrease cell growth in the drug sensitive HL 60 cell line but not in the drug resistant VLB or ADR cell lines. Poly vinyl alcohol itself was cytotoxic to the CEM cell line. The multidrug resistance reversing agents cyclosporin A and trifluoperazine were only capable of increasing cytotoxicity in the HL 60 cell line, with no effect in the drug resistant VLB or ADR cell lines.

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Livros sobre o assunto "Acute Leukaemia - Treatment"

National Institute for Clinical Excellence. Guidance on the use of imatinib for chronic myeloid leukaemia. London: National Institute for Clinical Excellence, 2003.

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National Institute for Clinical Excellence. Guidance on the use of imatinib for chronic myeloid leukaemia. London: National Institute for Clinical Excellence, 2002.

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Rooney, Maria Anne. An evaluation of the immune competence of children with common Acute Lymphoblastic Leukaemia, both during and post-treatment, by an investigation of the Lymphocyte sub-populations using monoclonal antibodies and the Alkaline Phosphatase Anti-Alkaline Phosphatase technique. [s.1: The Author], 1989.

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Mendez, Irvin. Acute Myeloid Leukaemia: Symptoms, Diagnosis and Treatment. Nova Science Publishers, Incorporated, 2018.

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M, Carella Angelo, ed. Chronic myeloid leukaemia: Biology and treatment. London: Martin Dunitz, 2001.

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Goldman, John M., Angelo M. Carella, George Q. Daley, Connie J. Eaves e Hehlmann Rudiger. Chronic Myeloid Leukaemia: Biology and Treatment. Taylor & Francis Group, 2003.

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McCann, Shaun R. Leukaemia. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0007.

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The word leukaemia still is associated with foreboding and a fear of premature death. Steady advances have been made in the treatment of childhood leukaemia but, with notable exceptions, the same is not true in adults. The so-called genetic/molecular revolution has extended the understanding of the pathogenesis of many forms of leukaemia but, as yet, has rarely facilitated cure. With the introduction of tyrosine kinase inhibitor therapy, chronic myeloid leukaemia is the obvious exception but it still needs to be seen as to whether the cytogenetic/molecular revolution can provide cures for many elderly patients with leukaemia, as such patients respond poorly to chemotherapy. Haematopoietic stem cell transplantation, although toxic, expensive, and difficult, still provides a cure for many patients. In spite of all these advances, however, most adults with acute leukaemia or myelodysplastic syndrome are destined to die from their disease, and the causes of these fatal illnesses continue to elude researchers.

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Cassidy, Jim, Donald Bissett, Roy A. J. Spence OBE, Miranda Payne e Gareth Morris-Stiff. Bone and soft tissue malignancies. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199689842.003.0025.

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Haematological malignancies examines the epidemiology, genetics, clinical presentation and classification of these diseases, and presents current treatment approaches for each. First are the acute leukaemias, and the management of acute lymphoblastic leukaemia (ALL) and acute myeloid leukaemia (AML). Chronic myeloid leukaemia, its genetics and sensitivity to tyrosine kinase inhibitors, is described. Myelodysplastic syndromes and their management, are followed by chronic lymphoid leukaemias, a large heterogeneous group of diseases, and their treatment. Hodgkin lymphoma, its pathology and presentation, staging and role of PET scanning, is described along with current treatment with chemotherapy and limited radiotherapy. Non-Hodgkin lymphoma is another heterogeneous group of diseases, divided into low-grade and high-grade pathology, and varying in their genetics, presentation, and management. Rituximab is a key component of chemotherapy regimens against B-cell lymphoma. Myeloma and other plasma cell dyscrasias are described, and treatment options reviewed. Myeloma remains incurable, but with appropriate management consistent with prolonged good quality life. Treatment includes chemotherapy, bisphosphonate therapy, analgesics and radiotherapy, Throughout this chapter is emphasised the importance of clinical trials in driving the rapid improvements in treatment of these diseases.

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Cutter, David, e Martin Scott-Brown. Treatment of cancer. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0325.

