Relevant bibliographies by topics / Leukemia cell

Academic literature on the topic 'Leukemia cell'

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Published: 10 March 2023

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Journal articles on the topic "Leukemia cell"

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Abdel-Wahab, Omar, and Ross L. Levine. "Metabolism and the leukemic stem cell." Journal of Experimental Medicine 207, no. 4 (April 5, 2010): 677–80. http://dx.doi.org/10.1084/jem.20100523.

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Acute leukemias are clonal disorders of hematopoiesis wherein a leukemic stem cell (LSC) acquires mutations that confer the capacity for unlimited self-renewal, impaired hematopoietic differentiation, and enhanced proliferation to the leukemic clone. Many recent advances in understanding the biology of leukemia have come from studies defining specific genetic and epigenetic abnormalities in leukemic cells. Three recent articles, however, further our understanding of leukemia biology by elucidating specific abnormalities in metabolic pathways in leukemic hematopoiesis. These studies potentially converge on the concept that modulation of reactive oxygen species (ROS) abundance may influence the pathogenesis and treatment of acute myeloid leukemia (AML).
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Ziegler-Heitbrock, HW, R. Munker, E. Thiel, I. Krebs, and G. Riethmuller. "Killer cell activity of human monoblastic leukemia cells as detected with a monocyte-specific target cell." Blood 65, no. 1 (January 1, 1985): 8–14. http://dx.doi.org/10.1182/blood.v65.1.8.8.

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Abstract Peripheral blood leukemia cells from patients with acute monoblastic leukemia (AMoL) were tested for killer cell activity against target cells that detected natural killer cell-mediated or monocyte-mediated spontaneous cytotoxicity. The fibrosarcoma cell line Wehi 164, pretreated with actinomycin D to induce susceptibility to lysis, specifically detects the activity of unstimulated human monocytes. In four of six cases of AMoL, high killer cell activity could be measured against this target. In three of these four cases, the killer cell activity could be assigned exclusively to the leukemic clone, based on the high leukocyte counts and the resultant dilution of normal cells, as evidenced by marker and by functional analysis. While leukemic cells with killer cell activity against Wehi 164 contained 34% to 45% cells that were positive for binding of the 63D3 monoclonal antibody, the two leukemic samples without killer cell activity contained only 1% and 12% 63D3-positive cells. Cell sorting of 63D3-positive and -negative cells from two leukemias with killer cell activity demonstrated that the killer cell activity was restricted to the 63D3-positive fraction of AMoL cells. These data demonstrate that monoblastic leukemia cells can be potent killer cells and that killing activity is linked to the 63D3- defined cell surface molecule.
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Ziegler-Heitbrock, HW, R. Munker, E. Thiel, I. Krebs, and G. Riethmuller. "Killer cell activity of human monoblastic leukemia cells as detected with a monocyte-specific target cell." Blood 65, no. 1 (January 1, 1985): 8–14. http://dx.doi.org/10.1182/blood.v65.1.8.bloodjournal6518.

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Peripheral blood leukemia cells from patients with acute monoblastic leukemia (AMoL) were tested for killer cell activity against target cells that detected natural killer cell-mediated or monocyte-mediated spontaneous cytotoxicity. The fibrosarcoma cell line Wehi 164, pretreated with actinomycin D to induce susceptibility to lysis, specifically detects the activity of unstimulated human monocytes. In four of six cases of AMoL, high killer cell activity could be measured against this target. In three of these four cases, the killer cell activity could be assigned exclusively to the leukemic clone, based on the high leukocyte counts and the resultant dilution of normal cells, as evidenced by marker and by functional analysis. While leukemic cells with killer cell activity against Wehi 164 contained 34% to 45% cells that were positive for binding of the 63D3 monoclonal antibody, the two leukemic samples without killer cell activity contained only 1% and 12% 63D3-positive cells. Cell sorting of 63D3-positive and -negative cells from two leukemias with killer cell activity demonstrated that the killer cell activity was restricted to the 63D3-positive fraction of AMoL cells. These data demonstrate that monoblastic leukemia cells can be potent killer cells and that killing activity is linked to the 63D3- defined cell surface molecule.
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I, Jamal. "Plasma Cell Leukemia: An Overview." Haematology International Journal 5, no. 1 (2021): 1–2. http://dx.doi.org/10.23880/hij-16000175.

