Relevant bibliographies by topics / AML acute myeloid leukaemia

Academic literature on the topic 'AML acute myeloid leukaemia'

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Published: 10 March 2023

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Journal articles on the topic "AML acute myeloid leukaemia"

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Budi, Luh Putu Rihayani, Ketut Ariawati, and Sianny Herawati. "NEONATAL ACUTE MYELOID LEUKAEMIA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 19, no. 3 (October 14, 2016): 211. http://dx.doi.org/10.24293/ijcpml.v19i3.417.

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Acute myeloid leukaemia (AML) is a. malignant, clonally disease that involves proliferation of blasts in bone marrow, blood, or other tissue. The blasts most often show myeloid or monocytic differentiation. The incidence of AML increases with age, but when neonatal leukaemia does occur, it is paradoxically AML rather than ALL. All the signs and symptoms that present on patient with AML are caused by the infiltration of the bone marrow with leukaemic cells and resulting failure of normal haematopoiesis. Without the normal haematopoietic elements, the patient is at risk for developing life-threatening complications of anaemia, infection due to functional neutropenia, and haemorrhage due to thrombocytopenia. Organomegaly is seen in approximately half of patient with AML due to hepatic and sphlanic infiltration with leukaemic blasts. Prognosis of neonatal leukaemia is poor with the 6-month survival rate is only one third despite aggressive chemotherapy. It has higher mortality rate than any other congenital cancer. The researchers reported two of AML diagnosed cases in neonatal period. The first case, a one-day-old male was referred with respiratory distress and suspect Down syndrome with spontaneous petechiae. The second case, a 17-day-old female presented with bloody diarrhoea and history of hypothyroid. Dysmorphic face and hepatosplenomegalia were found in both of the physical examination. Their complete blood count revealed leukocytosis and thrombocytopenia. Peripheral blood smear revealed myeloblast 30% on the first case and 23% on the second case. Both immunophenotyping revealed the population of blast expressing myeloid lineage (CD33 and CD34).
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Nurunnabi, Md, Mosammath Khadiza Mamdu, Ayesha Siddika, Farzana Zafreen, Md Abdul Wahab, and Shahana Shermin. "Morphological and Immunophenotypic Analysis in Diagnosis of Acute Leukaemia." Delta Medical College Journal 8, no. 1 (March 31, 2022): 15–20. http://dx.doi.org/10.3329/dmcj.v8i1.58958.

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Background: Leukaemias are neoplastic proliferations of haematopoietic stem cells and form a major proportion of haematopoietic neoplasms that are diagnosed worldwide. Objective: To differentiate between morphological and immunophenotypic analysis in the diagnosis of acute leukemia. Materials and method: This cross sectional study was conducted in the department of Haematology, Armed Forces Institute of Pathology (AFIP), Dhaka, Bangladesh from January 2008 to December 2008. Total 50 patients were included after fulfilling inclusion and exclusion criteria. Results: The total of 50 bone marrow samples from suspected cases of acute leukaemia were included in the study. Out of 50 samples, 48 cases were diagnosed as either acute myeloid leukaemia (19 or 38%) or acute lymphoblastic leukaemia (29 or 58%) and 02 (04%) cases were morphologically indistinguishable. All 50 cases were subjected to immunophenotypic study. Out of 50 cases immunophenotypically 14(28%) were acute myeloid leukaemia (AML), 32(64%) were acute lymphoblastic leukaemia (ALL), and bi-phenotypic leukaemia and acute undifferentiated leukaemia were 02(04%) each. In this study Male: Female ratio was 1.3:1. Out of 19(38%) cases of AML, 29(58%) cases of ALL and 02(04%) cases of indistinguishable diagnosed morphologically, 14(28%) were found to be AML, 32(64%) ALL, 02(04%) bi-phenotypic and 02(04%) were acute undifferentiated leukaemias on immunophenotyping respectively. Out of 29 cases identified as ALL on morphology 25(86.2%) were confirmed as ALL, 02(07%) turned out to be AML, 01(3.4%) was bi-phenotypic and 01(3.4%) was undifferentiated. Conclusion: In this study, acute lymphoblastic leukaemia was the commonest type of leukemia followed by acute myeloid leukaemia with male predominance seen in all types of leukaemia. Delta Med Col J. Jul 2020 8(1): 15-20
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Gruszka, Alicja, Debora Valli, Cecilia Restelli, and Myriam Alcalay. "Adhesion Deregulation in Acute Myeloid Leukaemia." Cells 8, no. 1 (January 17, 2019): 66. http://dx.doi.org/10.3390/cells8010066.

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Cell adhesion is a process through which cells interact with and attach to neighboring cells or matrix using specialized surface cell adhesion molecules (AMs). Adhesion plays an important role in normal haematopoiesis and in acute myeloid leukaemia (AML). AML blasts express many of the AMs identified on normal haematopoietic precursors. Differential expression of AMs between normal haematopoietic cells and leukaemic blasts has been documented to a variable extent, likely reflecting the heterogeneity of the disease. AMs govern a variety of processes within the bone marrow (BM), such as migration, homing, and quiescence. AML blasts home to the BM, as the AM-mediated interaction with the niche protects them from chemotherapeutic agents. On the contrary, they detach from the niches and move from the BM into the peripheral blood to colonize other sites, i.e., the spleen and liver, possibly in a process that is reminiscent of epithelial-to-mesenchymal-transition in metastatic solid cancers. The expression of AMs has a prognostic impact and there are ongoing efforts to therapeutically target adhesion in the fight against leukaemia.
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Gruszka, Alicja M., Debora Valli, and Myriam Alcalay. "Wnt Signalling in Acute Myeloid Leukaemia." Cells 8, no. 11 (November 7, 2019): 1403. http://dx.doi.org/10.3390/cells8111403.

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Acute myeloid leukaemia (AML) is a group of malignant diseases of the haematopoietic system. AML occurs as the result of mutations in haematopoietic stem/progenitor cells, which upregulate Wnt signalling through a variety of mechanisms. Other mechanisms of Wnt activation in AML have been described such as Wnt antagonist inactivation through promoter methylation. Wnt signalling is necessary for the maintenance of leukaemic stem cells. Several molecules involved in or modulating Wnt signalling have a prognostic value in AML. These include: β-catenin, LEF-1, phosphorylated-GSK3β, PSMD2, PPARD, XPNPEP, sFRP2, RUNX1, AXIN2, PCDH17, CXXC5, LLGL1 and PTK7. Targeting Wnt signalling for tumour eradication is an approach that is being explored in haematological and solid tumours. A number of preclinical studies confirms its feasibility, albeit, so far no reliable clinical trial data are available to prove its utility and efficacy.
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Niazmand, Mohammad Javad, Matthew Speckert, and Donna Johnston. "Acute myeloid leukaemia presenting as proptosis in an infant." BMJ Case Reports 14, no. 12 (December 2021): e247506. http://dx.doi.org/10.1136/bcr-2021-247506.

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Paediatric patients with acute myeloid leukaemia (AML) often present with symptoms associated with the disruption of normal haematopoiesis and subsequent cellular deficiencies. Periosteal reactions are common in paediatric leukaemia, but typically manifest as a thin, laminated pattern along long bones. Aggressive periosteal reactions are much less frequently seen. Here, we report a case of paediatric AML initially presenting with proptosis and periorbital swelling caused by aggressive, sunburst periosteal reactions surrounding the sphenoid and zygomatic bones. This unique presentation emphasises the importance of considering leukaemic infiltration in the differential for sunburst periosteal reaction in paediatric patients.
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Sun, Qian, Chi-Chiu So, Sze-Fai Yip, Thomas S. K. Wan, Edmond Shiu Kwan Ma, and LiChong Chan. "Functional Alterations of Lin−CD34+CD38+ Progenitors in Chronic Myelomonocytic Leukaemia and on Progression to Acute Leukaemia." Blood 110, no. 11 (November 16, 2007): 4119. http://dx.doi.org/10.1182/blood.v110.11.4119.4119.

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Abstract Chronic myelomonocytic leukaemia (CMML) is a clonal bone marrow stem cell disorder based on the presence of trilineage involvement, the association of myelodysplastic and myeloproliferative features and its ability to transform into acute myeloid leukaemia. The objectives of our study are to identify the cell population and its functional characteristics involved in evolution from CMML phase to acute myeloid leukaemia. We analysed Lin−CD34+ stem/progenitor population and performed cell proliferation, apoptotic assays, self-renewal ability and differentiation potential studies in purified populations of Lin−CD34+CD38− stem cells and Lin−CD34+CD38+ committed progenitors from peripheral blood of 16 patients with CMML and in six of the 16 after transformation to acute myeloid leukaemia (AML-t). We observed an expansion of the stem cell/progenitor pool (Lin−CD34+ cells) in AML-t comprising mainly of Lin−CD34+CD38+ committed progenitors within Lin−CD34+ cells. The Lin−CD34+CD38+ committed progenitors displayed highly proliferative activity in CMML and in AML-t; and additionally acquired resistance to apotosis and myeloid colony self-renewing ability in AML-t. Impairment of dendritic cell (DC) differentiation was observed with complete block in AML-t. Our findings suggest Lin−CD34+CD38+ committed progenitors instead of Lin−CD34+CD38− stem cells could be the target(s) of secondary genetic lesions underpinning progression from CMML to AML. These results have implications for the further study of the biology of leukaemic transformation and the design of new strategies for the effective treatment of CMML.
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Skarsgård, Lisa Stenman, Mattias K. Andersson, Marta Persson, Ann-Cathrine Larsen, Sarah E. Coupland, Göran Stenman, and Steffen Heegaard. "Clinical and genomic features of adult and paediatric acute leukaemias with ophthalmic manifestations." BMJ Open Ophthalmology 4, no. 1 (October 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, and Ricardo Ramina. "Acute myeloid leukaemia induced by mitoxantrone: case report." Arquivos de Neuro-Psiquiatria 63, no. 2a (June 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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Sarrou, Evgenia, Laura Richmond, Ruaidhrí J. Carmody, Brenda Gibson, and Karen Keeshan. "CRISPR Gene Editing of Murine Blood Stem and Progenitor Cells Induces MLL-AF9 Chromosomal Translocation and MLL-AF9 Leukaemogenesis." International Journal of Molecular Sciences 21, no. 12 (June 15, 2020): 4266. http://dx.doi.org/10.3390/ijms21124266.

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Chromosomal rearrangements of the mixed lineage leukaemia (MLL, also known as KMT2A) gene on chromosome 11q23 are amongst the most common genetic abnormalities observed in human acute leukaemias. MLL rearrangements (MLLr) are the most common cytogenetic abnormalities in infant and childhood acute myeloid leukaemia (AML) and acute lymphocytic leukaemia (ALL) and do not normally acquire secondary mutations compared to other leukaemias. To model these leukaemias, we have used clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9 gene editing to induce MLL-AF9 (MA9) chromosomal rearrangements in murine hematopoietic stem and progenitor cell lines and primary cells. By utilizing a dual-single guide RNA (sgRNA) approach targeting the breakpoint cluster region of murine Mll and Af9 equivalent to that in human MA9 rearrangements, we show efficient de novo generation of MA9 fusion product at the DNA and RNA levels in the bulk population. The leukaemic features of MA9-induced disease were observed including increased clonogenicity, enrichment of c-Kit-positive leukaemic stem cells and increased MA9 target gene expression. This approach provided a rapid and reliable means of de novo generation of Mll-Af9 genetic rearrangements in murine haematopoietic stem and progenitor cells (HSPCs), using CRISPR/Cas9 technology to produce a cellular model of MA9 leukaemias which faithfully reproduces many features of the human disease in vitro.
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Palma, Catalina A., Elise Tonna, Adam J. Bryant, Vivek Jayaswal, David Agapiou, Yee Hwa Yang, David Ma, and Mark Lutherborrow. "MicroRNA Expression in Acute Myeloid Leukaemia and Their Effects on the Differentiation of Acute Myeloid Leukaemia Cells." Blood 118, no. 21 (November 18, 2011): 2430. http://dx.doi.org/10.1182/blood.v118.21.2430.2430.

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Abstract Abstract 2430 Acute myeloid leukaemia (AML) is typified by an aberrant halt in maturation of myeloid progenitor cells, leading to uncontrolled proliferation of immature blasts. In the majority of cases of AML with normal karyotype, the underlying cause of the maturation arrest remains unclear. MicroRNAs, small inhibitory RNAs, are known to be dysregulated in cancers and have been postulated to play a causative role in leukaemogenesis. We aimed to investigate the contribution of aberrant microRNA expression to the inhibition of maturation in AML cells. MicroRNA expression profiling was performed on the bone marrow of 28 AML patients with normal karyotype and 8 normal controls. Differential expression was confirmed by qRT-PCR. We found that the expression of a panel of 12 microRNAs was able to accurately separate AML-M1 and AML-M5 subtypes. The AML-M1 subtype represents a more immature cell population when compared to the monoblast morphology observed in AML-M5. Four candidate microRNAs, miR-181a, -146a, -130a and -135b were selected for further investigation based in their putative targeting of key monocytic transcription factors as determined by in silico modelling followed by luciferase assays. In vitro monocyte and macrophage differentiation of HL60 and NB4 cell lines with 1,25-dihydroxyvitamin D3 and/or phorbol-12-myristate-13-acetate treatment resulted in a significant decrease in all four candidate microRNAs (measured by qRT-PCR), supporting the hypothesis that candidate microRNA over-expression in AML-M1 may contribute to its maturation arrest. Over-expression of the candidate microRNAs by transfection with Pre-miR microRNA precursor molecules (Ambion) into the HL60 and NB4 monocyte differentiation model, resulted in the significant suppression of CD14 (Figure, *p <0.05 compared to Scrambled control) and CD15 expression, markers of monocytes and granulocytes respectively. Conversely, knockdown of miR-181a, -146a, -130a and -135b with miRCURY LNA microRNA knockdown probes (Exiqon) induced an increase in CD14 expression in HL60 cells compared to non-targeting Scrambled control. An important regulatory role of these microRNAs in myeloid/monocytic differentiation is strongly suggested by their targeted suppression of the key transcription factors KLF4, MAFB, IRF8, HOXA10, MCL1 and PU.1 which was confirmed by luciferase reporter assay. This study provides evidence that the over-expressed microRNAs discovered in our profiling work between AML-M1 and AML-M5 are biologically relevant microRNAs, which have the potential to affect the maturation potential of AML cells. Disclosures: No relevant conflicts of interest to declare.
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Dissertations / Theses on the topic "AML acute myeloid leukaemia"

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Shah, Niraj Mayank. "The role of NRF2 in acute myeloid leukaemia (AML)." Thesis, University of Liverpool, 2018. http://livrepository.liverpool.ac.uk/3022789/.

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Acute Myeloid Leukaemia refers to the excess proliferation of myeloid progenitor cells. Whilst the 5-year survival rate is 40% in younger patients, this falls to 5% in patients over 65 and resistance to front-line chemotherapy agents remain a problem. We previously identified NRF2, a regulator of anti-oxidant genes, to be constitutively activated in AML and this correlated with resistance to chemotherapy. Recent studies have also suggested NRF2 also plays a more oncogenic role. To further understand NRF2's role in both chemotherapy resistance and oncogenesis we looked at its ability to regulate miRNA in AML. Using a miRNA array, we identified several miRNAs, including miR-125b and miR-29b, whose expression correlated with that of NRF2 in both cell lines and AML patient samples. Both miRNAs exist as paralogs, in that they contain the same miRNA sequence but exist in different genomic locations and we used qPCR to identify miR-125b1 and miR-29b1 as paralogs regulated by NRF2. Using a reporter assay we confirmed the activity of putative NRF2-ARE binding sites in both miRNA promoters. To understand the function of both in AML we manipulated their expression using miRNA 'mimics' or antagomIRs. Individual manipulation of either miRNA resulted in a slight increase in apoptosis. However, the miRNAs appeared to act synergistically as when expressed simultaneously a significant increase in apoptosis was seen both in cell lines and patient blasts. Manipulation of both miRNA also resulted in the increased sensitivity of AML cells to chemotherapy agents. BAK1, STAT3 and AKT2 were shown to be targets of both miRNAs providing a novel mechanism by which NRF2 expression can affect AML cells. To further study the role of NRF2 in AML we used CRISPR-Cas9 to generate NRF2-deficient cells. CRISPR guide RNA were designed to target NRF2 Exons 1, 2 and genome editing validated in HEK293T cells. Leukaemic cell lines (K562 and THP-1) were virally transduced with guides targeting Exon 4 of NRF2. Once editing was verified clones were derived by growing selected cells in Methycellulose-containing medium. Putative clones were initially screened using MG-132 (to stabilise NRF2) and further confirmed by treatment with the NRF2 inducers CDDO-Me and Sulforaphane. Verified clones were characterised by Sanger Sequencing. In addition to CRISPR-Cas9 we also validated a number of other gene-editing methodologies including CRISPR-Cpf-1 and TALENs. Overall these methodologies represent powerful tools to further characterise the role of NRF2 in AML.
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Bajuaifer, Nada A. "Translational regulation of ABCB1 gene in acute myeloid leukaemia (AML)." Thesis, University of Nottingham, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.594594.

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Introduction: Multidrug Resistance (MDR) was and remains a major obstacle in the way of successful chemotherapy for cancer patients and especially acute myeloid leukaemia (AML) patients. In AML, MOR mediated by ABCBl over-expression accounts for the majority of MOR cases. The ABCB1 gene encodes a surface protein known as P-glycoprotein (Pgp) which plays a major role in MOR by effluxing drugs out of cells leading to increased relapse rates in AML patients. The regulation of ABCBl and subsequently Pgp is multifactorial and can be altered at many levels. Common regulators of genes expression may play a role in the regulation of this gene such as genetic sequence variation in the form of single nucleotide polymorph isms and short noncoding RNAs known as microRNAs. Results and Discussion: Role of different regulators in the regulation of ABeBl gene was investigated; these were microRNAs and 3'UTR SNP (specifically rs3842). Microarray profiling of 11 AML cell lines and 45 NeRN AMLl4 and AMLl5 trial patients samples showed significant down-regulation of miR-34b and miR-503 in Pgp positive cell lines when compared with Pgp negative cell lines and miR-l48a, miR-45l, miR-659, miR-499-5p, miR-l97 and miR-642 in Pgp positive patient samples when compared with Pgp negative patient samples. This suggests a role of these miRs in MDR in AML. No significant up-regulation was found in the Pgp positive cell lines and patients samples when compared with the Pgp negative group. Functionally, no direct effect of miR-l48a and miR-34b on ASeSl3'UTR constructs and Pgp protein level (for miR-34b) was found but an indirect effect of these miRs on ASeS! still needs to be tested. Second, the role of rs3842 on regulation of ABeBl gene was investigated. rs3842 genotyping of 455 NCRN AMll4 and AML15 trial patients showed comparable distribution to the reported distribution of the genotypes of normal healthy European population. Furthermore, an effect of the rs3842 polymorphism on Pgp protein expression and function (but not at the mRNA level) was seen in the 35% of patients where ASeS! expression is high. Functionally, higher baseline activity of the ASeS! wild type 3'UTR construct was found when compared with the ABeBl variant 3'UTR construct and a further construct mutated by site-directed mutagenesis. On examination of the rs3842 polymorphism and surrounding sequence, it was predicted that miR-374a targets AseSl very close to the SNP. This went to show that miR-374a causes down-regulation of ASCSl 3'UTR activity but only when the wild type rs3842 allele A is expressed. In addition, an effect of miR-374a on Pgp protein expression was found at the protein level but not at the mRNA suggesting a role of miR-374a in the translational regulation of the ABCBl gene. To conclude, the role found of microRNAs (miR-374a) and rs3842 in ABCBl regulation in this work suggests a significant role of the 3'UTR of ABCBl gene in its regulation.
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Jawad, Mays Safa Hadi. "Genetic susceptibility to radiation-induced acute myeloid leukaemia (r-AML)." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/30366.

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CBA/H inbred mice are susceptible to radiation-induced acute myeloid leukaemia (r-AML) while C57BL/6 mice are resistant to r-AML. CBA/H mice also have higher haemopoietic stem cell number (HSC) than C57BL/6 mice raising the possibility that HSC frequency is a risk factor in r-AML. F2 mice were therefore analysed to map QTL that determine the frequency of phenotypically defined bone marrow cells. The Lin-Sca-1+c-Kit+ cell QTL in F2 mice mapped to chromosomes 1 (65cM), 17 (6cM), and 18 (21cM), genetic evidence that they are HSC, while the more mature Lin-Sca-1+FLK-2+ cell QTL mapped to chromosome 9 (33cM), a novel progenitor cell frequency QTL. The same F2 mice were also scored for difference in peripheral blood and bone marrow red blood cell counts (RBC), and spleen weight, so QTL were mapped for these phenotypes. Different autosomal loci affect bone marrow (chromosome 5, 9, 11, and 19) and peripheral blood RBC counts (chromosome 4), and spleen weight (chromosomes 3, 15, and 17). This suggests that the relative contributions of spleen and bone marrow erythropoiesis to peripheral RBC counts are genetically determined in mouse. A human AML genetic association study was carried out to assess the contribution of variant alleles to risk of AML in patients with de novo or therapy-related AML (t-AML) compared to age matched controls. In humans, a variant HLX1 allele was associated with a 4-fold increased risk of t-AML. Together with a variant RAD51 DNA repair allele, the variant HLX1 allele increased the risk of t-AML by 14-fold. The variant HLX1 gene may determine stem cell frequency (target size) during chemo-/radiotherapy therapy and a reduced ability to repair therapy-induced DNA damage will increase the risk of malignant transformation.
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Vlachou, T. "FUNCTIONAL AND GENETIC HETEROGENEITY IN ACUTE MYELOID LEUKAEMIA." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/471776.

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Acute myeloid leukaemia (AML) is the most frequent leukaemia in adults, and still represents a disease with an unmet medical need, with 50-60% of patients relapsing within 3 years after diagnosis. AMLs are characterised by a high degree of intra-tumour heterogeneity, both at the biological and the genetic level, which is critical for tumour maintenance and response to treatments. Biologically, AMLs are organised hierarchically, with rare stem-like cells (leukaemia stem cells, LSCs) endowed with the unique properties of self-renewal and differentiation. Genetically, AMLs harbour patient-specific combinations of different driver mutations, which are organised within individual cases in sub-clones with distinct growth properties. We hypothesized that tumour maintenance and relapse in AMLs are driven by the selective expansion of quiescent sub-clones within the LSC population, which serve as the genomic and functional reservoir of the tumour. The experimental strategy we employed to test this hypothesis is based on the xenotransplantation of human leukaemias, the implementation of an in vivo clonal tracking approach, the functional isolation of leukaemic subpopulations with diverse proliferation histories and whole-exome sequencing (WES) of bulk and isolated leukaemic subpopulations. Our aims were to assess the proliferative hierarchy of LSCs and to examine their intrinsic genetic heterogeneity. We identified two functional LSC classes, quiescent and cycling, that are in equilibrium in the tumour and largely share the same clonal architecture. We further observed that genetic leukaemic clones appear to consist of a high number of individual LSCs, the majority of which exhaust upon serial transplantation. Finally, by genetic analyses of isolated leukaemic subsets, we were able to detect a specific enrichment for rare mutations in the quiescent compartment of two patient xenografts. Our data indicate that tumour evolution is sustained by the quiescent LSC pool and suggest that their highly proliferating counterpart has a finite lifespan. We expect that the results of our studies will provide new insights into the mechanisms of disease progression and treatment response in AML, and potentially reveal novel therapeutic approaches.
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Gasiorowski, Robin. "CD300f As A Novel Therapeutic Antibody Target For Acute Myeloid Leukaemia." Thesis, The University of Sydney, 2017. http://hdl.handle.net/2123/17190.

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Current outcomes for patient with acute myeloid leukaemia (AML) are unsatisfactory, particularly for older patients where the median overall survival is less than six months. Monoclonal antibodies (mAb) have been used with great success in a range of malignancies and the promising results seen with gemtuzumab ozogamicin suggest they may improve outcomes in AML. CD300f is an immunoregulatory leucocyte cell surface molecule with myeloid restricted expression, which we have investigated as a potential antibody target in AML. We found that CD300f is expressed on blasts and leukaemic stem cells (LSC) from the majority of AML patients and that AML cells express multiple isoforms of CD300f. We showed that there is a range CD300f epitopes expressed on healthy and malignant cells, and developed a novel CD300f mAb, DCR2, which has in vitro and in vivo activity against AML. However we showed that CD300f, like CD33, is expressed on haematopoietic stem cells suggesting that targeting this antigen is likely to result in myelosuppression. We also investigated the expression and regulation of other CD300 family members on myeloid cells, with the results suggesting that this family of molecules has the potential to regulate dendritic cell responses. We identified CD302 as another novel target for AML antibodies, again showing its expression on the majority of AML blasts and LSC. Finally, using the HLDA10 panel of mAbs, we investigated the expression of novel and more established AML targets on both healthy and malignant cells. We showed that all of the tested targets are expressed on both healthy and malignant cells. A key issue for products based on these murine mAbs will be establishing the therapeutic window where there is efficacy against AML without excessive toxicity. The binding patterns of DCR2, and the other mAbs investigated in this thesis, will help to drive the preclinical and clinical testing required to achieve this. Keywords: Therapeutic antibody, AML, CD300f
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Marsico, Paolo. "The effects of targeted therapy on cell viability and apoptosis on CML and AML cell lines." Thesis, University of Chester, 2019. http://hdl.handle.net/10034/621798.

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Tyrosine kinase inhibitors (TKIs) are currently the first therapy option for chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) patients. However, many patients affected by CML and AML may develop resistance to TKIs or may not recover under this treatment regime. New potential and more effective treatments are recently emerging. Heat shock protein inhibitors (HSPIs) and the proteasome inhibitor Bortezomib are drugs which have been yet to be successfully tested on leukemic patients, despite being successful on other malignancies such as multiple myeloma (MM). The combination between HSPIs and Bortezomib could potentially be successful in killing leukemic cells, by enhancing their respective molecular mechanisms. Indeed, HSPIs would bind to HSP72 avoiding the protein to exert its ligase function to the proteasome, whilst Bortezomib could stop the ubiquitinated proteins to enter the proteasome and ultimately inducing apoptosis. To test the effects of such combination, cell viability was measured via MTS assay, apoptosis levels were tested through Annexin V\PI assays. Involvement of HSP72 and pro-survival protein Bcl-2 were measured via flow-cytometry. The cells were administered with HSPIs and Bortezomib first as single agents for 24 hours, to establish working minimal concentration. Also, the drugs were tested for a shorter time, to understand when the drugs start to be effective. It emerged that one hour is sufficient for the drugs to give an initial effect in terms of cell viability and apoptosis. Following, combination experiments of HSPIs and Bortezomib were performed; the first drug was administered for one hour, the second following one hour and the cells were incubated for 24 hours. This was repeated alternatively for both type of drugs on the different cell lines. MTS and Annexin V\PI showed that there is not a synergistic effect between drugs, but instead there is antagonism. No necrosis was found at any level of the study. The cells were then probed for HSP72 and Bcl-2, to investigate their involvement in apoptosis mechanisms. Following 6 hours of combined and single agent treatment, both type of drugs inhibit HSP72 but failed to reduce the expression of Bcl-2, particularly on AML cells. It is thus proposed that CML and AML cells may die by apoptosis following a short time of treatment with HSPIs and Bortezomib by an extrinsic pathway of apoptosis, independent from Bcl-2 involvement and from mitochondrial pathway of apoptosis. This study may be the first to indicate a potential use of HSPIs and Bortezomib on CML and AML patients for a short time of treatment, although not in combination. Future studies are needed to further investigate the mechanisms of action of these drugs, aiming to potentially give CML and AML patients another successful therapy option to overcome resistance to canonic chemotherapy.
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Bodini, M. "Genomics of treatment response in Acute Myeloid Leukemia." Doctoral thesis, Università degli Studi di Milano, 2017. http://hdl.handle.net/2434/469570.

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Acute Myeloid Leukaemia (AML) is a cancer of the myeloid lineage of blood cells characterised by rapid growth of undifferentiated myeloid precursors that accumulate in the bone marrow and suppress normal haematopoiesis. It is the most common adult leukaemia with an estimated number of more than 60’000 new cases for the US in 2016. Despite the high rates of complete remissions achieved after treatment (60-80% in young adults), the number of patient that will result cured after induction and consolidation therapy is very low (~12%). The molecular basis of relapsing disease is still unclear and the small number of identified predictive factors has small predictive power. To date, chemotherapy induction treatment is similar for all patients and consists in the administration of mainly three drugs (fludarabine, cytarabine, and idarubicin). Prediction markers for the outcome of chemotherapy would instead reduce useless treatments and direct research through new possible therapeutic targets that would enhance AML treatment. In three successive studies, Ding et al., Corces-Zimmerman et al. and Krönke et al., described four possible behaviours for relapse patients: the return of the first leukaemia (dominant clone or a subclone), with or without additional evolution, or the emergence of ancestral clones, also in this case, with or without additional mutations. In this thesis, endowed of the NGS technologies advancement, we decided to delineate the possible process of relapse formation in order to be able in the future to predict which patients are more susceptible to relapse. Our experimental plan includes the whole exome analysis of 30 pairs of primary/relapsed AML samples using NGS to identify relapse-specific mutations, the bioinformatics analysis of the clonal evolution of the disease and the identification of pathways that correlate with the relapsing disease.
The methods for the analysis of NGS data, at present, are still in a refinement phase, especially for the high level analysis (detection of variants and definition of their role in the pathogenesis). We broadly analysed the existing methods for the treatment of NGS data (aligners, mutation callers, CNV callers and methods to reconstruct clonal composition) in order to determine those better fitting to our cohort of patients and purposes: occasionally, we had the possibility to choose the best tool meeting our investigative needs, discovering that other methods were valuable as well, in other cases we verified that more improvements are needed to obtain reliable results. Our analysis shows that the genomic landscapes of primary and relapse AMLs are similar and in the majority of the patients (76%) some relapse clones were already present in the primary tumour and reappeared after chemotherapy at similar or augmented cellular frequencies. We also identified some functional gene categories (DNA methylation pathway, cohesin complex and chromatin modifiers) more prone to resistance and peculiar genes (e.g. ASXL1, TET2) presenting growing VAFs at relapse. In 4 out of 29 patients (14%) we were able to identify driver mutations in the blood sample of the complete remission at low frequency; we hypothesise that more sophisticated diagnostic tools, based on NGS analysis, would help in driving the treatment to obtain better outcomes for patients.
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MALLARDO, MARIA. "DISSECTING THE ROLE OF THE CYTOPLASMIC MUTANT NUCLEOPHOSMIN IN ACUTE MYELOID LEUKAEMIA DEVELOPMENT." Doctoral thesis, Università degli Studi di Milano, 2014. http://hdl.handle.net/2434/234152.

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Acute myeloid leukaemia (AML) is a genetic heterogeneous group of diseases, with the largest subgroup showing a mutation in the Nucleophosmin gene (NPM1). Normally the NPM protein localizes mainly in the nucleolus, but in AML blasts it is aberrant localized to the cytoplasm (NPMc+AML). Notably, NPMc+AML patients show peculiar gene expression profiles, treatment response and prognosis. Hence, it has been proposed as an independent category for leukaemia classification according to WHO in 2008. In view of the relevance of NPMc+ mutation to AML pathogenesis and prognosis, understanding its role in leukaemia development represents a major issue in the field. The aim of this PhD project is to get further insight into the relevance of NPMc+ mutations to AML development. To this scope, here it is reported a characterization of a novel mouse model expressing the mutated protein. The hematopoietic restricted expression of the protein induces leukaemia in mice. This data definitively clarify that NPMc+ is an initiating mutation for leukaemia development. However, the long latency and low penetrance of disease onset strongly support the need of cooperating mutations. Since, the high frequency of FLT3-ITD mutations in NPMc+AML, we genetically tested the synergisms between the two abnormalities. To this scope, NPMc+ mice were crossed with FLT3-ITD mice (Lee, 2007). Double mutated mice developed leukaemia with sort latency and full penetrance indicating effective cooperation. Moreover, our data support the two hits model of tumourigenesis, where functional complementary mutations contribute to disease onset. Another major challenge of this project is to understand how NPMc+ affect the biology of normal HSPC and imposes the transition from normal to cancer stem cells. We found that NPMc+ expression perturbs the homeostasis of HSCP and expand the number of LT-HSC by increasing the proliferation rate. However, this enhanced proliferation is not associated to loss of quiescent and functional HSC, which may represent a reservoir of persistent pre-malignant cells available for the accumulation of additional genetic alteration. Further investigation into the biology of per-leukaemic stem cells may give insights into the molecular mechanisms imposed by the oncogene for malignancy transformation and finally may contribute for the development of new therapeutic strategies.
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GILIOLI, DIEGO. "Dissecting the role of cellular senescence in acute myeloid leukaemia immune-surveillance and response to therapy." Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/133076.

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Tzelepis, Konstantinos. "Identification of novel genetic vulnerabilities and therapeutic targets in acute myeloid leukaemia using CRISPR dropout screens." Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/271130.

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Acute myeloid leukaemia (AML) is an aggressive cancer with a poor prognosis, for which mainstream treatments have not changed for decades. To identify novel therapeutic targets in AML, I have optimized a genome-wide clustered regularly interspaced short palindromic repeats (CRISPR) screening platform and use it to identify genetic vulnerabilities in AML cells. This work led to the identification of 492 AML-specific cell-essential genes, including several established therapeutic targets such as that represent new clinically actionable candidates. I have validated selected genes using DOT1L, BCL2, MEN1 and many other genes genetic and pharmacological inhibition, and chose candidates for downstream studies. Both the epigenetic modifier KAT2A and SRPK1 as promising KAT2A and spliceosome kinase SRPK1 inhibition demonstrated anti-AML activity by inducing myeloid differentiation and apoptosis, and suppressed the growth of primary human AMLs while sparing normal hemopoietic stem-progenitor cells. My findings propose that KAT2A and SRPK1 inhibition should be investigated as new therapeutic strategies in AML and also provide a large number of novel genetic vulnerabilities of this leukaemia that can be pursued in downstream studies. As these screens were performed in immortalised AML cell lines, I then went on to develop a method for the performance of dropout screens in genotypically-defined primary murine AMLs developed in our lab and arising in Cas9-expressing mice. Through this work, I successfully carried out the first such screen in AML cells driven by mutant Npm1 (NPM1c) and Flt3-ITD, the commonest two-mutation combination in human AML. Downstream analysis of the results revealed the excellent potential of this type of screen and enabled me to investigate the molecular effects on mutant Npm1, which are currently poorly understood. Overall, my results demonstrate that unbiased CRISPR dropout screens can identify novel therapeutic targets in cancer while, in parallel, revealing novel biological insights.
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Books on the topic "AML acute myeloid leukaemia"

1

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

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K, Burnett Alan, ed. Acute myeloid leukaemia. London: Baillière Tindall, 2001.

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Olwill, Shane. Annexin II expression in acute myeloid leukaemia. [S.l: The author], 2003.

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Barge, A. Acute myeloid leukaemia: The role of haematopoietic growth factors. Macclesfield: Gardner-Caldwell Communications, 1998.

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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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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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Hyde, K. The development of a CFU-GM Bioassay and its relationship to the French American British classification of acute Myeloid Leukaemia. Salford: University of Salford, 1991.

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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Leukaemia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0004.

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Acute myeloblastic leukaemia (AML) - Acute lymphoblastic leukaemia (ALL) - Chronic myeloid leukaemia (CML) - Chronic lymphocytic leukaemia (B-CLL) - Prolymphocytic leukaemia (PLL) - Hairy cell leukaemia and variant - Large granular lymphocyte leukaemia (LGLL) - Adult T-cell leukaemia-lymphoma (ATLL)
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Hassan Al-Sader. Leukaemia. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0004_update_001.

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Acute myeloblastic leukaemia (AML) - Acute lymphoblastic leukaemia (ALL) - Chronic myeloid leukaemia (CML) - Chronic lymphocytic leukaemia (B-CLL) - Prolymphocytic leukaemia (PLL) - Hairy cell leukaemia and variant - Large granular lymphocyte leukaemia (LGLL) - Adult T-cell leukaemia-lymphoma (ATLL)
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Goldman, John M., Angelo M. Carella, George Q. Daley, Connie J. Eaves, and Hehlmann Rudiger. Chronic Myeloid Leukaemia: Biology and Treatment. Taylor & Francis Group, 2003.

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Book chapters on the topic "AML acute myeloid leukaemia"

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Vavro, Hrvoje. "Pachymeningial Involvement in Acute Myeloid Leukaemia (AML)." In Neuroradiology - Images vs Symptoms, 141–45. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-69213-1_19.

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Goldstone, A. H., A. R. Perry, L. G. Robinson, K. Wheatley, and A. K. Burnett. "Stem Cell Transplants in Acute Myeloid Leukaemia (AML)." In Haematology and Blood Transfusion / Hämatologie und Bluttransfusion, 906–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-71960-8_126.

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Ferrand, Christophe, and Alessandro Rambaldi. "Myeloid Malignancies." In The EBMT/EHA CAR-T Cell Handbook, 97–103. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_18.

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AbstractIn addition to chemotherapy, which remains the basic treatment, the treatment panel for acute myeloid leukaemia (AML) has expanded considerably in recent years. Clinicians now have a large choice of therapies: targeted therapies (anti-IDH1/2, anti-FLT3, and anti-BCL2 therapies, among others), drugs targeting epigenetic mechanisms, kinase inhibitors (FLT3, MAPK, and JAK2, etc.), immunotherapies (monoclonal antibodies linked or not to a toxin, dual/bispecific), and cellular immunotherapies. Moreover, despite its toxicities, allogeneic transplantation often remains an effective final therapeutic alternative. However, most patients are refractory or relapsed (R/R) after several lines of therapy. Thus, there is a clinical need in AML R/R patients, and CAR-T cells may be an option and can find a place in the treatment to reduce tumour burden and clinical evolution of the disease (Fig. 18.1, modified from Roussel et al. (2020)).
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Marcus, R. E., D. Catovsky, H. G. Prentice, A. C. Newland, J. M. Chessells, R. F. Stevens, I. M. Hann, J. M. Goldman, A. V. Hoffbrand, and D. A. G. Galton. "Intensive Induction and Consolidation Chemotherapy for Adults and Children with Acute Myeloid Leukaemia (AML) Joint AML Trial 1982–1985." In Acute Leukemias, 346–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71213-5_56.

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Strand, Roger, and Caroline Engen. "Filled with Desire, Perceive Molecules." In Human Perspectives in Health Sciences and Technology, 251–67. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92612-0_15.

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AbstractCould there be a Taoist philosophy of Acute Myeloid Leukaemia (AML)? This chapter discusses why a molecular treatment of AML has been so hard to find but still so intensely researched, and exposes some of the ethical dilemmas involved when treating this aggressive blood cancer. It does so by applying the concepts and style of the ancient Chinese masterpiece Tao Te Ching, the essence of which is that the real world is richer than what can be expressed by language.
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Sokolov, A., E. Parovitchnikova, V. Isaev, S. Kulikov, and V. Savchenko. "Long Remissions After Late Relapse of Acute Myeloid Leukaemia (AML) with Idarubicin + Cytarabine Conventional Doses Treatment." In Haematology and Blood Transfusion Hämatologie und Bluttransfusion, 404–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59358-1_66.

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Montesinos, Pau, and David Martínez-Cuadrón. "Secondary AML." In Acute Myeloid Leukemia, 71–101. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_4.

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Willoughby, M. L. N., and B. Lampkin. "Acute Myeloid Leukaemia." In Cancer in Children, 107–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84722-6_10.

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Smith, Matthew L., and Thomas McKerrell. "Acute myeloid leukaemia." In The Genetic Basis of Haematological Cancers, 133–202. Chichester, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118527948.ch3.

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Mughal, Tariq I. "Acute Myeloid Leukaemia." In Precision Haematological Cancer Medicine, 40–56. Boca Raton, FL : CRC Press, Taylor & Francis Group, [2018]: CRC Press, 2018. http://dx.doi.org/10.1201/9781315380513-4.

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Conference papers on the topic "AML acute myeloid leukaemia"

1

Bykowska, K., S. Lapaciuk, M. Janczarski, Z. Wegrzynowicz, and M. Kopec. "PLASMA FIBRONECTIN IN ACUTE LEUKAEMIAS AND DURING STREPTOKINASE THERAPY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643557.

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We have previously shown that digestion of fibronectin (FN) by trypsin, kallikrein and plasmin influences strongly the FN quantitation by electroimmunoassay (EIA) and immunoturbidimetric assay (ITA). Proteolytic degradation led to an overestimation of FN by EIA but to a decline of results in ITA (Thromb.Haemostas., 53:377, 1985). In this study plasma FN was determined in parallel by EIA and ITA in adult patients with acute leukaemia prior to chemotherapy and in patients treated with SK for DVT. It has been assumed that in leukaemias leukocytic proteases can degrade FN. In 24 control subjects, mean values of plasma FN determined by EIA (285 ± 61 mg/1) and by ITA (268 ± 61 mg/1) did not differ. In contrast, significantly higher values were found by EIA (268 ± 100 mg/1) than by ITA ( 214 ± 65 mg/1, p < 0.01) in 38 patients with acute myeloid leukaemia (AML) and in 12 with blast crisis (BC) in chronic granulocytic leukaemia (245±73 mg/1 and 182 ± 46 mg/1 respectively, p < 0.05). Difference in results of two assays in 10 patients with acute lymphoblastic leukaemia (ALL) was not significant. A decrease in plasma FN when compared with controls was detected only by ITA but not by EIA in AML and BC (p < 0.001). The results of two immunoassays showed a high correlation in control group (r = 0.940) and in ALL (r = 0.838), lower in BC (r = 0.570) and poor in AML (r = 0.163). Discrepant were also results of parallel FN determination by EIA ai]dTJTA in 4 patients treated with SK. Higher values of EIA than of ITA could indicate plasmin mediated FN proteolysis. We have not confirmed recent reports on a frequent occurrence in leukaemias of slowly migrating peak of plasma FN complexes in two-dimensional crossed Immunoelectrophoresis. Such peaks were detected in only 3 of the 46 examined plasma samples. In conclusion the parallel FN determination by EIA and ITA can provide an ’ indirect evidence for the occurrence of proteolytic degradation of plasma FN in vivo.
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Skelding, K., J. Gilchrist, E. Pearsall, M. Chi, N. Bowden, and L. Lincz. "PO-144 Role of increased expression of brain and acute leukaemia, cytoplasmic (BAALC) in acute myeloid leukaemia (AML) DNA damage repair pathways." 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-eacr25.185.

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Yasinska, I., B. Gibbs, L. Varani, R. Hussain, G. Siligardi, E. Fasler-Kan, L. Calzolai, and V. Sumbayev. "PO-409 Highly specific targeting of human acute myeloid leukaemia (AML) cells using functionalised gold nanoparticles." 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-eacr25.920.

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Armenteros-Monterroso, E., L. Zhao, J. de Boer, and O. Williams. "Investigating Reptin function in Acute Myeloid Leukaemia." In 30. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch-onkologische Forschung. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1602188.

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Alameri, M., J. Bartram, O. Williams, and J. de Boer. "Epigenetics profiling for minimal residual disease in paediatric acute myeloid leukaemia." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687157.

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Cazzola, A., I. Jansen, and A. Kraemer. "PO-457 Is 8-azaguanine selectively active against aneuploid acute myeloid leukaemia?" 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-eacr25.478.

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Issa, H., R. Bhayadia, and JH Klusmann. "Therapeutic application of the tumour suppressive miR-193b in Acute Myeloid Leukaemia." In 32. Jahrestagung der Kind-Philipp-Stiftung für pädiatrisch onkologische Forschung. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1687144.

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Licandro, Roxane, Thomas Schlegl, Michael Reiter, Markus Diem, Michael Dworzak, Angela Schumich, Georg Langs, and Martin Kampel. "WGAN Latent Space Embeddings for Blast Identification in Childhood Acute Myeloid Leukaemia." In 2018 24th International Conference on Pattern Recognition (ICPR). IEEE, 2018. http://dx.doi.org/10.1109/icpr.2018.8546177.

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Tuszynski, George P., and Vicki Rothman. "Abstract 5392: Angiocidin induces differentiation of acute myeloid leukemia (AML) cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5392.

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Koh, Youngil, Dae-Yoon Kim, Jong-Kwang Kim, Yeun-June Chung, Sung-Soo Yoon, and Hyung-Lae Kim. "Abstract 4756: Genomic profile of AML-ETO rearranged acute myeloid leukemia." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4756.

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Reports on the topic "AML acute myeloid leukaemia"

1

Jiang, Zhiping, Ao Zhang, Shuxing Wang, Quanlei Ren, and Yizhu Wang. Prognostic value of ASXL1 mutations in patients with myelodysplastic syndromes and acute myeloid leukemia: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0013.

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Review question / Objective: A meta-analysis was performed to investigate prognostic value of ASXL1 mutations in patients with myelodysplastic syndromes and acute myeloid leukemia. Condition being studied: Some MDS or AML patients have ASXL1 mutations while others haven’t. Main outcome(s): We used OS as the primary endpoint and AML transformation as the secondary endpoint. OS was defined as either death (failure) or survival at the last follow-up. AML transformation was defined as starting when the patient entered the trial and proceeding to the time of AML diagnosis.Combined HRs and 95% CIs for OS and AML transformation were used to evaluate the prognostic effect of ASXL1 mutations using the generic inverse variance method.
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Kungwankiattichai, Smith, Ben Ponvilawa, Claudie Roy, Pattaraporn Tunsing, Florian Kuchenbauer, and Weerapat Owattanapanich. Maintenance with Hypomethylating Agents after Allogeneic Stem Cell Transplantation in Acute Myeloid Leukemia and Myelodysplastic Syndrome: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0078.

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Review question / Objective: P: Patients with AML or MDS after allo-SCT; I: Hypomethylating agents after allo-SCT; C: Observation after allo-SCT; O: Overall survival rates. Condition being studied: Hypomethylating agents (HMAs) seem to have a range of properties favorable to post-allogeneic hematopoietic stem cell transplantation (allo-SCT) maintenance in acute myeloid leukemia (AML) patients. This meta-analysis was performed to review all relevant studies to compare the outcomes of patients undergoing allo-SCT for AML or MDS receiving HMA maintenance therapy with observation only. Information sources: The systematic search of the Embase and MEDLINE databases identified 4,416 articles, from which 512 duplicates were removed. This resulted in 3,904 articles available for title and abstract review. Subsequently, 3,875 articles were excluded as the article type and study design did not fulfill the inclusion criteria, or there was no report on a primary outcome of interest. The remaining 29 articles underwent full-length review and 18 of those were excluded for the aforementioned reasons. Ultimately, the eligibility criteria for our meta-analysis were met by 11 studies: 2 RCTs, 1 prospective cohort study, and 8 retrospective cohort studies.
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