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The variety of conditions that are considered to be ‘cancer’ is extremely wide, with marked variation in the management approach from disease to disease. A common feature in the management of malignant conditions, however, is the involvement of a wide range of medical professionals at different stages of the patient pathway. This commonly includes physicians, surgeons, radiologists, pathologists, medical oncologists, radiation oncologists, and specialist nurses, as well as a plethora of other allied disciplines. As such, a practice that has been widely adopted is to work as a multidisciplinary team (MDT), with regular meetings to decide the appropriate treatment for each patient with a cancer diagnosis, on an individual and case-by-case basis. The main treatment modalities for the treatment of cancer are surgery, radiotherapy, and chemotherapy. While these are often combined to form a multimodality therapy, they are all, in isolation, potentially radical (curative) therapies for certain conditions. For example, surgery (in the case of a Stage I colon adenocarcinoma), radiotherapy (in the case of early laryngeal squamous cell carcinoma), and chemotherapy (in the case of acute lymphoblastic leukaemia) are all curative as single-modality treatments. It is commonly the case, however, for a patient to require more than one mode of therapy to achieve the best outcome, for example a combination of surgery, chemotherapy, and radiotherapy for early breast cancer. It can also be the case that two or more different management strategies are thought to give equivalent oncological results, for example surgery or radiotherapy for early prostate cancer. In this situation, the MDT and the patient need to decide on the ‘best’ management plan for the individual, based on their personal and professional opinions and on the differing toxicity profiles of the alternate treatments.

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McCann, Shaun R. Molecules, genes, and gene therapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0009.

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The twenty-first century has brought many innovations in haematology, with improved diagnostic technology, which may inform treatment choices for malignant diseases, and a better understanding of the genetics and/or epigenetics underlying many diseases. Unfortunately, the aetiology of most of these diseases still eludes us, and some common diseases such as sickle cell disease await simple, inexpensive, and widely available curative treatment. For reasons that are often obscure, some diseases have become fashionable and attract large research financial backing, whereas some do not. With the advent of advanced technology and an improved understanding of disease mechanisms, most haematological malignancies should enjoy the same success as the treatment of childhood acute lymphoblastic leukaemia and chronic myeloid leukaemia.

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Capítulos de livros sobre o assunto "Acute Leukaemia - Treatment"

Jacobs, P., L. Wood e N. Novitzky. "Treatment of Adult Acute Lymphoblastic Leukaemia". In Acute Leukemias II, 428–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74643-7_79.

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Bader, Peter, Franco Locatelli e Christina Peters. "Paediatric Acute Lymphoblastic Leukaemia (ALL)". In The EBMT/EHA CAR-T Cell Handbook, 57–59. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_10.

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AbstractAcute lymphoblastic leukaemia (ALL) is the most frequent malignant disease in childhood and adolescence, with an annual incidence of approximately 3–4 cases per 100,000 children under 15 years of age. Multimodal chemotherapy forms the base of current ALL treatment. Based on excellent national and international collaboration in consecutive prospective, randomized clinical trials, the prognosis of childhood ALL has significantly improved over time. Currently, up to 90% of all paediatric patients with ALL will survive.

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Rees, J. K. H., R. Gray e F. G. J. Hayhoe. "The Ninth British Medical Research Council Trial for the Treatment of Acute Myeloid Leukaemia". In Acute Leukemias, 35–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71213-5_6.

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Ortega, J. J., G. Javier e T. Olive. "Treatment of Standard- and High-Risk Childhood Acute Lymphoblastic Leukaemia with Two CNS Prophylaxis Regimens". In Acute Leukemias, 483–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71213-5_85.

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Reizenstein, Peter. "The Use of Biological Response Modifiers in Acute Myeloid Leukaemia". In New Approaches to the Treatment of Leukemia, 79–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75484-5_3.

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McCulloch, E. A. "Biological Characteristics of Acute Myeloblastic Leukaemia Contributing to Management Strategy". In New Approaches to the Treatment of Leukemia, 87–116. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75484-5_4.

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Davis, C. L., A. Z. S. Rohatiner, J. Amess, J. Lim e T. A. Lister. "Treatment of Recurrent Acute Myelogenous Leukaemia at a Single Centre Over a 10-Year Period". In Acute Leukemias II, 339–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74643-7_64.

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Rohatiner, A. Z. S., R. Bassan, R. Battista, J. E. Kingston, J. Amess, M. Carter, A. M. Oza et al. "High-Dose Cytosine Arabinoside in the Treatment of Acute Lymphoblastic Leukaemia". In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 437–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78350-0_78.

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Barnett, M. J., J. E. Kingston, A. Miller, A. Z. S. Rohatiner, M. A. Horton, M. F. Greaves, J. S. Malpas e T. A. Lister. "Treatment of Minimal Residual Disease in “Poor Risk” Acute Lymphoblastic Leukaemia with High-Dose Cytosine Arabinoside". In Minimal Residual Disease in Acute Leukemia 1986, 205–10. Dordrecht: Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4273-8_19.