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Krivtsov, Andrei V., Amit U. Sinha, Matthew C. Stubbs, Andrew Kung, and Scott Armstrong. "Cell of Origin Influences Leukemia Stem Cell Phenotype." Blood 114, no. 22 (November 20, 2009): 3459. http://dx.doi.org/10.1182/blood.v114.22.3459.3459.

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Abstract Abstract 3459 Poster Board III-347 MLL-fusion proteins can transform either hematopoietic stem cells (HSC) or granulocyte macrophage progenitors (GMP) into leukemia stem cells (LSC). However, the leukemogenic process in HSC may differ from that in GMP. We transduced HSC and GMP with MLL-AF9 or control retroviruses. Single-cell sorted MLL-AF9 expressing HSC or GMP could be serially replated for over 9 passages. Upon transplantation into syngeneic mice, 86.3% (n=22) of HSC:MLL-AF9 single cell derived clones (SCC) induced AML with a median latency of 61 days, while 33.3% of GMP:MLL-AF9 SCC induced AMLs with median latency of 100 days. Immunophenotype analysis of the resultant leukemias demonstrated that long-term repopulating HSC (LT-HSC) and GMP-derived leukemias were quite similar, with a GMP-like (LGMP) population enriched in LSC in both cases. Gene expression analysis demonstrated that globally the LGMP isolated from HSC derived AMLs (AML:HSC) and GMP derived AMLs (AML:GMP) were similar to each other but possessed specific genetic programs reminiscent of the cell of origin (HSC or GMP). For example Evi1, Jun, and Fos oncogenes were highly expressed in HSC and AML:HSC, but expressed at low level in GMP or AML:GMP. The genetic program that distinguished LGMP:HSC from LGMP:GMP was found to be enriched in hematopoietic stem cells compared to more differentiated myeloid progenitors and correlate with genetic programs in and human MLL-rearranged AML associated with a poor clinical outcome in two independent MLL-rearranged AML data sets. In order to directly assess differences in treatment response for leukemias derived from different cells of origin, we treated leukemic mice with a chemotherapeutic agent often used to treatment human AMLs. Treatment of leukemic mice with Etoposide reduced the spleen weights in mice transplanted with AML:HSC to a lesser extent (28%) than in mice transplanted with AML:GMP (88%). Altogether, these data indicate that cell of origin of AML can influence the genetic program of fully developed leukemia, and thus could account for some of the heterogeneity in human leukemias and perhaps outcome. Disclosures No relevant conflicts of interest to declare.
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Cardoso, Angelo A., J. Pedro Veiga, Paolo Ghia, Hernani M. Afonso, W. Nicholas Haining, Stephen E. Sallan, and Lee M. Nadler. "Adoptive T-Cell Therapy for B-Cell Acute Lymphoblastic Leukemia: Preclinical Studies." Blood 94, no. 10 (November 15, 1999): 3531–40. http://dx.doi.org/10.1182/blood.v94.10.3531.422k14_3531_3540.

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We have previously shown that leukemia-specific cytotoxic T cells (CTL) can be generated from the bone marrow of most patients with B-cell precursor acute leukemias. If these antileukemia CTL are to be used for adoptive immunotherapy, they must have the capability to circulate, migrate through endothelium, home to the bone marrow, and, most importantly, lyse the leukemic cells in a leukemia-permissive bone marrow microenvironment. We demonstrate here that such antileukemia T-cell lines are overwhelmingly CD8+ and exhibit an activated phenotype. Using a transendothelial chemotaxis assay with human endothelial cells, we observed that these T cells can be recruited and transmigrate through vascular and bone marrow endothelium and that these transmigrated cells preserve their capacity to lyse leukemic cells. Additionally, these antileukemia T-cell lines are capable of adhering to autologous stromal cell layers. Finally, autologous antileukemia CTL specifically lyse leukemic cells even in the presence of autologous marrow stroma. Importantly, these antileukemia T-cell lines do not lyse autologous stromal cells. Thus, the capacity to generate anti–leukemia-specific T-cell lines coupled with the present findings that such cells can migrate, adhere, and function in the presence of the marrow microenvironment enable the development of clinical studies of adoptive transfer of antileukemia CTL for the treatment of ALL.
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Yan, Ying, Peter Steinherz, Xiuqin Guan, Ann Jakubowski, Joesph P. McGuirk, and Richard J. O’Reilly. "Growth Potential of Human Leukemia Blast Cells in SCID Mice and Association with Prognosis of Human Acute Leukemias." Blood 104, no. 11 (November 16, 2004): 1900. http://dx.doi.org/10.1182/blood.v104.11.1900.1900.

