Relevant bibliographies by topics / Myeloid leukemia

Academic literature on the topic 'Myeloid leukemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 March 2023

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Journal articles on the topic "Myeloid leukemia":

Swatler, Julian, Laura Turos-Korgul, Ewa Kozlowska, and Katarzyna Piwocka. "Immunosuppressive Cell Subsets and Factors in Myeloid Leukemias." Cancers 13, no. 6 (March 10, 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.

Namikawa, R., R. Ueda, and S. Kyoizumi. "Growth of human myeloid leukemias in the human marrow environment of SCID-hu mice." Blood 82, no. 8 (October 15, 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.

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, no. 17 (October 27, 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.

Shvachko, L. P. "EMT-mechanizm induces the leukemic stemness phenotype in myeloid leukemias." Faktori eksperimental'noi evolucii organizmiv 23 (September 9, 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.

Jamieson, Catriona, Sidd Jaiswal, David Traver, Jason Gotlib, Mark Chao, and Irving L. Weissman. "Increased Expression of CD47 Is a Constant Marker in Mouse and Human Myeloid Leukemias." Blood 106, no. 11 (November 16, 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.

ENACHE, Tatiana Cristina, Ana-Maria VLĂDĂREANU, Horia BUMBEA, Minodora ONISÂI, and Ion DUMITRU. "EPIDEMIOLOGICAL AND IMMUNOPHENOTYPIC CHARACTERIZATION OF ACUTE MYELOID LEUKEMIAS." Romanian Journal of Medical Practice 12, no. 4 (December 31, 2017): 234–39. http://dx.doi.org/10.37897/rjmp.2017.4.11.

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Acute leukemias are a group of hematopoietic stem cell malignancies characterized by the proliferation and accumulation of immature cell (blasts) clones that associate medullary insufficiency syndrome (anemia, neutropenia, thrombocytopenia). Depending on the origin of the malignant clone, two major categories of acute leukemias are: acute lymphocytic leukemia (ALL) and acute myeloid leukemia (AML). Studies show an annual incidence of acute leukemias in European adults of 5-6 cases per 100,000 people with an increase in over 70 years of age, reaching an incidence of about 15-20 / 100,000 people. Of the total acute myeloid leukemias, 20% occur in children and 80% are among adults. Diagnosis of acute leukemias is based on the recognition of morphological, cytochemical, immunophenotypic, cytogenetic and molecular biology changes. Immunophenotyping plays a major role in the diagnosis and classification of acute leukemias, in differentiation of acute myeloid and lymphocytic leukemias and in detection of minimal residual disease.

Войцеховский, Валерий, Valeriy Voytsekhovskiy, Татьяна Заболотских, Tat'yana Zabolotskikh, Алексей Григоренко, Aleksey Grigorenko, Екатерина Филатова, and Ekaterina Filatova. "DAMAGE OF THE BRONCHOPULMONARY SYSTEM IN PATIENTS WITH CHRONIC HEMOBLASTOSIS." Bulletin physiology and pathology of respiration 1, no. 69 (October 5, 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.

Padmanabhan, Dr K. "An Interesting Case of Acute Myeloid Leukemia." Journal of Medical Science And clinical Research 05, no. 02 (February 28, 2017): 18166–68. http://dx.doi.org/10.18535/jmscr/v5i2.150.

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Jones, Letetia, Sabina Sevcikova, Vernon Phan, Sachi Jain, Angell Shieh, Joshua Dubansky, Min Li, et al. "Myc Drives Chromosomal Gain in Acute Myeloid Leukemia." Blood 112, no. 11 (November 16, 2008): 792. http://dx.doi.org/10.1182/blood.v112.11.792.792.

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Abstract Acute Myeloid Leukemia (AML) is a disease characterized by diverse genetic pathogenesis, including both balanced and unbalanced chromosomal aberrations. Much is known regarding the pathogenic effects of balanced rearrangements in AML, whereas our understanding of how unbalanced aberrations contribute to leukemia is more limited. The balanced t(15;17) chromosomal rearrangement is a nearly constant feature of acute promyeloctyic leukemia (APL), a subtype AML. The translocation fuses the promyelocytic leukemia gene (PML) to the retinoic acid receptor α gene (RARA). Trisomy 8 is the most common secondary karyotypic lesion observed in APL, and it has been speculated but not proven that the MYC gene contributes to this chromosomal gain. We previously reported that mouse chromosome 15, which contains the mouse Myc gene in a region syntenic to human chromosome 8q24, is commonly gained in the MRP8 PML-RARA mouse model of APL. We now report our work to assess the hypothesis that increased MYC cooperates with PML-RARα to accelerate disease and that gain of MYC/Myc drives +8 in humans and +15 in mice. Expressing MYC with a retroviral vector in PML-RARA bone marrow led to the rapid development of APL-like leukemias (3 months vs. 8.5 months with PML-RARA alone). Chromosome 15 was not gained in any of the leukemias, although 70% had other clonal karyotypic abnormalities. This finding suggests that when MYC is overexpressed, there is no selective pressure to gain chromosome 15, supporting our hypothesis that Myc is driving this gain. We also generated PML-RARA mice haploinsufficient for Myc to examine the effect of decreasing MYC levels. The median latency among leukemic animals was 258 days for mice with PML-RARA and two wild-type Myc alleles, whereas the latency was increased to 339 days for PML-RARA Myc haploinsufficient mice. Hence, lower MYC expression served as a check on leukemic transformation. Furthermore, the majority of the leukemias that arose in Myc haploinsufficient mice had gained wild-type Myc. These data demonstrate a selective pressure for Myc gain. Additional experiments showed that as MYC expression increases there is a decrease in both latency and genetic complexity of leukemias that arise, that MYC and PML-RARα interact to disrupt myeloid differentiation in vivo and that although MYC cooperates with PML-RARα to cause leukemia, additional events are required for completing transformation even at high levels of MYC. Altogether our studies of increased and decreased MYC expression in PML-RARA mice show a strong correlation between MYC dosage and leukemic transformation. Our results suggest that agents that target MYC might be useful for the treatment of AML.

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Dissertations / Theses on the topic "Myeloid leukemia":

Cheung, Man-sze, and 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.

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.

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.

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.

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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Books on the topic "Myeloid leukemia":

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

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Röllig, Christoph, and Gert J. Ossenkoppele, eds. 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, ed. 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, and Haojian Zhang, eds. 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, ed. 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, and Larry J. Kricka, eds. 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, and Deininger Michael, eds. Chronic myeloid leukemia. New York: Informa Healthcare, 2007.

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Bain, Barbara J. Chronic myeloid leukaemias. Oxford: Clinical Pub., 2012.

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Hughes, Timothy P., David M. Ross, and 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, and Marlton Paula, eds. Myeloid leukemia: Methods and protocols. Totowa, N.J: Humana Press, 2006.

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Book chapters on the topic "Myeloid leukemia":

Voso, Maria Teresa, Eleonora De Bellis, and 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, and 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, and 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, and 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, and 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, and 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, and 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, and 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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Conference papers on the topic "Myeloid leukemia":

DeMarco, B., M. O. Al-Qadi, S. S. Carson, and 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, and 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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Abstract:

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.

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, and 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., and 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, and 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, and 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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Ramos, Doralina do Amaral Rabello, Vivian D'Afonseca da Silva Ferreira, Maria Gabriela Berzoti-Coelho, Sandra Mara Burin, Cíntia Leticia Magro, Maira da Costa Cacemiro, Belinda Pinto Simões, Felipe Saldanha-Araujo, Fabíola Attié Castro, and Fábio Pittella-Silva. "Abstract 366: Association ofMLL2/KMT2DandMLL3/KMT2Cwith chronic myeloid leukemia." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-366.

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Adi, Y. A., F. Adi-Kusumo, L. Aryati, and M. S. Hardianti. "Modelling inhibition of AKT phosphorylation in acute myeloid leukemia." In THE 2016 CONFERENCE ON FUNDAMENTAL AND APPLIED SCIENCE FOR ADVANCED TECHNOLOGY (CONFAST 2016): Proceeding of ConFAST 2016 Conference Series: International Conference on Physics and Applied Physics Research (ICPR 2016), International Conference on Industrial Biology (ICIBio 2016), and International Conference on Information System and Applied Mathematics (ICIAMath 2016). Author(s), 2016. http://dx.doi.org/10.1063/1.4953987.

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de Leeuw, Dave C., Willemijn van den Ancker, Fedor Denkers, Rene X. Menezes, Theresia M. Westers, Gert J. Ossenkoppele, Arjan A. van de Loosdrecht, and Linda Smit. "Abstract LB-246: MicroRNA profiling can classify acute leukemias of ambiguous lineage as either acute myeloid leukemia or acute lymphoid leukemia." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-lb-246.

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Reports on the topic "Myeloid leukemia":

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, October 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, October 1999. http://dx.doi.org/10.21236/ada391284.

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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, June 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, June 2007. http://dx.doi.org/10.21236/ada482354.

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Sorror, Mohamed L., Barry E. Storer, and Elihu H. Estey. Comparing Hematopoietic Cell Transplant versus Other Treatments for Adults with Acute Myeloid Leukemia. Patient-Centered Outcomes Research Institute (PCORI), January 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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Gong, Jun. Diminishing oncometabolic havoc: Approved IDH1 and IDH2 inhibitors in relapsed or refractory acute myeloid leukemia. Science Repository OU, December 2018. http://dx.doi.org/10.31487/j.aco.2018.01.004.

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Getz, Kelly D., Julia E. Szymczak, Farah Contractor, Brian T. Fisher, and Richard Aplenc. Comparing Chemotherapy Recovery at Home versus in the Hospital for Children with Acute Myeloid Leukemia. Patient-Centered Outcomes Research Institute (PCORI), January 2021. http://dx.doi.org/10.25302/01.2021.cer.140922827.

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Academic literature on the topic 'Myeloid leukemia'

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Contents

Journal articles on the topic "Myeloid leukemia":

Dissertations / Theses on the topic "Myeloid leukemia":

Books on the topic "Myeloid leukemia":

Book chapters on the topic "Myeloid leukemia":

Conference papers on the topic "Myeloid leukemia":

Reports on the topic "Myeloid leukemia":