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Tobler, A., e H. P. Koeffler. "Differentiation inducers and their potential use in the treatment of acute myelogenous leukaemia". In Cancer Biology and Medicine, 163–81. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-009-0385-2_6.

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Trabalhos de conferências sobre o assunto "Acute Leukaemia - Treatment"

Guindo, P. Nieto, H. Mateo Carrasco, FD Fernandez Gines e E. Molina Cuadrado. "CP-137 Economic analysis of azacitidine versus decitabine for the treatment of acute myeloid leukaemia". In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.136.

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Megías-Vericat, JE, P. Montesinos, MJ Herrero, V. Bosó, F. Moscardó, L. Rojas, D. Martínez-Cuadrón, SF Aliño, MA Sanz e JL Poveda. "PKP-003 Influence of cytarabine metabolic pathway polymorphisms in effectiveness of acute myeloid leukaemia induction treatment". In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.431.

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Soliman, Ranin, Carl Heneghan, Nancy Bolous, Iman Sidhom, Sonia Ahmed, Nia Roberts, Jason Oke e Alaa Elhaddad. "122 Systematic review of costs and cost-effectiveness of treatment for relapsed/refractory acute leukaemia in children". In EBM Live. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ebm-2022-ebmlive.37.

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Soliman, Ranin, Carl Heneghan, Nancy Bolous, Iman Sidhom, Sonia Ahmed, Nia Roberts, Jason Oke e Alaa Elhaddad. "173 Systematic review of costs and cost-effectiveness of treatment for relapsed/refractory acute leukaemia in children". In Preventing Overdiagnosis Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/bmjebm-2022-podabstracts.94.

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Agraz-Doblas, A., C. Bueno, P. Schneider, C. Revilla, T. Moreno, P. Ballerini, M. Bardini, RW Stam, P. Menéndez e I. Varela. "PO-315 The mutational and transcriptome landscape of infant B-cell acute lymphoblastic leukaemia: the INTERFANT treatment protocol experience". In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.345.

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Lopez-Montero, E., A. Mosquera-Torre, M. Touris-Lores, B. Sanchez-Iglesias, B. Bernardez-Ferran e MJ Lamas-Diaz. "PS-086 Adding low dose allopurinol as hepatoprotector to the maintenance treatment with mercaptopurine in children with acute lymphoblastic leukaemia". In 22nd EAHP Congress 22–24 March 2017 Cannes, France. British Medical Journal Publishing Group, 2017. http://dx.doi.org/10.1136/ejhpharm-2017-000640.592.

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Grey, HET, e A. Davidson. "G555(P) Does the type of steroid used in the treatment of acute lymphoblastic leukaemia in childhood influence adult weight?" In Royal College of Paediatrics and Child Health, Abstracts of the RCPCH Conference and exhibition, 13–15 May 2019, ICC, Birmingham, Paediatrics: pathways to a brighter future. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-rcpch.538.

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Valencia, JC del Río, MRuiz de Villegas Garcia Pelayo, RTamayo Bermejo e I. Muñoz Castillo. "4CPS-105 Blinatumomab for the treatment of the relapse b-precursor acute lymphoblastic leukaemia in a paediatric patient: a case report". In Abstract Book, 23rd EAHP Congress, 21st–23rd March 2018, Gothenburg, Sweden. British Medical Journal Publishing Group, 2018. http://dx.doi.org/10.1136/ejhpharm-2018-eahpconf.196.

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Huynh, T., D. Vidovic, C. Dean, K. Lee, I. Weaver e P. Marcato. "PO-372 Investigating the epigenetic changes underlying combination treatment of acute promyelocytic leukaemia with all-trans retinoic acid and arsenic trioxide". In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.400.

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Del Río Valencia, JC, C. Ortega De La Cruz, T. Chinchilla Alarcón e I. Muñoz Castillo. "4CPS-113 Inotuzumab–ozogamizin for the treatment of relapse B precursor acute lymphoblastic leukaemia in an adult patient: a case report". In 25th EAHP Congress, 25th–27th March 2020, Gothenburg, Sweden. British Medical Journal Publishing Group, 2020. http://dx.doi.org/10.1136/ejhpharm-2020-eahpconf.214.

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