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Abstract We have described a severe combined immunodeficiency (SCID) mouse model that permits the subcutaneous growth of primary human acute leukemia blast cells into a measurable subcutaneous nodule which may be followed by the development of disseminated disease. Utilizing the SCID mouse model, we examined the ability of patient-derived leukemic blasts to generate leukemic growth in the animals after subcutaneous inoculation without conditioning treatment. Leukemia blasts derived from 133 patients with acute leukemias, (67 acute lymphoblastic leukemia (ALL) and 66 acute myeloid leukemia (AML)), were inoculated into SCID mice. The leukemias displayed three distinct growth patterns: "aggressive", "indolent", or "no tumor growth". Out of 133 patients, leukemia samples 46 (34.5%) displayed an aggressive growth pattern, 14 (10.5%) indolent growth and 73 (55.0%) did not grow in SCID mice. The growth probability of leukemias from relapsed and/or refractory disease was 3 fold higher than that from patients with newly diagnosed disease. Serial observations found that leukemic blasts from the same individual, which did not initiate tumor growth at initial presentation and/or at early relapse, may engraft and grow in the later stages of disease, suggesting that the ability of leukemia cells for engraftment and proliferation was gradually acquired following the process of leukemia progression. Nine autonomous growing leukemia cell lines were established in vitro. These displayed an aggressive proliferation pattern, suggesting a possible correlation between the capacity of human leukemia cells for autonomous proliferation in vitro and an aggressive growth potential in SCID mice. It was demonstrated that patients whose leukemic blasts displayed an aggressive growth and dissemination pattern in SClD mice had a poor clinical outcome in patients with ALL as well as AML. Patients whose leukemic blasts grew indolently or whose leukemia cells failed to induce growth had a significantly longer DFS and more favorable clinical course.
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Tschanter, Petra, Nicole Baeumer, Lisa Lohmeyer, Frank Berkenfeld, Lara Tickenbrock, Sven Diederichs, Martin Stehling, et al. "Loss of the Cell Cycle Regulator p26INCA1 Induces Exhaustion of Leukemic Stem Cells." Blood 116, no. 21 (November 19, 2010): 96. http://dx.doi.org/10.1182/blood.v116.21.96.96.

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Abstract Abstract 96 Acute myeloid leukemia is a clonal disease characterized by a malignant proliferation and accumulation of myeloid progenitor cells. Current therapeutic strategies are often not able to eradicate the leukemic cells. Malignancy is associated with deregulation of cell cycle check- points and the deregulation of checkpoints is associated with altered stem cell properties. A better understanding of malignant stem cells and their cell cycle regulation might help to develop new therapies. Recently, we identified p26INCA1 as a novel cell cycle regulator. GST pulldown assays revealed binding of INCA1 predominantly to CDK2- specific Cyclins and we demonstrated an inhibitory effect of INCA1 on CDK2/ CyclinA complexes in kinase activity assays. The loss of INCA1 and its inhibitory effect on the cell cycle regulation led to an increased cell cycling and consequently to an enlarged stem cell pool in vivo. Upon cytotoxic stress, the loss of Inca1 enhanced cell cycling and bone marrow exhaustion. To analyze a potential role of INCA1 in leukemogenesis we retrovirally transduced wildtype and Inca1−/− bone marrow cells with AML1-ETO9a (A1E9a) and transplanted these cells into wildtype recipients. Most of the wildtype cell- transplanted recipients died due to AML. In contrast, only one of the Inca1−/− cell- transplanted mice developed AML. Engraftment was higher upon transplantion of Inca1−/− cells but engraftment was not sustained. To consider the repopulation capacity of the leukemic cells we performed transplantation of primary leukemic cells into secondary recipients. A1E9a induced leukemia in Inca1 wildtype cells was transplantable and lethal. However Inca1−/− leukemic cells were severely impaired in leukemia development in secondary recipients. Colony forming units and replating capacity were significantly reduced in A1E9a Inca1−/− bone marrow cells although these cells showed increased CDK2 activity. Exhaustion of leukemic cells in the absence of Inca1 was confirmed by cloning efficiency assays. Further analyses were performed with c-myc induced leukemias. Interestingly, Inca1 deletion precluded the development of leukemias in secondary recipients. Taken together, these findings identify an important role for p26INCA1 in the maintenance of leukemia and potentially the self-renewal capacity of leukemic stem cells. Disclosures: No relevant conflicts of interest to declare.
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Gilliland, D. Gary, Craig T. Jordan, and Carolyn A. Felix. "The Molecular Basis of Leukemia." Hematology 2004, no. 1 (January 1, 2004): 80–97. http://dx.doi.org/10.1182/asheducation-2004.1.80.

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Abstract Major strides have been made in our understanding of the molecular basis of adult and pediatric leukemias. More than one hundred disease alleles have been identified and characterized in cell culture and murine models of leukemia. In some instances, molecularly targeted therapies have been developed based on these insights that are currently in clinical trials, such as small molecule inhibitors of FLT3. In addition, it has recently been appreciated that, as with normal hematopoiesis, there is a hierarchical organization among leukemic cells that includes a rare population of leukemic stem cells that have properties of self-renewal. Understanding the characteristics of these leukemic stem cells may provide new insights into leukemia therapies that target self-renewal pathways. In Section I, Dr. Craig Jordan reviews the data that supports the existence of a “leukemia stem cell.” He provides an overview of the functional properties of leukemic stem cells, their relationship to hematopoietic stem cells, and the relevance of leukemic stem cells in other human malignancies including solid tumors. He briefly discusses what is known of the pathways that regulate properties of self-renewal. Dr. Gary Gilliland provides an overview of the genetics of adult leukemias in Section II and ongoing genome-wide strategies for discovery of new disease alleles. He describes the clinical and therapeutic implications of these findings and provides examples of bench-to-bedside translation of molecularly targeted therapies for AML, including the use of FLT3 inhibitors. In Section III, Dr. Carolyn Felix reviews recent advances in our understanding of the genetics and therapy of pediatric leukemias. She provides an overview of leukemias that are common in pediatric malignancies but rarely observed in adults, including the TEL-AML1 (ETV6-RUNX1) fusion associated with pediatric B-cell ALL, the OTT-MAL fusion associated with infant megakaryoblastic leukemia, PTPN11 mutations in juvenile myelomonocytic leukemia, and MLL fusion genes in leukemogenesis, among others.
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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.
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Dissertations / Theses on the topic "Leukemia cell"

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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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Osuji, Nnenna. "Leukemias of Mature T-Cell Phenotype with Gene Expression Profiling in T-Cell prolymphocytic Leukemia." Thesis, Institute of Cancer Research (University Of London), 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.498887.

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Morisot, Sebastien. "Détermination of the frequency of leukemia stem cells in childhood precursor B cell acute lymphoblastic leukemias." Paris 11, 2009. http://www.theses.fr/2009PA11T022.

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COLOMAR, CARANDO NATALIA. "Novel insights into NK cell/leukemia molecular interactions and possible tools to potentiate the anti-leukemia NK cell activity." Doctoral thesis, Università degli studi di Genova, 2022. http://hdl.handle.net/11567/1079072.

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Natural killer (NK) cells are extremely promising for cellular antitumor therapy in terms of efficacy and safety, particularly in the control of hematological malignancies. The aim of this thesis was to provide deeper insights on receptor/ligand leukemia interactions and investigate possible tools to enhance the NK cell anti-leukemia activity. Two clinical contexts of haploidentical hematopoietic stem cell transplantation (haplo-HSCT) were under evaluation 1) αβT-cell and B-cell depleted haplo-HSCT in pediatric leukemia patients, and 2) haplo-HSCT with post-transplant cyclophosphamide (PT-Cy) in adult AML patients. Regarding the first platform, we tested the in vitro effect of different NK cell engagers (NKCEs), which can trigger either NKp46 or NKp30 together with CD16A, and target either CD19 or CD20 to induce killing of pediatric B cell precursor acute lymphoblastic leukemia (BCP-ALL). We used as target cells different BCP-ALL cell lines and primary leukemias, and as effector cells resting NK cells derived from healthy donors and pediatric leukemia patients after αβT/B-depleted haplo-HSCT. The NKCEs potentiated the killing of NK-cell resistant BCP-ALL cells and enhanced the degranulation and cytokine production of NK cells. These data strongly support the therapeutic use of NKp46/CD16A/CD19-NKCE to fight relapsed/refractory leukemia in pre- or post-transplantation setting. Regarding the other platform, we investigated the phenotype of NK cells after transplantation, and we evaluated the effect of immune checkpoint inhibitor (ICI), targeting NKG2A, to unleash NK-cell activity against leukemia. The data pave the way for the use of an anti-NKG2A antibody (as Monalizumab) at early-time points after transplantation to enhance the anti-leukemia activity of NK cells.
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Papayannidis, Cristina <1980&gt. "Pre-clinical and clinical development of leukemia stem cell inhibitors in acute leukemias." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5596/1/TesiPapayannidisDottorato2013_Copy.pdf.

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In Leukemias, recent developments have demonstrated that the Hedgehog pathway plays a key-role in the peculiar ability of self renewal of leukemia stem cells. The aim of this research activity was to investigate, through a first in man, Phase I, open label, clinical trial, the role and the impact, mainly in terms of safety profile, adverse events and pharmacokinetics, of a Sonic Hedgehog inhibitor compound on a population of heavely pretreated patients affected by AML, CML, MF, or MDS, resistant or refractory to standard chemotherapy. Thirty-five patients have been enrolled. The drug was administered orally, in 28 days cycles, without rest periods. The compound showed a good safety profile. The half life was of 17-35 hours, justifying the daily administration. Significant signs of activity, in terms of reduction of bone marrow blast cell amount were seen in most of the patients enrolled. Interestingly, correlative biological studies demonstrated that, comparing the gene expression profyiling signature of separated CD34+ cells before and after one cycle of treatment, the most variably expressed genes were involved in the Hh pathway. Moreover, we observed that many genes involved in MDR (multidrug resistance)were significantly down regulated after treatment. These data might lead to future clinical trials based on combinatory approaches, including, for instance, Hh inhibitors and conventional chemotherapy.
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Papayannidis, Cristina <1980&gt. "Pre-clinical and clinical development of leukemia stem cell inhibitors in acute leukemias." Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5596/.

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In Leukemias, recent developments have demonstrated that the Hedgehog pathway plays a key-role in the peculiar ability of self renewal of leukemia stem cells. The aim of this research activity was to investigate, through a first in man, Phase I, open label, clinical trial, the role and the impact, mainly in terms of safety profile, adverse events and pharmacokinetics, of a Sonic Hedgehog inhibitor compound on a population of heavely pretreated patients affected by AML, CML, MF, or MDS, resistant or refractory to standard chemotherapy. Thirty-five patients have been enrolled. The drug was administered orally, in 28 days cycles, without rest periods. The compound showed a good safety profile. The half life was of 17-35 hours, justifying the daily administration. Significant signs of activity, in terms of reduction of bone marrow blast cell amount were seen in most of the patients enrolled. Interestingly, correlative biological studies demonstrated that, comparing the gene expression profyiling signature of separated CD34+ cells before and after one cycle of treatment, the most variably expressed genes were involved in the Hh pathway. Moreover, we observed that many genes involved in MDR (multidrug resistance)were significantly down regulated after treatment. These data might lead to future clinical trials based on combinatory approaches, including, for instance, Hh inhibitors and conventional chemotherapy.
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Matsubara, Yasushi. "Delineation of immunoregulatory properties of adult T cell leukemia cells." Kyoto University, 2007. http://hdl.handle.net/2433/135653.

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O'Neill, Kieran. "Automated analysis of single cell leukemia data." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/50867.

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Acute myeloid leukemia (AML) is a high grade malignancy of non-lymphoid cells of the hematopoietic system. AML is a heterogeneous disease, and numerous attempts have been made to risk-stratify AML so that appropriate treatment can be offered. Single cell analysis methods could provide insights into the biology of AML leading to risk-stratified and functionally tailored treatments and hence improved outcomes. Recent advances in flow cytometry allow the simultaneous measurement of up to 17 antibody markers per cell for up to millions of cells, and it is performed routinely during AML clinical workup. However, despite vast amounts of flow cytometry data being gathered, comprehensive, objective and automated studies of this data have not been undertaken. Another method, strand-seq, elucidates template strand inheritance in single cells, with a range of potential applications, none of which had been automated when this thesis work commenced. I have developed bioinformatic methods enabling research into AML using both these types of data. I present flowBin, a method for faithfully recombining multitube flow cytometry data. I present flowType-DP, a new version of flowType, able to process flow cytometry and other single cell data having more than 12 markers (including flowBin output). I demonstrate the application of flowBin to AML data, for digitally isolating abnormal cells, and classifying AML patients. I also use flowBin in conjunction with flowType to find cell types associated with clinically relevant gene mutations in AML. I present BAIT, a software package for accurately detecting sister chromatid exchanges in strand-seq data. I present functionality to place unbridged contigs in late-build genomes into their correct location, and have, with collaborators, published the corrected locations of more than half the unplaced contigs in the current build of the mouse genome. I present contiBAIT, a software package for assembling early-build genomes which consist entirely of unanchored, unbridged contigs. ContiBAIT has the potential to dramatically improve the quality of many model organism genomes at low cost. These developments enable rapid, automated, objective and reproducible deep profiling of AML flow cytometry data, subclonal cell analysis of AML cytogenetics, and improvements to model organisms used in AML research.
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Machado, Parrula Maria Cecilia. "Measles Virotherapy in Adult T cell Leukemia." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1261413581.

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Lam, Wilbur Aaron. "Cell mechanics of leukostasis in acute leukemia." Diss., Search in ProQuest Dissertations & Theses. UC Only, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3311343.

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Thesis (Ph.D.)--University of California, San Francisco with the University of California, Berkeley, 2008.
Source: Dissertation Abstracts International, Volume: 69-06, Section: B, page: 3693. Adviser: Daniel Fletcher.
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Books on the topic "Leukemia cell"

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1939-, Polliack Aaron, and Tallman Martin S, eds. Hairy cell leukemia. Amsterdam: Harwood Academic, 2000.

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C, Cawley J., ed. Hairy-cell leukaemia. London: Springer, 1996.

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Vogt, Peter K., ed. Human T-Cell Leukemia Virus. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70113-9.

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Watanabe, Toshiki, and Takuya Fukushima, eds. Adult T-cell Leukemia/Lymphoma. Tokyo: Springer Japan, 2017. http://dx.doi.org/10.1007/978-4-431-56523-9.

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1932-, Vogt P. K., ed. Human T-cell leukemia virus. Berlin: Springer, 1985.

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McCredie, Kenneth B. Selected abstracts on hairy cell leukemia. Bethesda, MD: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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D, Catovsky, ed. The Leukemic cell. 2nd ed. Edinburgh: Churchill Livingstone, 1991.

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1939-, Huang Andrew T., and Rundles Symposium on Hairy Cell Leukemia and Chronic Lymphocytic Leukemia (1985 : Duke University Medical Center), eds. Hairy cell and chronic lymphocytic leukemia: Thirty years of progress. New York: Elsevier, 1987.

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Kiyoshi, Takatsuki, ed. Adult T-cell leukaemia. Oxford: Oxford University Press, 1994.

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Takashi, Uchiyama. Adult T cell leukemia and related diseases. New York: Springer-Verlag, 1995.

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Book chapters on the topic "Leukemia cell"

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Haas, W., and H. von Boehmer. "T Cell Proliferation and Differentiation." In Leukemia, 21–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69722-7_3.

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Paul, W. E. "Induction of B Cell Proliferation and Differentiation." In Leukemia, 69–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69722-7_5.

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Strzelecka, Paulina M., Anna M. Ranzoni, and Ana Cvejic. "Single-Cell Transcriptomic Analysis of Hematopoietic Cells." In Leukemia Stem Cells, 135–58. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0810-4_9.

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Joseph, