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Literatura científica selecionada sobre o tema "Leukaemic Stem Cells"

Autor: Grafiati

Publicado: 14 de março de 2023

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Artigos de revistas sobre o assunto "Leukaemic Stem Cells"

1

Sarrou, Evgenia, Laura Richmond, Ruaidhrí J. Carmody, Brenda Gibson e 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, n.º 12 (15 de junho de 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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Blair, A., e D. H. Pamphilon. "Leukaemic stem cells". Transfusion Medicine 13, n.º 6 (dezembro de 2003): 363–75. http://dx.doi.org/10.1111/j.1365-3148.2003.00464.x.

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Shlush, L. I., e T. Feldman. "The evolution of leukaemia from pre‐leukaemic and leukaemic stem cells". Journal of Internal Medicine 289, n.º 5 (29 de janeiro de 2021): 636–49. http://dx.doi.org/10.1111/joim.13236.

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4

Lutz, Christoph, Petter Woll, Anders Castor, Helen Ferry, Christina Jensen, Joanne Green, Helene Dreau et al. "Selective Persistence of Distinct Stem/B Leukaemic Stem Cells In Childhood Acute Lymphoblastic Leukaemia In Clinical Remission." Blood 116, n.º 21 (19 de novembro de 2010): 1585. http://dx.doi.org/10.1182/blood.v116.21.1585.1585.

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Abstract Abstract 1585 Recent studies utilising surrogate leukaemic stem cell (LSC) assays have suggested that LSCs in acute lymphoblastic leukaemias (ALLs) might be neither rare, nor phenotypically or functionally distinct. However, studies of candidate LSCs in surrogate assays might not recapitulate the full leukaemic potential of candidate LSCs in patients, and in particular their responsiveness and resistance to therapeutic targeting. Therefore, we have investigated the identity, molecular and functional properties, and persistence of different subsets of candidate LSCs in childhood ALL, at diagnosis and during the course of clinical and molecular remissions in response to chemotherapy, and their relationship to subsequent relapses. First, we investigated 6 patients diagnosed with “good prognosis” TEL-AML1+ ALL, and at diagnosis we found TEL-AML1+ leukaemic cells within the immature B cell progenitor compartment (proB: 34+38+19+), mature B-cells (34-19+), as well as in a population expressing an aberrant combination of stem cell (34+38-/lo) and B-cell (19+) cell surface markers. These stem/B (34+38-/lo19+) cells were all TEL-AML1+ and not present in age-matched normal bone marrow controls. In contrast, haematopoietic stem cells (HSC: 34+38-19-) were not part of the TEL-AML1+ leukaemic clone in any of the patients. 15 days into chemotherapy, all TEL-AML1+ mature B-cells were eliminated in all patients, and this was followed by a clearance of leukaemic proB cells by day 28 of treatment. In striking contrast, leukaemic stem/B cells were still detectable at day 28, but in all TEL-AML1 patients, at later stages all leukaemic cells including the stem/B cells were undetectable, and at the same time these patients went into complete remission with less than 1 leukaemic cell in 10e4 cells detectable. A similar pattern was observed in a case of “high risk” BCR-ABL+ ALL: BCR-ABL+ proB and B-cells were efficiently eliminated by day 90 of the course of chemotherapy, and up to 180 days into the treatment only 34+38-/lo19+ stem/B cells remained part of the BCR-ABL+ clone. In agreement with the persistence of BCR-ABL+ 34+38-/lo19+ stem/B cells, this patient relapsed 17 months after the initiation of chemotherapy. In order to understand the underlying mechanisms of the observed functional and therapeutic heterogeneity seen in leukaemic subpopulations, we performed comparative gene-expression analysis of diagnostic leukaemic stem/B and proB cells of TEL-AML1+ patients. This analysis revealed a differential gene expression pattern between leukaemic stem/B and proB cells, with positive regulators of cell cycle being the most distinctly up regulated genes in leukaemic proB cells. In agreement with this, cell cycle analysis of 3 diagnostic TEL-AML1+ cases also showed proB cells to be more actively cycling compared to the more quiescent state of the leukaemic stem/B compartment (proB: G0 42%; G1 40%; S,G2,M 18% vs. stem/B: G0 81%; G1 18%; S,G2,M 1%), providing a potential mechanistic basis for the relative therapy resistance of ALL stem/B cells. Taken together the present studies suggest that quiescent 34+38-/lo19+ stem/B cells are selectively resistant to chemotherapy, and most likely the origin of relapses when these occur in childhood ALL. Disclosures: No relevant conflicts of interest to declare.

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Noman, Helal Mohammed Mohammed Ahmed, Yahya Saleh Al-Matary, Subbaiah Chary Nimmagadda, Pradeep Kumar Patnana, Longlong Liu, Lanying Wei, Daria Frank, Georg Lenz e Cyrus Khandanpour. "Leukaemia Cells Induced Metabolic Alterations in AML Associated Mesenchymal Stem Cells Via Notch Signalling". Blood 138, Supplement 1 (5 de novembro de 2021): 4347. http://dx.doi.org/10.1182/blood-2021-144468.

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Abstract Introduction: Acute myeloid leukaemia (AML) is a haematological malignancy with a high relapse rate and poor prognosis. Leukaemia cell proliferation is dependent on its interaction with the bone marrow (BM) microenvironment. AML associated mesenchymal stem cells (AML-MSCs) supported the proliferation of leukaemia cells and contributed to disease progression. Stromal microenvironment promoted a metabolic switch but precise underlying molecular mechanisms are poorly understood. Previous studies have demonstrated transfer of functional mitochondria from AML-MSCs to AML blasts facilitating energy requirements. To further improve our understanding of the crosstalk between leukaemia and AML-MSCs, we sought to determine contribution of AML-MSCs and signalling cascades regulating metabolic processes. Methods: Sorted MSCs from non-leukaemic and MLL-AF9 leukaemic mice were isolated, and gene expression profiling was performed using RNA microarray. Additionally sorted MSCs from long-term cultures were cultured alone or with MLL-AF9 leukaemia cells and analysed by RNA-sequencing. Gene set enrichment analysis (GSEA) was used to identify the hallmark gene sets overrepresented in AML-MSCs. We further cocultured murine wild type BM-MSCs alone or together with murine AML cells (C1498 and MLL-AF9) or the control lineage negative cells (Lin -). Metabolic alterations, oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) were analysed by Agilent Seahorse XFe96 analyser. Additionally, glucose consumption, lactate secretion and mitochondrial DNA copy number were measured. Results: Microarray analysis in sorted MSCs from leukaemic and non-leukaemic mice have identified hallmark oxidative phosphorylation (p<0.01, NES=-1.6) and glycolysis (p<0.01, NES=-1.3) gene sets to be negatively enriched in AML-MSCs. Interestingly, both the gene sets were also negatively enriched in sorted AML-MSCs when cocultured with leukaemia but not control cells. To validate these findings, we analysed OCR and EACR in WT-MSCs in an identical setting. The oxidative phosphorylation was significantly decreased in MSCs cocultured with C1498 (p<0.0001) and MLL-AF9 (p<0.005) but not with Lin - cells. Interestingly, glycolysis rate, glucose consumption, lactate secretion were significantly decreased in MSCs cocultured with leukaemia cells. Mitochondrial DNA copy number were significantly decreased in MSCs cocultured with C1498 (p<0.001) or MLL-AF9 (p<0.005) but not with control cells. Recent evidence from the lab has demonstrated an essential role for Notch signalling in the leukaemia and AML-MSCs interaction. To functionally determine the crosstalk of leukaemia-MSC interaction and subsequent Notch signalling, we ectopically expressed the Notch intracellular domain (Notch-ICN1) to mimic Notch activation in a murine stromal cell line, MS-5. Confirming Notch activation, Hes1 mRNA expression (encoding a transcriptional target of Notch signalling) was significantly increased in these cells. Underscoring a role for Notch signalling and activation, Notch-ICN1 overexpression in MS-5 cells demonstrated less oxidative phosphorylation and glycolysis rates as compared to MS-5 cells transduced with empty vector. Conclusion: In line with our microarray and GSEA analysis, our findings confirmed that leukaemia cells indeed induced metabolic alterations decreasing oxidative phosphorylation and glycolysis, and thereby potentially altering AML-MSCs function. At the molecular level, Notch signalling (via upregulated Notch1 and 2 expressions and Notch-ICN) in AML-MSCs contributed to metabolic alterations. Therefore, therapeutically interfering this pathway could target the bidirectional interaction between leukaemia and AML-MSCs improving therapeutic efficacy of AML. Disclosures Khandanpour: GSK: Honoraria; Takeda: Honoraria; Janssen: Honoraria; AstraZeneca: Honoraria, Research Funding; Pfizer: Honoraria; Sanofi: Honoraria, Research Funding; BMS/Celgene: Honoraria.

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Bonnet, Dominique. "Normal and leukaemic stem cells". British Journal of Haematology 130, n.º 4 (agosto de 2005): 469–79. http://dx.doi.org/10.1111/j.1365-2141.2005.05596.x.

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Brown, Geoffrey, Lucía Sánchez e Isidro Sánchez-García. "Are Leukaemic Stem Cells Restricted to a Single Cell Lineage?" International Journal of Molecular Sciences 21, n.º 1 (19 de dezembro de 2019): 45. http://dx.doi.org/10.3390/ijms21010045.

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Cancer-stem-cell theory states that most, if not all, cancers arise from a stem/uncommitted cell. This theory revolutionised our view to reflect that cancer consists of a hierarchy of cells that mimic normal cell development. Elegant studies of twins who both developed acute lymphoblastic leukaemia in childhood revealed that at least two genomic insults are required for cancer to develop. These ‘hits’ do not appear to confer a growth advantage to cancer cells, nor do cancer cells appear to be better equipped to survive than normal cells. Cancer cells created by investigators by introducing specific genomic insults generally belong to one cell lineage. For example, transgenic mice in which the LIM-only 2 (LMO2, associated with human acute T-lymphoblastic leukaemia) and BCR-ABLp210 (associated with human chronic myeloid leukaemia) oncogenes were active solely within the haematopoietic stem-cell compartment developed T-lymphocyte and neutrophil lineage-restricted leukaemia, respectively. This recapitulated the human form of these diseases. This ‘hardwiring’ of lineage affiliation, either throughout leukaemic stem cell development or at a particular stage, is different to the behaviour of normal haematopoietic stem cells. While normal cells directly commit to a developmental pathway, they also remain versatile and can develop into a terminally differentiated cell that is not part of the initial lineage. Many cancer stem cells do not have this versatility, and this is an essential difference between normal and cancer stem cells. In this report, we review findings that support this notion.

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Bonnet, D. "Cancer stem cells: AMLs show the way". Biochemical Society Transactions 33, n.º 6 (26 de outubro de 2005): 1531–33. http://dx.doi.org/10.1042/bst0331531.

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The blood-related cancer leukaemia was the first disease where human CSCs (cancer stem cells), or LSCs (leukaemic stem cells), were isolated. The haematopoietic system is one of the best tissues for investigating CSCs, since the developmental hierarchy of normal blood formation is well defined. Leukaemia can now be viewed as aberrant haematopoietic processes initiated by rare LSCs that have maintained or reacquired the capacity for indefinite proliferation through accumulated mutations and/or epigenetic changes. Yet, despite their critical importance, much remains to be learned about the developmental origin of LSCs and the mechanisms responsible for their emergence in the course of the disease. This report will review our current knowledge on LSC development and finally demonstrate how these discoveries provide a paradigm for identification of CSCs from solid tumours.

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Kuek, Vincent, Anastasia M. Hughes, Rishi S. Kotecha e Laurence C. Cheung. "Therapeutic Targeting of the Leukaemia Microenvironment". International Journal of Molecular Sciences 22, n.º 13 (26 de junho de 2021): 6888. http://dx.doi.org/10.3390/ijms22136888.

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In recent decades, the conduct of uniform prospective clinical trials has led to improved remission rates and survival for patients with acute myeloid leukaemia and acute lymphoblastic leukaemia. However, high-risk patients continue to have inferior outcomes, where chemoresistance and relapse are common due to the survival mechanisms utilised by leukaemic cells. One such mechanism is through hijacking of the bone marrow microenvironment, where healthy haematopoietic machinery is transformed or remodelled into a hiding ground or “sanctuary” where leukaemic cells can escape chemotherapy-induced cytotoxicity. The bone marrow microenvironment, which consists of endosteal and vascular niches, can support leukaemogenesis through intercellular “crosstalk” with niche cells, including mesenchymal stem cells, endothelial cells, osteoblasts, and osteoclasts. Here, we summarise the regulatory mechanisms associated with leukaemia–bone marrow niche interaction and provide a comprehensive review of the key therapeutics that target CXCL12/CXCR4, Notch, Wnt/b-catenin, and hypoxia-related signalling pathways within the leukaemic niches and agents involved in remodelling of niche bone and vasculature. From a therapeutic perspective, targeting these cellular interactions is an exciting novel strategy for enhancing treatment efficacy, and further clinical application has significant potential to improve the outcome of patients with leukaemia.

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Shlush, Liran I., Sasan Zandi, Amanda Mitchell, Weihsu Claire Chen, Joseph M. Brandwein, Vikas Gupta, James A. Kennedy et al. "Identification of pre-leukaemic haematopoietic stem cells in acute leukaemia". Nature 506, n.º 7488 (12 de fevereiro de 2014): 328–33. http://dx.doi.org/10.1038/nature13038.

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Mais fontes

Teses / dissertações sobre o assunto "Leukaemic Stem Cells"

1

Lewis, Ian D. "Characterisation of normal and leukaemic stem cells in chronic myeloid leukaemia /". Title page, contents and abstract only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phl6745.pdf.

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2

POTETI, MARTINA. "The metabolic profile of Chronic Myeloid Leukaemia: stem cells as a target to overcome resistance to therapy". Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1071850.

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Chronic Myeloid Leukaemia (CML) is a stem cell-driven disorder treated with Tyrosine Kinase inhibitors (TKi) with impressive efficacy. However, TKi are unable in most cases to prevent the relapse of disease, as even a very successful response to treatment results in the persistence of a state of Minimal Residual Disease (MRD). Our hypothesis predicts that MRD is sustained by the persistence of Leukaemic Stem Cells (LSC) capable to survive and cycle independently of BCR/Abl kinase activity within Bone Marrow (BM) stem cell niches where severe oxygen and glucose shortage would result in BCR/Ablprotein suppression. In this study, we addressed the role of the availability of glutamine, among a number of other metabolites possibly relevant in this context, in the control of BCR/Ablprotein expression in CML cell cultures where energy supply is markedly restricted, i.e. maintained under conditions likely mimicking those of stem cell niches in vivo. We found that glutamine drives accelerated BCR/Ablprotein suppression and that this phenomenon is paralleled by the kinetics of glucose consumption from culture medium. The relationship between presence of glutamine and glucose consumption was deepened by investigating the effects of different metabolic inhibitors. We found that the inhibition of glycolysis via treatment with 2-DG or 3PO, as well as that of Pentose Phosphate Pathway (PPP) via treatment with 6-AN, prevented the effects of the presence of glutamine on BCR/Ablprotein expression, confirming that BCR/Ablprotein suppression requires the presence of glutamine and depends on glucose consumption irrespective of the pathway driving this consumption. On the contrary, the inhibition of OxPhos by means of metformin did not interfere with the effects of the presence or absence of glutamine on BCR/Ablpr otein expression. The effects of the presence or the absence of glutamine were also tested on the maintenance of stem cell potential in low oxygen. Using our in vitro LSC assay, Culture-Repopulation Ability (CRA) assay, we found that cells grown in the absence of glutamine exploited their stem cell potential promptly upon transfer to permissive conditions. The treatment of glutamine-free cultures with metformin did not interfere with the pattern of LC2 repopulation. On the contrary, BCR/Ablprotein-negative cells were affected by metformin treatment. The treatment with BPTES, a GLS1 inhibitor, in either the presence or the absence of glutamine, favored the maintenance of BCR/Ablprotein expression in low oxygen, so that LSC transferred to permissive conditions were capable to exploit their stem cell potential rapidly, driving prompt LC2 repopulation. This result could represent the basis of an innovative CML treatment strategy using inhibitors of glutamine metabolism in combination with TKi to determine LSC eradication together with induction or maintenance of remission.

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Volpe, Giacomo. "Regulation of flt3 gene expression in haematopoietic and leukaemic stem cells". Thesis, University of Birmingham, 2010. http://etheses.bham.ac.uk//id/eprint/822/.

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The interaction between the tyrosine kinase receptor Flt3 and its ligand leads to signalling during the commitment of haematopoietic stem cells (HSCs). Constitutive activation of the Flt3/FL pathway is a key factor in enhanced survival and expansion in acute myeloid leukaemia (AML). Although there is extensive knowledge regarding mutations leading to the constitutive activation of Flt3 receptor activity, the molecular mechanisms underlying the regulation of the \(flt3\) gene in HSCs, and how such mechanisms might be altered in leukaemia, are still poorly understood. Here, by using HSC and leukaemic cell lines, I locate several regulatory elements in the \(flt3\) locus by DNaseI mapping and have characterized their epigenetic environment. Analysis of the methylation and acetylation status of histones H3 and H4 around \(flt3 cis\)-regulatory regions highlights a distinct combination of epigenetic modifications specific to AML cells in a region that distinguishes the Flt3\(^-\) and Flt3\(^+\) stages of HSC differentiation. Moreover, I show the link between the \(in vivo\) binding of C/EBP and c-Myb on regulatory elements and epigenetic remodelling in the differential regulation of \(flt3\) in leukaemic cells. Finally, I identify the histone modifiers TIP60 and CBP as potential mediators of the epigenetic regulation of \(flt3\) in AML cells.

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Kuntz, Elodie Marie. "An investigation of metabolic vulnerabilities in chronic myeloid leukaemic stem cells". Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/8615/.

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Chronic myeloid leukaemia (CML) is a myeloproliferative disorder that originates at the haematopoietic stem cell (HSC) level. CML is driven by BCR-ABL, a fusion oncoprotein with a constitutive tyrosine kinase activity. The discovery of imatinib, a c-Abl specific tyrosine kinase inhibitor (TKI), revolutionised the treatment of CML by inducing cytogenetic and molecular responses in the majority of CML patients in chronic phase. However, imatinib and second/third generation TKIs do not eradicate leukaemic stem cells (LSCs), leading to disease persistence with associated risk of toxicity, drug resistance and relapse. This suggests that effective eradication of CML LSCs requires identification of novel target(s) that can be exploited therapeutically in combination with TKI treatment. In recent years, a plethora of studies have demonstrated that cancer cells rewire their metabolism to fuel their high energy demands and targeting these metabolic alterations can be of therapeutic benefit. Thus far, investigation of CML LSCs metabolism has been restricted by technical limitations. In this study, we aimed to identify and target the metabolic dependencies in CML LSCs using stem cell-enriched (CD34+) primary cells isolated from CML patients and healthy donors. We initially investigated the metabolism of differentiated CD34- and primitive CD34+ cells and demonstrated that glucose and fatty acid oxidation was elevated in CD34+ CML cells. We as well demonstrated that CML CD34+ cells displayed an increase in their mitochondrial oxygen consumption rate (OCR). Next, we compared the metabolism of CD34+ and CD34+CD38- CML cells to their respective normal counterparts, which revealed that stem cell-enriched CML cells possess increased mitochondrial functions in comparison to normal cells. Of clinical significance, we show that the antibiotic tigecycline, an inhibitor of mitochondrial translation, reduced this aberrant oxidative metabolism. The combination of imatinib and tigecycline targeted primitive CML cells at a clinically achievable concentration while having minimal effect on colony formation potential of CD34+ cells derived from healthy donors. To validate these findings in vivo, human CML CD34+ cells were injected into irradiated immune-deficient mice. Remarkably, four-week combination treatment with tigecycline and imatinib in vivo eliminated the majority of CML LSCs, targeting 95% of the cells. Moreover, mice maintained low levels of CML LSCs upon discontinuation of the combination treatment whereas imatinib-treated mice showed signs of relapse. These results indicate that oxidative phosphorylation is crucial for the survival of CML LSCs and inhibition of mitochondrial metabolism with tigecycline, in combination with imatinib treatment, might be a suitable therapeutic strategy to selectively target these cells and improve cure rates.

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Robinson, Simon N. "Proliferation regulation of haematopoietic stem cells in normal and leukaemic haematopoiesis". Thesis, University of St Andrews, 1992. http://hdl.handle.net/10023/14965.

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The cellular integrity of the blood is maintained by the cellular output of the haematopoietic stem cell population which produces the specialized precursors and differentiated cells which constitute the blood. The investigation of haematopoietic stem cell behaviour and regulation has been hampered by both the difficulty in their identification and the development of relevant assay systems. The purpose of this investigation was to study the behaviour and regulation of the haematopoietic stem cell population in normal and leukaemic haematopoiesis using an in vitro assay of a primitive haematopoietic precursor. The use of a combination of haematopoietic colony-stimulating factors [interleukin 3 (IL3)/multi-CSF and macrophage colony-stimulating factor (M-CSF/CSF-1)] in semi-solid agar culture of murine haematopoietic tissue, stimulated the proliferation of a haematopoietic colony-forming cell, defined as the "HPP-CFCIL3+CSF-1" population, which was characterized by a high proliferative potential, a multipotency and behavioural and regulatory properties consistent with its being a primitive haematopoietic precursor and possibly a component of the haematopoietic stem cell population. The proportion of the in vitro HPP-CFCIL3+csf-1 population in S-phase in normal murine marrow, was determined to be relatively low at approximately 10%, increasing to approximately 40% in sublethally X-irradiated, regenerating murine marrow and the respective presence of the haematopoietic stem cell proliferation inhibitor and stimulator was demonstrable by the induction of appropriate kinetic changes in the in vitro HPP-CFCIL3+CSF-1 population. In leukaemic haematopoiesis, leukaemic proliferation often occurs at the expense of apparently suppressed normal haematopoiesis. In vitro HPP-CFCIL3+CSF-1 assay of the haematopoietic stem cell proliferation regulators in a number of murine, myeloid leukaemic cell lines, failed to demonstrate either increased levels of the haematopoietic stem cell proliferation inhibitor, or evidence of a direct-acting, leukaemia- associated proliferation inhibitor, however, evidence of a leukaemia- associated impairment of inhibitor and stimulator production was observed and this may be a possible mechanism by which the leukaemic population develops a proliferative advantage over normal haematopoietic tissue. The identification of a possible mechanism of leukaemic progression and suppression of normal haematopoiesis may subsequently allow the development of potentially more effective disease treatment and management regimes. The endogenous haemoregulatory tetrapeptide: Acetyl-N-Ser- Asp-Lys-Pro [AcSDKP, Mr=487 amu] is reported to prevent the G0-G1 transition of haematopoietic stem cells into S-phase. The mechanism of action of AcSDKP and a number of related peptides, was investigated in relation to the stem cell proliferation stimulator and inhibitor. AcSDKP demonstrated no direct haemoregulatory role against the in vitro HPP-CFCIL3+CSF-1 population, which is consistent with reports that AcSDKP is not active against cells already in late G1, or S-phase, rather it appeared to act indirectly by impairing the capacity of the haematopoietic stem cell proliferation stimulator to increase the proportion of the in vitro HPP-CFCIL3+CSF-1 population in S-phase. An apparent impairment of stimulator action may explain the reported AcSDKP-associated 'block' of haematopoietic stem cell recruitment. A putative endogenous AcSDKP precursor and synthetic and degradative enzyme systems have been reported and the possible physiopathological role of AcSDKP in a number of myeloproliferative disorders has been implicated. The potential application of AcSDKP as a 'haemoprotective' agent administered prior to the use of S-phase- specific chemotherapy may be of clinical significance. The in vitro HPP-CFCIL3+CSF-1 assay of a primitive haematopoietic precursor cell population, which may be a component of the haematopoietic stem cell population, should play a significant role in the investigation of haematopoietic stem cell behaviour and regulation in both normal and aberrant haematopoiesis. With the characterization of the mechanism(s) of action of the haematopoietic stem cell proliferation inhibitor and stimulator and the haemoregulatory tetrapeptide AcSDKP, the manipulation of the haematopoietic system to clinical advantage can be envisaged, while the identification of the aberrant regulatory mechanism(s) in haematopoietic dysfunction may allow, the development of more effective disease treatment and management regimes.

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江卓庭 e Cheuk-ting Kong. "Understanding the function of the Mll-een leukaemic fusion gene by embryonic stem cell approaches". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B31244312.

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7

Taylor, Alan. "The role of leukaemia inhibitory factor and a leukaemic associated inhibitor in the control of the proliferation of haematopoietic stem cells". Thesis, University of St Andrews, 1996. http://hdl.handle.net/10023/14962.

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Activities associated with, or interacting with, leukaemic cell populations were assayed for the ability to influence in vitro haematopoiesis. The first of these, the glycoprotein leukaemia inhibitory factor (LIF), has a role in aspects of murine, non human primate and human haematopoiesis. It is thought to be particularly important in the development of megakaryocytes and is also known to induce the terminal differentiation of certain leukaemic cell lines. LIF was assayed both for direct and indirect effects on the proliferation of haematopoietic precursor cell populations in vitro. As a direct acting agent in semi-solid agar culture of haematopoietic cell populations derived from normal bone marrow or 15 day foetal liver, LIF was unable to support colony formation. In cultures of cells derived from normal bone marrow stimulated with single, or combinations of, growth factors, the addition of LIF had no statistically significant effect on the level of colony formation. In cultures of cells derived from foetal liver, stimulated with particular growth factor combinations (medium conditioned by the Wehi3B leukaemic cell line + medium conditioned by the lung fibroblast cell line, L929); GM-CSF + M-CSF; IL-la + IL-3 + M-CSF), LIF, was shown to decrease the level of colony formation. LIF did not directly alter the proportion of the population in DNA synthesis in cell populations derived from normal femoral marrow, 15 day foetal liver or y- irradiated femoral marrow. As an indirect acting agent LIF failed to block the synthesis of a stem cell stimulator, or it's action, on a population of high proliferative potential colony forming cells derived from normal femoral marrow, cloned in the presence of Wehicm+L929cm. (HPP-CFC (Wehicm + L929cm)) LIF's actions on clones of a murine myeloid leukaemia (SA2JMB1) were also assessed. LIF had no statistically significant effect on colony formation or the level of DNA synthesis in populations of SA2JMB1 leukaemic cells. A second group of associated activities was produced by the X- irradiation induced murine myeloid leukaemia (SA2JMB1). Medium conditioned by the leukaemic cells was assayed in vitro both for direct and indirect effects on the proliferation of haematopoietic cells derived from femoral marrow. As a direct acting agent in 7 and 14-day semi-solid agar culture of femoral marrow, leukaemic conditioned medium alone stimulated limited colony formation. In 7 and 14 day cultures stimulated with single and combinations of specific colony stimulating factors: (rmGM-CSF, rhM-CSF, rhIL-1a) a significant increase in colony number was noted in all cases when cultures were supplemented with leukaemic conditioned medium. SA2JMBlcm was shown to support the proliferation of an IL-3 dependent cell line (FDCP-A4 cells). The colony enhancing ability of SA2JMBlcm was shown to be blocked by pretreatment with antibodies to IL-3. This suggested that SA2JMB1 conditioned medium contained IL-3 or an IL-3 like activity, as one of its components. The conditioned medium failed to directly alter the level of DNA synthesis in a population of HPP-CFC (Wehicm+L929cm) derived from normal bone marrow or y- irradiated bone marrow. As an indirect acting agent the conditioned medium did block the action of a stem cell proliferation stimulator on normal bone marrow derived HPP-CFC (Wehicm+L929cm). This leukaemia associated activity was shown to be larger than 50KD, sensitive to heat treatment and able to act in a different manner to the stem cell inhibitor MIP-1-a. Thus this novel activity may be important in blocking stimulator action in haematopoietic stem cells and thus contribute to the haematopoietic insufficiency seen in leukaemia.

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Austin, Pamela M. "Defining biological properties of the leukaemic stem cell in Hoxa9Meis1-induced leukaemia". Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80222.

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A subset of the leukaemic clone, the leukaemic stem cell (L-HSC), is responsible for the maintenance and propagation of a leukaemia. Most current therapies, however, do not target this population. In this thesis, I show that a determinant of disease phenotype is the frequency of the leukaemic stem cell within the leukaemic population. Moreover, the frequency of L-HSC in a leukaemia is predetermined by the inherent properties of the cell that is transformed and can be attributed to the ontogenic origin of the cell. Ideal therapies would specifically target mechanistic defects in leukaemic stem cells; however, the pathways that are involved and what oncogenic defects can be targeted for therapy remain to be discovered. As it is not known if all oncogenes can be targeted or what the determinants of oncogenic dependency are, I have developed a system to further elucidate this as described herein.

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9

Carlens, Stefan. "Leukaemic relapse after allogeneic haematopoietic stem cell transplantation and the use of the graft-versus-leukaemia effect /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4310-9/.

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Taussig, David. "Characterisation of acute myeloid leukaemia stem cells". Thesis, Queen Mary, University of London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424766.

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Mais fontes

Livros sobre o assunto "Leukaemic Stem Cells"

1

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

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2

Collins, Graham, e Chris Bunch. Acute leukaemia. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0286.

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Acute leukaemias are rapidly progressive, clonal haematopoietic stem cell disorders resulting in the accumulation of immature blood cell precursors (known as blasts) in the bone marrow. There are two main types, defined by the presence of myeloid lineage or lymphoid markers on the blast cells: acute myeloid leukaemia and acute lymphoblastic leukaemia. This chapter addresses the causes, diagnosis, and management of the acute leukaemias.

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3

Bunch, Chris. Chronic leukaemia. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0287.

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In the chronic leukaemias, leukaemogenesis occurs in two different cell types (and possibly even two different anatomical sites), leading to two very different forms of the disease: chronic myeloid leukaemia and chronic lymphocytic leukaemia. Chronic myeloid leukaemia is best thought of as a myeloproliferative disorder. It is a clonal disorder of the haematopoietic stem cell, leading to overproduction of the myeloid cells: neutrophils and their precursors, basophils and eosinophils. By contrast, chronic lymphocytic leukaemia can be viewed as a low-grade lymphoma. It is a clonal disorder of mature B-lymphocytes (possibly memory B-cells). This chapter reviews the causes, diagnosis, and management of these two forms of chronic leukaemia.

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McCann, Shaun R. Radiation and transplantation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198717607.003.0006.

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There is a paradoxical relationship between ionizing radiation and leukaemia. On the one hand, it is known that exposure to high doses of ionizing radiation causes leukaemia; on the other hand, the preparative regimens for stem cell transplantation, which can cure leukaemia, often contain total body irradiation. This chapter discusses the effect war has had on medical technology, with specific regard to the use of stem cells for the treatment of blood disorders such as leukaemia and sickle cell anaemia. The transfer of laboratory techniques to the clinical practice of stem cell transfer and bone marrow transplantation is also discussed.

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Ajithkumar, Thankamma, Ann Barrett, Helen Hatcher e Natalie Cook. Paediatric malignancies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235636.003.0015.

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Leukaemia is the commonest cancer (accounting for >40% of cases) in children. It is a clonal proliferation of stem cells which leads to bone marrow failure and tissue infiltration.• Acute lymphoblastic leukaemia (ALL): 4/100,000• Acute myeloid leukaemia (AML): 0.7/100,000• Chronic myeloid leukaemia (CML): 0.2/100,000...

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6

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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7

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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8

Bunch, Chris. Myelodysplasia. Editado por Patrick Davey e David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0288.

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The myelodysplastic syndromes (or myelodysplasias) comprise a spectrum of disorders characterized by dysplastic or ineffective haemopoiesis that leads to variable anaemia, neutropenia, and thrombocytopenia. There is often a degree of red-cell macrocytosis. The majority are clonal stem cell disorders in which the abnormal clone predominates and expands only slowly over a number of years. Myelodysplasias have a tendency to develop ultimately into acute leukaemia in some patients; for this reason, they are sometimes referred to as ‘preleukaemias’, even though two-thirds of patients will never develop this complication. This chapter addresses the causes, diagnosis, and management of myelodysplastic syndromes.

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Capítulos de livros sobre o assunto "Leukaemic Stem Cells"

1

Marks, David I. "Allogeneic Stem Cell Transplantation for Acute Lymphoblastic Leukaemia in Adults". In Allogeneic Stem Cell Transplantation, 193–202. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-478-0_13.

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2

Berger, Marc G., e Céline Bourgne. "Contribution of Chronic Myeloid Leukaemia (CML) as a Disease Model to Define and Study Clonal Heterogeneity". In Stem Cells Heterogeneity in Cancer, 171–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-14366-4_10.

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3

Goldstone, A. H., A. R. Perry, L. G. Robinson, K. Wheatley e 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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4

Geißler, K., W. Hinterberger, P. Bettelheim, P. Höcker, M. Fischer e K. Lechner. "Circulating Stem Cells in Patients with Akute Leukaemia in Remission". In 11th Annual meeting of the EBMT, 50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-662-40457-7_35.

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5

Viale, Andrea, e Pier Giuseppe Pelicci. "Regulation of Self-Renewing Divisions in Normal and Leukaemia Stem Cells". In Cell Cycle Deregulation in Cancer, 109–25. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1770-6_7.

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6

Rehmann-Sutter, Christoph, Martina Jürgensen, Madeleine Herzog e Christina Schües. "Open Questions". In Philosophy and Medicine, 231–36. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04166-2_16.

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AbstractThe families we approached have two exceptional things in common: they all experienced the dramatic event of a life-threatening disease such as leukaemia affecting one of their children; and, in all of these families, that child was treated with a stem cell transplant taken from a sibling’s body. In this last chapter of the book we reflect very briefly on our interview experiences, analysis, and discussions. In the end, we identify open questions and further areas which may invite further research.

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7

Marks, David I. "Allogeneic Stem Cell Transplantation for Acute Lymphoblastic Leukaemia in Adults". In Adult Acute Lymphocytic Leukemia, 297–304. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-707-5_18.

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8

Green, A. R. "The Stem Cell Leukaemia Gene: A Critical Regulator of Haemopoiesis Vasculogenesis". In Haematology and Blood Transfusion Hämatologie und Bluttransfusion, 119–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59358-1_21.

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9

Blaise, Didier, e Sabine Fürst. "Post-CAR-T Cell Therapy (Consolidation and Relapse): Lymphoma". In The EBMT/EHA CAR-T Cell Handbook, 169–71. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-94353-0_33.

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AbstractEven after a decade of use, CAR-T cell therapy for non-Hodgkin lymphoma (NHL) is still evolving, and disease control is now the main concern in the majority of experienced centres. Indeed, despite highly appealing objective response (OR) rates in refractory patients, the long-term overall survival (OS) of this population has only slightly improved. Pivotal studies have suggested that 2-year OS rates do not surpass 30%, even though results improve when complete response (CR) is achieved within the first 3 months after treatment (Wang et al. 2020; Schuster et al. 2019; Neelapu et al. 2017). Although achieving this exceptionally high level of OR is praiseworthy, similar improvements have not been made regarding OS, and current OS probabilities are not satisfactory. Of course, there are multiple reasons for this; a substantial proportion of patients either do not achieve an initial response or experience progression very soon after treatment, with poor OS (Chow et al. 2019). Both populations present with disease burden or aggressive cancer prior to CAR-T cell therapy, possibly having been referred too late in the course of treatment or waited too long before CAR-T cells were processed for them. Both of these issues have potential solutions, such as more widely publicizing the efficacy of CAR-T cells, which may increase referrals at an earlier stage, and developing methods, which are already being heavily investigated, for shortening the manufacturing process (Rafiq et al. 2020). In the latter case, the use of allogeneic lymphocytes could allow for already prepared cells to be readily used when needed and would most likely be the most efficient strategy as long as the risk of graft-versus host disease is offset (Graham and Jozwik 2018). Thus, achieving CR is a crucial step in increasing OS, as patients with partial response (PR) or stable disease (SD) present with lower OS, while currently, recurrence appears to be rare when CR is maintained for more than 6 months (Komanduri 2021). However, the disease will likely recur in more than half of patients in the months following treatment, possibly due to issues such as the poor persistence of CAR-T cells (which may not be as crucial as once thought for acute lymphoblastic leukaemia (Komanduri 2021)) or the loss of target antigen expression (which has been regularly documented (Rafiq et al. 2020)). Both of these mechanisms could potentially be used to develop methods that reduce recurrence after CAR-T cell therapy. In fact, the most popular approaches currently being investigated are attempting to either use two CAR-T cell types that each target different antigens or to create CAR-T cell constructs that target either multiple antigens or an antigen other than CD19 (Shah et al. 2020). The concomitant infusion of CAR-T cells with targeted therapies is also being explored in other B-cell malignancies and appears to both increase the CR rate and decrease recurrence (Gauthier et al. 2020). When recurrence does occur, patient OS is rather dismal, and the best remaining option would most likely be inclusion in a clinical trial. If this option is not available, salvage therapy may be attempted, although cytotoxic treatments are extremely limited given that most diseases have been refractory to numerous lines of treatment prior to immunotherapy. A few case reports and studies with a small patient population receiving anti-PD-1 antibodies, ibrutinib, or ImiDs have been reported with largely anecdotal supporting evidence (Byrne et al. 2019). However, even in the case of a new objective response (OR), the subsequent risk of recurrence is substantial and may invite further consolidation with allogeneic haematopoietic stem cell transplantation (Byrne et al. 2019), which has already been performed in patients treated for acute lymphoblastic leukaemia (Hay et al. 2019). However, the efficacy of this strategy remains to be validated in NHL patients in clinical trials. Further supporting evidence, although limited, has recently been reported concerning an additional treatment with CAR-T cells inducing an OR. Of the 21 NHL patients included in the study, the OR rate after the second infusion was 52% (CR, n = 4; PR, n = 7), with some durable responses inviting further investigations (Gauthier et al. 2021). Overall, with such poor outcomes after recurrence, current efforts are also focused on predicting the patients most likely to experience disease progression and that are potential candidates for preemptive consolidation therapy, although there is no doubt that patients who do not achieve a rapid CR should be the first candidates. Additionally, immune monitoring should encompass not only CAR-T cell survival but also the detection of circulating tumour DNA (Komanduri 2021) because this could aid in detecting subclinical recurrence and in deciding whether consolidation or maintenance therapy should be administered. However, currently, all these approaches are highly speculative and require further clinical study.

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10

Rehmann-Sutter, Christoph, e Christina Schües. "A Donor by Coincidence or by Conception – My Sister’s Keeper Revisited". In Philosophy and Medicine, 19–29. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-04166-2_2.

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AbstractThirteen-year-old Anna Fitzgerald has been conceived in order to be a matching donor for her older sister Kate, who has a rare form of leukaemia. The story in the novel “My Sister’s Keeper” by Jody Picoult, and Nick Cassavetes’ movie, has many striking similarities to the situations that we heard from the families we studied – despite one significant difference: Anna is created to be a saviour sibling, whereas the stem cell donors we interviewed already existed and were found to be matching. We discuss the film as an emotionally complex, multi-layered narrative that gives insight into the perspectives of different family members and into some key aspects of a paradigmatic family conflict. The temporal order of the film’s story-telling using multiple flash-backs and retakes represents the entangled temporalities of experience and memory.

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Trabalhos de conferências sobre o assunto "Leukaemic Stem Cells"

1

Rovida, E., I. Tusa, G. Cheloni, A. Gozzini, X. Deng, NS Gray, S. Li e P. Dello Sbarba. "PO-145 ERK5 pathway inhibitors inhibit the maintenance of chronic myeloid leukaemia stem cells". 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-eacr25.186.

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2

Elster, Doris, e Julia Holzer. "PROMOTION OF HEALTH LITERACY IN THE CONTEXT OF STEM CELL DONATION FOR LEUKAEMIA PATIENTS". In 15th annual International Conference of Education, Research and Innovation. IATED, 2022. http://dx.doi.org/10.21125/iceri.2022.1790.

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3

Osorio, F., A. Rosendahl Huber, F. Camargo e R. Van Boxtel. "30 Whole-genome sequencing of normal stem cells provides novel insights into human native hematopoiesis and leukaemia aetiology". 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-eacr25.30.

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4

Park, ES, YJ Chung e PD Aplan. "PO-020 Discrepancy in efficacy of disulfiram between NUP98-PHF23 fusion acute myelogenous leukaemia cell line andin vivomouse model: sharing normal hematopoietic stem cells niche". 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-eacr25.555.

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5

Holzer, Julia, e Doris Elster. "INVESTIGATING PREDICTORS OF ADOLESCENTS’ INTENTION TO DONATE STEM CELLS TO LEUKAEMIA PATIENTS: A STUDY BASED ON THE THEORY OF PLANNED BEHAVIOUR". In 14th International Conference on Education and New Learning Technologies. IATED, 2022. http://dx.doi.org/10.21125/edulearn.2022.1107.

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Bandeira, Deborah, Mariana Rietmann da Cunha Madeira, Marianne Borges Landau e Andréa Rodrigues Cordovil Pires. "2022-RA-1062-ESGO Uterine granulocytic sarcoma as an extra-medullary relapse of acute myeloid leukaemia in an allogeneic hematopoietic stem cell transplantation recipient". In ESGO 2022 Congress. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-esgo.430.

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