Thematische Bibliographien / Myeloid leukemia

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Auswahl der wissenschaftlichen Literatur zum Thema „Myeloid leukemia“

Autor: Grafiati

Veröffentlicht am 4. Juni 2021

Zuletzt aktualisiert am 29. Juli 2024

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Zeitschriftenartikel zum Thema "Myeloid leukemia"

Swatler, Julian, Laura Turos-Korgul, Ewa Kozlowska und Katarzyna Piwocka. „Immunosuppressive Cell Subsets and Factors in Myeloid Leukemias“. Cancers 13, Nr. 6 (10.03.2021): 1203. http://dx.doi.org/10.3390/cancers13061203.

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Both chronic myeloid leukemia and acute myeloid leukemia evade the immune response during their development and disease progression. As myeloid leukemia cells modify their bone marrow microenvironment, they lead to dysfunction of cytotoxic cells, such as CD8+ T cells or NK cells, simultaneously promoting development of immunosuppressive regulatory T cells and suppressive myeloid cells. This facilitates disease progression, spreading of leukemic blasts outside the bone marrow niche and therapy resistance. The following review focuses on main immunosuppressive features of myeloid leukemias. Firstly, factors derived directly from leukemic cells – inhibitory receptors, soluble factors and extracellular vesicles, are described. Further, we outline function, properties and origin of main immunosuppressive cells - regulatory T cells, myeloid derived suppressor cells and macrophages. Finally, we analyze interplay between recovery of effector immunity and therapeutic modalities, such as tyrosine kinase inhibitors and chemotherapy.

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Namikawa, R., R. Ueda und S. Kyoizumi. „Growth of human myeloid leukemias in the human marrow environment of SCID-hu mice“. Blood 82, Nr. 8 (15.10.1993): 2526–36. http://dx.doi.org/10.1182/blood.v82.8.2526.2526.

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Abstract It has been shown previously that multilineage human hematopoiesis is maintained within human fetal bone marrow (BM) fragments implanted into severe combined immunodeficient (SCID) mice. We describe here an application of this animal model, the SCID-hu mouse, to the study of human myeloid leukemias. BM cells from 8 patients with various types of myeloid leukemias were injected directly into human bone grafts in the SCID-hu mouse. Cells from 7 patients grew in the human marrow without spreading to the mouse marrow. Cells from 6 of these patients were successfully transferred in vivo to secondary SCID-hu recipients. The surface phenotype and the cytologic features of the leukemia cells were conserved during passage in vivo. Thus, human myeloid leukemia cells could be reproducibly propagated in the human marrow environment in SCID-hu mice. The differentiation of promyelocytic leukemia cells in the SCID-hu mice was induced by all-trans retinoic acid, suggesting that the biologic features of the leukemia cells were maintained as well. Finally, evidence for a leukemic progenitor cell population in one case of acute myelogenous leukemia was provided with this system. This model may provide a useful tool for studying the biology of human myeloid leukemia as well as for evaluating new therapeutic modalities for myeloid leukemias.

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It has been shown previously that multilineage human hematopoiesis is maintained within human fetal bone marrow (BM) fragments implanted into severe combined immunodeficient (SCID) mice. We describe here an application of this animal model, the SCID-hu mouse, to the study of human myeloid leukemias. BM cells from 8 patients with various types of myeloid leukemias were injected directly into human bone grafts in the SCID-hu mouse. Cells from 7 patients grew in the human marrow without spreading to the mouse marrow. Cells from 6 of these patients were successfully transferred in vivo to secondary SCID-hu recipients. The surface phenotype and the cytologic features of the leukemia cells were conserved during passage in vivo. Thus, human myeloid leukemia cells could be reproducibly propagated in the human marrow environment in SCID-hu mice. The differentiation of promyelocytic leukemia cells in the SCID-hu mice was induced by all-trans retinoic acid, suggesting that the biologic features of the leukemia cells were maintained as well. Finally, evidence for a leukemic progenitor cell population in one case of acute myelogenous leukemia was provided with this system. This model may provide a useful tool for studying the biology of human myeloid leukemia as well as for evaluating new therapeutic modalities for myeloid leukemias.

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Aue, Georg, Yang Du, Susan M. Cleveland, Stephen B. Smith, Utpal P. Davé, Delong Liu, Marc A. Weniger et al. „Sox4 cooperates with PU.1 haploinsufficiency in murine myeloid leukemia“. Blood 118, Nr. 17 (27.10.2011): 4674–81. http://dx.doi.org/10.1182/blood-2011-04-351528.

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Abstract Cooperation of multiple mutations is thought to be required for cancer development. In previous studies, murine myeloid leukemias induced by transducing wild-type bone marrow progenitors with a SRY sex determining region Y-box 4 (Sox4)–expressing retrovirus frequently carried proviral insertions at Sfpi1, decreasing its mRNA levels, suggesting that reduced Sfpi1 expression cooperates with Sox4 in myeloid leukemia induction. In support of this hypothesis, we show here that mice receiving Sox4 virus-infected Sfpi1ko/+ bone marrow progenitors developed myeloid leukemia with increased penetrance and shortened latency. Interestingly, Sox4 expression further decreased Sfpi1 transcription. Ectopic SOX4 expression reduced endogenous PU.1 mRNA levels in HL60 promyelocytes, and decreased Sfpi1 mRNA levels were also observed in the spleens of leukemic and preleukemic mice receiving Sox4 virus-infected wild-type bone marrow cells. In addition, Sox4 protein bound to a critical upstream regulatory element of Sfpi1 in ChIP assays. Such cooperation probably occurs in de novo human acute myeloid leukemias, as an analysis of 285 acute myeloid leukemia patient samples found a significant negative correlation between SOX4 and PU.1 expression. Our results establish a novel cooperation between Sox4 and reduced Sfpi1 expression in myeloid leukemia development and suggest that SOX4 could be an important new therapeutic target in human acute myeloid leukemia.

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Shvachko, L. P. „EMT-mechanizm induces the leukemic stemness phenotype in myeloid leukemias“. Faktori eksperimental'noi evolucii organizmiv 23 (09.09.2018): 256–60. http://dx.doi.org/10.7124/feeo.v23.1024.

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Aim. To study the targeted expression EMT-induced markers N-cadherin, Snail and Twist in patients with the chronic and acute myeloid leukemias. Methods. RT-PCR, electroforesic in agarose gel, TotalLab v. 2.01 densitometry. Results. Have been investigated the relative levels of mRNA expression of N-cadherin and transcriptional factors Snail and Twist, associated with epithelial-to-mesenchymal induction (EMT) in patients with the essential polycytemia (EP), the chronic mieloid leukemia CML), the acute myeloid leukemia (AML) and the acute lymphoblastic leukemia (ALL). Conclusions. Have been highlighted the EMT stemness mechanism in Leukemic stem cell progression. Keywords: the epithelial-to-mesencymal transition (EMT), EMT-inducer marker, N-cadherin, Snail, Twist, myeloid leukemias, leuklemic stem cell progression.

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Jamieson, Catriona, Sidd Jaiswal, David Traver, Jason Gotlib, Mark Chao und Irving L. Weissman. „Increased Expression of CD47 Is a Constant Marker in Mouse and Human Myeloid Leukemias.“ Blood 106, Nr. 11 (16.11.2005): 3260. http://dx.doi.org/10.1182/blood.v106.11.3260.3260.

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Abstract CD47, also known as integrin associated protein, is a ubiquitously expressed cell surface glycoprotein that interacts with a number of integrins, modulating leukocyte adhesion, migration, cell motility and platelet activation. CD47 is also the ligand for the macrophage inhibitory receptor signal regulatory protein α (SIRP α) and thus, impairs macrophage-mediated phagocytosis. Recent reports suggest that increased CD47 expression may play a role in the pathogenesis of lymphoproliferative disorders such as CLL (Mateo et al, Nat Med.1999; 5:1277) and multiple myeloma, and that a bivalent single-chain antibody fragment against human CD47 induces apoptosis of myeloma cells (Kikuchi et al, Leukemia Research2005; 29:445). However, little is known about the role of CD47 in the pathogenesis of myeloid leukemias or the stage of hematopoiesis at which CD47 is expressed. In order to identify the stage of hematopoiesis at which alterations in CD47 arise and its role in the pathogenesis of myeloid leukemias, we analyzed CD47 expression in hematopoietic stem cells (HSC), progenitors, and lineage-positive cells derived from three mouse transgenic models of myeloid leukemia including: 1) mice homozygous for overexpression of human bcl-2 in the myeloid lineage (hMRP8 bcl-2 x bcl-2); 2) mice deficient in Fas together with myeloid targeted overexpression of bcl-2 (Faslpr/lpr hMRP8 bcl-2); and 3) mice with both human bcl-2 and BCR-ABL targeted to the myeloid lineage (hMRP8-BCR-ABLxhMRP8-bcl-2). Quantitative RT-PCR analysis demonstrated a 3.01+/− 1.54 fold increase in CD47 transcripts in leukemic compared with control (bcl2+) bone marrow (normalized to b-actin) while FACS analysis revealed approximately a 10-fold increase in CD47 protein expression, as measured by mean fluorescence intensity (MFI), in leukemic GMP compared with wild type GMP. Moreover, transplantation experiments revealed that all mice with both primary (n=14 mice) and secondary (n=19 mice) leukemic transplantation potential had an expansion of granulocyte-macrophage progenitors (GMP) with high level CD47 expression. Human CD47 expression analysis was performed via FACS on human normal, pre-leukemic myeloproliferative disorder (MPD) or AML HSC, progenitors, and lineage positive cells derived from marrow or peripheral blood. MPD samples (n=63) included polycythemia vera (PV; n=15), post-polycythemic myeloid metaplasia/myelofibrosis (PPMM/MF; n=5), essential thrombocythemia (ET; n=8), atypical chronic myelogenous leukemia (aCML; n=2), CML (n=7), chronic eosinophilic leukemia (CEL; n=1), chronic myelomonocytic leukemia (CMML; n= 13) and acute myelogenous leukemia (AML; n=12). As noted with the transgenic leukemic mouse models, progression of human myeloproliferative disorders to AML (n=12) was associated with an expansion of the GMP pool (70.6% +/− S.D. 2.15) compared with normal bone marrow (14.7% +/− S.D. 2.3). Furthermore, FACS analysis revealed that CD47 expression first increased 1.7 fold in AML compared with normal HSC and then increased to 2.2 fold greater than normal with commitment of AML progenitors to the myeloid lineage. CD47 was over-expressed by AML primitive progenitors and their progeny but not by the majority of MPD (MFI 2.3+/−S.D. 0.43) compared with normal bone marrow (MFI 1.9 +/−S.D. 0.07). Thus, increased CD47 expression may serve as a useful diagnostic marker for progression to AML and may represent a novel therapeutic target.

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Войцеховский, Валерий, Valeriy Voytsekhovskiy, Татьяна Заболотских, Tat'yana Zabolotskikh, Алексей Григоренко, Aleksey Grigorenko, Екатерина Филатова und Ekaterina Filatova. „DAMAGE OF THE BRONCHOPULMONARY SYSTEM IN PATIENTS WITH CHRONIC HEMOBLASTOSIS“. Bulletin physiology and pathology of respiration 1, Nr. 69 (05.10.2018): 25–35. http://dx.doi.org/10.12737/article_5b975083a62278.59044240.

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In 185 patients with chronic hemoblastosis (chronic lymphocytic leukemia, chronic myeloid leukemia, idiopathic myelofibrosis, multiple myeloma) after autopsy, the pathology of the bronchopulmonary system was studied. It was found out that in addition to immunodeficiency, an important role in the occurrence of respiratory diseases in chronic lymphocytic leukemia, as well as in chronic myeloid leukemia and idiopathic myelofibrosis in the stage of blast crisis is played by specific leukemic infiltration of the lungs, bronchi, pleura and diaphragm; the presence of leukostasis in the vessels of medium and small caliber with violation of microcirculation; compression of the diaphragm by significantly increased spleen and liver; in some cases (especially in chronic lymphocytic leukemia) hyperplasia of the lymphoid follicles of the bronchial tree. In chronic myeloid leukemia and idiopathic myelofibrosis, hyperthrombocytosis with the development of the sludge syndrome in small vessels of the lungs is essential. Pulmonary localization of inflammatory processes in patients with multiple myeloma is facilitated by lymphoid and plasma cell infiltration of the lungs, paraproteinosis of the lungs, localization of myeloma nodes in the ribs, lung tissue and bronchi.

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Bento, Marta Leal, Luís Carvalho, Zhewei Chen, Ana Coelho, Cong Tang und Gonçalo Bernardes. „Acute Myeloid and Lymphoblastic Leukemias: A NPM1 Targeting Strategy“. Blood 142, Supplement 1 (28.11.2023): 7147. http://dx.doi.org/10.1182/blood-2023-172497.

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Leukemia, a wide spectrum of diseases with altered proliferation and differentiation capacity of myeloid and lymphoid blood progenitors, is the most frequent type of cancer in children and one of the most common in adults. We discovered a covalent small-molecule “probe” for the treatment of acute myeloid and lymphoblastic leukemias that allows for post-translational modulation of the proteome in these leukemia cells. The probe dramatically induces apoptosis of leukemic cells at sub-toxic doses and consistently reduces proliferation, impairs cellular metabolism and promotes chemosensitization to “standard-of-care” chemotherapy regimens. Our proteomic analysis found specific targets that are critical to the leukemia cell survival, namely Nucleophosmin (NPM1) protein, which is a nucleolar phosphoprotein that performs diverse biological functions including molecular chaperoning, ribosome biogenesis, DNA repair, and genome stability. NPM1 gene mutations represent the most common genetic lesion in adult acute myeloid leukemia and their prognostic relevance earned them recognition as a distinct entity in the 2017 World Health Organization (WHO) classification of hematopoietic neoplasms. Our findings suggest a critical role of covalent inhibition of NPM1 in maintaining acute myeloid and lymphoblastic leukemia cells survival. This finding provides a rationale for therapeutic NPM1 modulation in acute leukemias.

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Longo, Giuseppe S. A., Richard Gorlick, William P. Tong, Emine Ercikan und Joseph R. Bertino. „Disparate Affinities of Antifolates for Folylpolyglutamate Synthetase From Human Leukemia Cells“. Blood 90, Nr. 3 (01.08.1997): 1241–45. http://dx.doi.org/10.1182/blood.v90.3.1241.

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Abstract Previous work showed that acute myelocytic leukemia blasts accumulate less long chain polyglutamates of methotrexate (MTX) than acute lymphocytic leukemia blasts when incubated with this radiolabeled antifolate. This difference likely explains the increased sensitivity of lymphoid leukemias to short-term exposure of MTX as compared with myeloid leukemias. In this study, we examined the basis for differences between long chain MTX polyglutamate accumulation between different leukemia cell types using both leukemia cell lines and blasts freshly isolated from blood of leukemic patients. The major difference found between leukemia cells that accumulate long chain polyglutamates and those that do not were differences in Km values for the enzyme folylpolyglutamate synthetase. Km values did not change with partial purification of this enzyme, indicating that interfering substances in crude lysates were not responsible for this difference. We postulate that there may be differences in the properties of this enzyme related to tissue specific expression. In contrast to MTX, both Tomudex (Zeneca Pharmaceuticals, Wilmington, DE) and 1843U89, potent inhibitors of thymidylate synthetase, have low Kms for folylpolyglutamate synthetase, and polyglutamate forms of these inhibitors are accumulated to the same degree in both myeloid and lymphoid acute leukemia cells, paralleling the equivalent cytotoxicity found between myeloid and lymphoid leukemia cell lines. Based on these results, we believe a clinical trial of Tomudex in patients with acute myeloid leukemia is warranted.

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Previous work showed that acute myelocytic leukemia blasts accumulate less long chain polyglutamates of methotrexate (MTX) than acute lymphocytic leukemia blasts when incubated with this radiolabeled antifolate. This difference likely explains the increased sensitivity of lymphoid leukemias to short-term exposure of MTX as compared with myeloid leukemias. In this study, we examined the basis for differences between long chain MTX polyglutamate accumulation between different leukemia cell types using both leukemia cell lines and blasts freshly isolated from blood of leukemic patients. The major difference found between leukemia cells that accumulate long chain polyglutamates and those that do not were differences in Km values for the enzyme folylpolyglutamate synthetase. Km values did not change with partial purification of this enzyme, indicating that interfering substances in crude lysates were not responsible for this difference. We postulate that there may be differences in the properties of this enzyme related to tissue specific expression. In contrast to MTX, both Tomudex (Zeneca Pharmaceuticals, Wilmington, DE) and 1843U89, potent inhibitors of thymidylate synthetase, have low Kms for folylpolyglutamate synthetase, and polyglutamate forms of these inhibitors are accumulated to the same degree in both myeloid and lymphoid acute leukemia cells, paralleling the equivalent cytotoxicity found between myeloid and lymphoid leukemia cell lines. Based on these results, we believe a clinical trial of Tomudex in patients with acute myeloid leukemia is warranted.

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Dissertationen zum Thema "Myeloid leukemia"

Cheung, Man-sze, und 張敏思. „Characterization of Leukemic stem cells in acute myeloid Leukemia“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687582.

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Cheung, Man-sze. „Characterization of Leukemic stem cells in acute myeloid Leukemia“. Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687582.

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Yaseen, Mumtaz. „Proteomics of Acute Myeloid Leukemia:“. Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-69882.

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Gunnarsson, Niklas. „Chronic myeloid leukemia and cancer“. Doctoral thesis, Umeå universitet, Medicin, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-141144.

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Background Chronic myeloid leukemia (CML) is a relatively rare hematological malignancy with a constant incidence of approximately 90 new cases each year in Sweden (0.9 cases/100 000 inhabitants). The etiology is largely unknown but high doses of ionizing radiation are a known but rare risk factor. The treatment options were for a long time limited to chemotherapies i.e. hydroxyurea and busulfan, interferon’s and allogeneic hematopoietic stem cell transplantation and the median survival were only about four years. Since the beginning of the 21st century a new way of treating CML has been introduced, the tyrosine kinase inhibitors (TKI), leading to a rapid decrease in leukemic cells and symptoms. Due to the TKIs, the overall 5-year survival is nowadays approximately 85 % and CML patients have time to develop other diseases, including other malignancies. The aims of this thesis was to investigate the present and future prevalence of CML and the prevalence of other malignancies prior and subsequent to the diagnosis of CML, malignancies among first-degree relatives of persons with CML. In addition, the incidence of autoimmune and chronic inflammatory diseases among patients with CML was also investigated. Methods From the Swedish CML register, data over nearly all Swedish CML patients from 2002 and forward were obtained for paper II-IV. For paper I, the Swedish cancer register was used to identify all Swedish CML patients since 1970 and the Swedish cause of death register was used to identify an eventual date of death for these patients. With a constant incidence and the relative survival rates for CML patients between 2006 and 2012 as a model, the present and future prevalence was calculated. For paper II-IV, data from the Swedish cancer register was used to identify other malignancies than CML. For paper II, information about autoimmune and chronic inflammatory diseases was retrieved from the Swedish national patient register. For paper II and IV, five controls matched for year of birth, gender and county of residence were randomly selected from the Swedish register of the total population. To calculate odds ratio (OR), conditional logistic regression was used. To calculate the risk of a second malignancy for paper III, Standardized incidence ratio (SIR) was used. In paper IV, first-degree relatives (parents, siblings and offsprings) for both cases and controls were retrieved from the Swedish multi-Generation Register, where persons born later than 1932 and registered in Sweden at some time since 1961 are registered. Results Prevalence and survival As shown in paper I, the 5-year overall survival for CML patients increased remarkably from 0.18 to 0.82 between 1970 and 2012. The prevalence increased from 3.9 to 11.9 per 100 000 inhabitants in Sweden between 1985 and 2012. By assuming no further improvements in relative survival as compared to the survival rates between 2006 and 2012, the prevalence by 2060 is expected to increase to 22.0 per 100 000 inhabitants. This corresponds to 2 587 CML patients as compared to 1 137 CML patients in 2012. Malignancies, autoimmune and chronic inflammatory diseases prior to CML In study II, more than 45 000 person-years of follow-up were evaluated in 984 CML patients diagnosed between 2002 and 2012. With an OR of 1.47 (95 % CI 1.20–1.82) and 1.55 (95 % CI 1.21–1.98), respectively, the prevalence of prior malignancies and autoimmune diseases were significantly increased as compared to matched controls. On the other hand, no association between CML and chronic inflammatory diseases was shown. Second malignancies In 868 CML patients, diagnosed between 2002 and 2011, 52 malignancies were observed in the Swedish cancer register, as shown in paper III. When compared to expected rates in the background population, a significantly increased risk of second malignancies with a SIR of 1.52 (95 % CI 1.13–1.99) was shown. When looking at specific cancer types, gastrointestinal as well as nose and throat cancer were significantly increased. Familial aggregation of malignancies 984 CML patients were identified in paper IV. However, 184 had a birth date prior to 1932, subsequently only 800 patients were analyzed. Among them, 4 287 first-degree relatives were identified, compared to 20 930 first-degree relatives of the matched controls. 611 malignancies were retrieved; no significant increase of malignancies in first-degree relatives of CML patients was shown (OR 1.06; 95 % CI: 0.96–1.16). Conclusion Since CML patients nowadays have a high survival rate, the calculations in this thesis shows that the prevalence of CML will almost double by 2060. CML patients have an increased risk of developing malignancies prior and subsequent to the diagnosis of CML, suggesting a hereditary or acquired predisposition to develop cancer. Since there is no familial aggregation of malignancies in CML patients, a hereditary predisposition to develop cancer is unlikely to be part of the pathogenesis of CML, leaving an acquired predisposition more likely.

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VARINELLI, MARCO. „MODELLING CHRONIC MYELOID LEUKEMIA IN ZEBRAFISH“. Doctoral thesis, Università degli studi di Brescia, 2021. http://hdl.handle.net/11379/544088.

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Cornforth, Terri Victoria. „Characterising the cell biology of leukemic stem cells in acute myeloid leukemia“. Thesis, University of Oxford, 2013. http://ora.ox.ac.uk/objects/uuid:654b2176-fd50-427e-86f2-74e928054bef.

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Acute Myeloid leukemia (AML) is an aggressive haematological malignancy that mainly affects the elderly. Relapse is common and is thought to be due to the presence of chemotherapy resistant leukemic stem cells (LSC). Within the CD34+ disease (>5% of the blast cells expressing CD34) , two subtypes have been identified; an LMPP/GMPlike expanded type and a MPP/CMP-like expanded type, the former is the most common, accounting for around 80% of CD34+ AML. Both the GMP-like and LMPPlike expanded populations show LSC activity. To improve our understanding of the disease and gain better insight in to how to develop treatments, the molecular basis of the disease needs to be investigated. I investigated miRNAs in the GMP/LMPP-like expanded AML. miRNAs are small non-coding RNAs involved in the regulation of mRNA. In recent years miRNAs have been shown to be implicated in many different diseases. To investigate the role miRNAs play in AML, miRNA expression was profiled in leukemic and normal bone marrow. Bioinformatic analysis was then used to examine the different miRNA expression profiles between normal and leukemic marrow. Our study showed that miRNAs are dysregulated in AML. miRNAs from the miR-17-92 and its paralogous cluster miR-106b-92 were amongst the miRNAs to be found down regulated in AML As had been seen previously at an mRNA level, on an miRNA level the LSC populations more closely resembled more mature progenitor populations than HSC and MPP populations, however the LSC populations did display an aberrant stem cell-like miRNA signature.

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Zhang, Lu [Verfasser]. „Immunogenicity of leukemia stem cells in acute myeloid leukemia / Lu Zhang“. Ulm : Universität Ulm. Medizinische Fakultät, 2012. http://d-nb.info/1020022574/34.

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García, Montolío Marc 1991. „The Role of PHF19 in myeloid leukemia“. Doctoral thesis, Universitat Pompeu Fabra, 2019. http://hdl.handle.net/10803/667911.

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Polycomb group (PcG) of proteins are a group of highly conserved epigenetic regulators involved in many biological functions such as embryonic development, stem cell self-renewal, cell proliferation, and cancer. PHD finger protein 19 (PHF19) is an associated factor of Polycomb Repressor Complex 2 (PRC2) that has been proposed to regulated its activity in embryonic stem cells. PHF19 has been shown to be up-regulated in different human cancers as well as cancer cell lines. In particular, myeloid leukemia cell lines show increased levels of PHF19, yet little is known about its function. Here, we have characterized the role of PHF19 in myeloid leukemia cell lines. We have demonstrated that PHF19 depletion decreases cell proliferation and induces erythroid differentiation. Mechanistically, we have demonstrated that PHF19 regulates the proliferation of chronic myeloid leukemia cell lines through its interaction with cell cycle regulator p21. Furthermore, we have observed that MTF2, a PHF19 homolog, occupies PHF19 target genes when PHF19 is depleted. Taken together, our results show that PHF19 is a key transcriptional regulator in myeloid leukemic cell lines and suggest that PHF19 inhibition could be a potential target to be explored for myeloid leukemia treatment.
El complejo de proteínas Polycomb (PcG), es un grupo de reguladores epigenéticos altamente conservados que participan en distintas funciones biológicas como el desarrollo embrionario, la auto renovación de las células madre, la proliferación y están involucradas también en cáncer. La proteína PHD finger 19 (PHF19), es un factor asociado al complejo represor Polycomb 2 (PRC2). PHF19 ha sido propuesta como reguladora de la actividad de PRC2 en células madre embrionarias. También se ha visto que esta sobreexpressada en diferentes canceres y líneas celulares cancerígenas. Nosotros hemos demostrado que la eliminación de PHF19 disminuye la proliferación de las líneas celulares mieloides cancerígenas. Hemos demostrado que la depleción de PHF19 en las células de leucemia crónica mieloide las induce a diferenciarse hacia eritrocitos. Mecánicamente, hemos demostrado que PHF19 regula la proliferación de esta línea celular mediante su interacción con el regulador de ciclo celular p21. Además, hemos observado que MTF2, un homólogo de PHF19, se deposita en aquellos genes donde previamente estaba PHF19. En conjunto, nuestros resultados muestran que PHF19 es un factor transcripcional clave en líneas celulares mieloides y sugieren que la inhibición de PHF19 podría ser una potencial diana para ser explorada para el tratamiento de la leucemia mieloide.

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Palle, Josefine. „Optimizing Chemotherapy in Childhood Acute Myeloid Leukemia“. Doctoral thesis, Uppsala University, Department of Women's and Children's Health, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-9189.

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Despite major advances in our understanding of the biology of childhood acute myeloid leukemia (AML) and the development of new cytotoxic drugs, the prognosis of long-term survival is still only 60-65 %.

In the present research, we studied the pharmacokinetics of drugs used in the induction therapy of childhood AML and performed in vitro drug sensitivity testing of leukemic cells from children with AML.

The aims of the studies were to correlate the results of the analysis to biological and clinical parameters and to identify subgroups of AML with specific drug sensitivity profiles in order to better understand why treatment fails in some patients and how therapy may be improved.

Blood samples were analysed to study the pharmacokinetics of doxorubicin (n=41), etoposide (n=45) and 6-thioguanine (n=50). Doxorubicin plasma concentration and total body clearance were correlated to the effect of induction therapy, and doxorubicin plasma concentration was an independent factor for complete remission, both in univariate and multivariate analysis including sex, age, and white blood cell count at diagnosis. For etoposide and 6-thioguanine no correlation was found between pharmacokinetics and clinical effect. Children with Down syndrome (DS) tended to reach higher blood concentrations of etoposide and thioguanine nucleotides, indicating that dose reduction may be reasonable to reach the same drug exposure as in children without DS.

Leukemic cells from 201 children with newly diagnosed AML, 15 of whom had DS, were successfully analysed for in vitro drug sensitivity by the fluorometric microculture cytotoxicity assay (FMCA). We found that samples from children with DS were highly sensitive to most drugs used in AML treatment. In non-DS children, the t(9;11) samples were significantly more sensitive to cytarabine (p=0.03) and doxorubicin (p=0.035) than other samples. The findings might explain the very favorable outcome reported in children with DS and t(9;11)-positive AML. A specific drug resistance profile was found for several other genetic subgroups as well. A detailed study of MLL-rearranged leukemia showed that cellular drug sensitivity is correlated both to partner genes and cell lineage, findings that support the strategy of contemporary protocols to include high-dose cytarabine in the treatment of patients with MLL-rearrangement, both in AML and acute lymphoblastic leukemia (ALL).

Our results indicate that drug resistance and pharmacokinetic studies may yield important information regarding drug response in different sub-groups of childhood AML, helping us to optimize future chemotherapy in childhood AML.

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Watson, Alexander Scarth. „Autophagy in hematopoiesis and acute myeloid leukemia“. Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:2e66c5c3-4774-44d1-8345-d0dc827da16d.

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Acute myeloid leukemia (AML) develops following oncogenic alterations to hematopoietic stem (HSC) and progenitor cells (HSPCs) in the bone marrow, resulting in dysregulated proliferation of immature myeloid progenitors that interferes with normal hematopoiesis. Understanding the mechanisms of HSPC protection against damage and excessive division, and how these pathways are altered during leukemic progression, is vital for establishing effective therapies. Here, we show that autophagy, a lysosomal degradation pathway, is increased in HSPCs using a novel imaging flow cytometry autophagy assay. Loss of hematopoietic autophagy following deletion of key gene Atg5 resulted in increased HSC proliferation, leading to HSC exhaustion and bone marrow failure. Although erythrocyte and lymphocyte populations were negatively impacted by autophagy loss, myeloid cells showing immature characteristics were expanded. Deletion of Atg5 in an AML model resulted in increased proliferation under metabolic stress, dependent on the glycolytic pathway, and aberrant upstream mTOR signaling. Moreover, modulation of Atg5 altered leukemic response to culture with stromal cells. Finally, primary AML cells displayed multiple markers of decreased autophagy. These data suggest a role for autophagy in preserving HSC function, partially through suppression of HSPC proliferation, and indicate that decreased autophagy may benefit AML cells. We postulate that modulation of autophagy could help maintain stem cell function, for example during transplantation, and aid AML therapy in a setting-specific manner.

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Bücher zum Thema "Myeloid leukemia"

Harry, Iland, Hertzberg Mark und Marlton Paula. Myeloid Leukemia. New Jersey: Humana Press, 2005. http://dx.doi.org/10.1385/1597450170.

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Röllig, Christoph, und Gert J. Ossenkoppele, Hrsg. Acute Myeloid Leukemia. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8.

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Hehlmann, Rüdiger, Hrsg. Chronic Myeloid Leukemia. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-71913-5.

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Li, Shaoguang, und Haojian Zhang, Hrsg. Chronic Myeloid Leukemia. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-4011-0.

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Hehlmann, Rüdiger, Hrsg. Chronic Myeloid Leukemia. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33198-0.

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Fortina, Paolo, Eric Londin, Jason Y. Park und Larry J. Kricka, Hrsg. Acute Myeloid Leukemia. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7142-8.

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E, Cortés F. Jorge, und Deininger Michael, Hrsg. Chronic myeloid leukemia. New York: Informa Healthcare, 2007.

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Hughes, Timothy P., David M. Ross und Junia V. Melo. Handbook of Chronic Myeloid Leukemia. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08350-6.

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Harry, Iland, Hertzberg Mark und Marlton Paula, Hrsg. Myeloid leukemia: Methods and protocols. Totowa, N.J: Humana Press, 2006.

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Saglio, Giuseppe, und Carmen Fava. The Treatment of Chronic Myeloid Leukemia. Unitec House, 2 Albert Place, London N3 1QB, UK: Future Medicine Ltd, 2013. http://dx.doi.org/10.2217/9781780842738.

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Buchteile zum Thema "Myeloid leukemia"

Voso, Maria Teresa, Eleonora De Bellis und Tiziana Ottone. „Diagnosis and Classification of AML: WHO 2016“. In Acute Myeloid Leukemia, 23–54. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_2.

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Kayser, Sabine, und Uwe Platzbecker. „Management of Acute Promyelocytic Leukemia“. In Acute Myeloid Leukemia, 177–97. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_8.

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Jaramillo, Sonia, und Richard F. Schlenk. „Treatment of Relapsed and Refractory AML: Intensive Approach in Fit Patients“. In Acute Myeloid Leukemia, 233–40. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_11.

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Bornhäuser, Martin. „Allogeneic Hematopoietic Cell Transplantation“. In Acute Myeloid Leukemia, 255–65. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_13.

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Itzykson, Raphael, Marco Cerrano und Jordi Esteve. „Prognostic Factors in AML“. In Acute Myeloid Leukemia, 127–75. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_7.

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Wierzbowska, Agnieszka, und Magdalena Czemerska. „Clinical Manifestation and Diagnostic Workup“. In Acute Myeloid Leukemia, 119–26. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_6.

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Sprute, Rosanne, und Oliver A. Cornely. „Special Clinical Scenarios: Infectious Complications and Prophylaxis“. In Acute Myeloid Leukemia, 285–92. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_16.

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Venditti, Adriano, Peter J. M. Valk, Nigel H. Russell und Sylvie D. Freeman. „Future Developments: Measurable Residual Disease“. In Acute Myeloid Leukemia, 317–37. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_18.

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Bug, Gesine, und Halvard Bonig. „Special Clinical Scenarios: Hyperleukocytosis“. In Acute Myeloid Leukemia, 267–73. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_14.

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Estey, Elihu. „Future Developments: Innovative Trial Design“. In Acute Myeloid Leukemia, 349–58. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72676-8_20.

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Konferenzberichte zum Thema "Myeloid leukemia"

DeMarco, B., M. O. Al-Qadi, S. S. Carson und S. Ghosh. „Leukemic Pleural Effusion in Acute Myeloid Leukemia“. In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4863.

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Rosenbluth, Michael J., Wilbur A. Lam und Daniel A. Fletcher. „Contribution of Cell Mechanics to Acute Leukemia“. In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59881.

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Leukostasis is a life-threatening condition that occurs when leukemia cells accumulate in the vasculature of organs such as the brain and lungs. Recent evidence has shown that leukostasis is not simply due to the physical overcrowding of leukemia cells, as previously thought, but may result from specific mechanical properties of the cells and interactions between cells. Using atomic force microscopy (AFM), we obtained direct measurements of two mechanical properties that are likely involved in this condition: (1) stiffness of individual leukemia cells and (2) non-specific adhesion forces between leukemia cells. We found that myeloid leukemia cells were significantly stiffer than lymphoid leukemia cells. Cell-cell adhesion forces of the cell lines were not found to be statistically different. These results may help to explain the clinical observation that leukostasis occurs in myeloid leukemia at lower white blood cell counts than in lymphoid leukemia.

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Ahmed Mustafa, Srwa, und Gullanar M Hadi. „Automated Leukemia Detection using K-means Clustering for Feature Extraction“. In 5TH INTERNATIONAL CONFERENCE ON COMMUNICATION ENGINEERING AND COMPUTER SCIENCE (CIC-COCOS'24). Cihan University-Erbil, 2024. http://dx.doi.org/10.24086/cocos2024/paper.1529.

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Leukemia is a kind of blood cancer that may cause significant damage to a person's general health. It is characterized by the production of an excessive number of white blood cells. To address leukemia quickly and effectively, it is important to have a diagnosis that is both correct and quick. Not too long ago, experts started using AI methods to help find cancer much earlier. One of the hardest parts of making a method to find leukemia is separating the nuclei from the rest of the picture. When medical staff use quick and accurate division methods, they can find patients faster and treat them more effectively. So far, hybrid clustering algorithms have been very helpful in the process of picture segmentation in the field of medical image processing. To find leukemias like chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL), this study looks into segmentation methods that use machine learning (ML) and deep learning (DL). The study looks at how many ML and DL algorithms can be used to automatically diagnose different types of leukemia. It is checked to see how well the ML and DL algorithms do at segmentation, pre-processing, feature extraction, selection, and total classification accuracy.

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Kulkarni, Shrinidhi. „CRISPR Solution to Cure Acute Myeloid Leukemia“. In 8th North American Conference on Industrial Engineering and Operations Management. Michigan, USA: IEOM Society International, 2023. http://dx.doi.org/10.46254/na8.20230275.

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Sultonova, Sherozakhon. „CLINICAL-HEMATOLOGICAL FEATURES OF CHRONIC MYELOID LEUKEMIA“. In RICERCHE SCIENTIFICHE E METODI DELLA LORO REALIZZAZIONE: ESPERIENZA MONDIALE E REALTÀ DOMESTICHE, chair Din Mohammad, Khamid Karimov, Kodirjon Boboyev und Khamida Kazakbayeva. European Scientific Platform, 2021. http://dx.doi.org/10.36074/logos-26.11.2021.v3.22.

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Verhagen, Han, Marjon Smit, David de Leeuw, Arjo Rutten, Mei-Ling Tsui, Fedor Denkers, Monique Terwijn et al. „Abstract 2339: IGFBP7 eradicates leukemic stem and progenitor cells in 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.am2015-2339.

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Shin, J. W., und D. J. Mooney. „Myeloid leukemia subtype-dependent sensitivity to matrix mechanics“. In 2014 40th Annual Northeast Bioengineering Conference (NEBEC). IEEE, 2014. http://dx.doi.org/10.1109/nebec.2014.6972939.

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Dai, Aili, Chen Zhao, C. Cameron Yin, Ling Chen, Xiaoping Sun, Sanat Dave, Xiaoyan Huang, Yu H. Zhang, Xin Han und M. James You. „Abstract 170: Hypermethylation ofDBCCR1gene in acute myeloid leukemia“. In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-170.

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Al-Qadi, M. O., M. Hunsucker und J. Akulian. „Acute Myeloid Leukemia Arising from Pleural Extramedullary Hematopoiesis“. In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a6702.

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Rahman, Rabi’Atul’Adawiyah Abdul, Mohd Yusoff Mashor, Rafikha Aliana Binti A. Raof, Rosline Hassan, Nazahah Binti Mustafa, Siti Nurul Aqmariah Binti Mohd Kanafiah, Khairul Shakir Bin Ab Rahman und Razan Hayati Zulkeflee. „Feature Targeted Image Enhancement for Acute Myeloid Leukemia“. In 2023 International Workshop on Artificial Intelligence and Image Processing (IWAIIP). IEEE, 2023. http://dx.doi.org/10.1109/iwaiip58158.2023.10462885.

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Berichte der Organisationen zum Thema "Myeloid leukemia"

Jangid, Ajay, Anurag Mishra, Rachit Raj, Sumit Kumar, Priyanka Munjal und Neha Pandey. Chronic Myeloid Leukemia (CML) as Surgical Emergency. Science Repository, März 2024. http://dx.doi.org/10.31487/j.ajscr.2024.01.02.

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Ileal perforation peritonitis is a critical surgical emergency often encountered in developing countries, commonly associated with typhoid fever, tuberculosis, trauma, and non-specific enteritis. This case report presents a unique instance of nonspecific enteritis associated with chronic myeloid leukemia (CML). A 16-year-old girl with a history of pulmonary tuberculosis presented with symptoms, leading to the diagnosis of ileal perforations and CML. Surgical intervention involved ileal resection and double barrel ileostomy. The postoperative course included complications and chemotherapy with imatinib, demonstrating the challenges and management strategies in such cases. The discussion emphasizes the varied aetiologies of non-traumatic ileal perforation in different regions and sheds light on the rare gastrointestinal manifestations of CML. Notably, this report underscores the significance of prompt imatinib therapy in controlling CML while highlighting the need for vigilant monitoring and dose adjustments due to chemotherapy-related adverse effects.

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Muller-Sieburg, Christa. Myeloid-Biased Stem Cells as Potential Targets for Chronic Myelogeneous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada447669.

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FLORIDA UNIV GAINESVILLE. Dissection of the Pathogenesis of Neurofibromatosis Type 1-Associated myeloid Leukemia. Fort Belvoir, VA: Defense Technical Information Center, Oktober 1998. http://dx.doi.org/10.21236/ada359875.

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Brannan, Camilynn I. Dissection of the Pathogenesis of Neurofibromatosis Type 1-Associated Myeloid Leukemia. Fort Belvoir, VA: Defense Technical Information Center, Oktober 1999. http://dx.doi.org/10.21236/ada391284.

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Untaaveesup, Suvijak, Sasinipa Trithiphen, Kamolchanok Kulchutisin, Tarinee Rungjirajittranon, Sujitra Panyoy, Thanapon Kaokunakorn, Nattawut Leelakanok und Weerapat Owattanapanich. Genetic Alterations in Extramedullary Leukemia among Acute Myeloid Leukemia Patients: Insights from a Cohort Study and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2023. http://dx.doi.org/10.37766/inplasy2023.8.0091.

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Zhang, Chengcheng. Dissecting the Role of IGFBP-2 in Development of Acute Myeloid Leukemia. Fort Belvoir, VA: Defense Technical Information Center, Juni 2011. http://dx.doi.org/10.21236/ada555017.

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Zhang, Dong-Er. Protein ISG15 Modification in the Development and the Treatment of Chronic Myeloid Leukemia. Fort Belvoir, VA: Defense Technical Information Center, Juni 2007. http://dx.doi.org/10.21236/ada482354.

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Sorror, Mohamed L., Barry E. Storer und Elihu H. Estey. Comparing Hematopoietic Cell Transplant versus Other Treatments for Adults with Acute Myeloid Leukemia. Patient-Centered Outcomes Research Institute (PCORI), Januar 2021. http://dx.doi.org/10.25302/01.2021.ce.13047451.

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Tremblay, Michel. Contribution of Protein Tyrosine Phosphateses to the Ontogeny and Progression of Chronic Myeloid Leukemia. Fort Belvoir, VA: Defense Technical Information Center, April 2006. http://dx.doi.org/10.21236/ada462811.

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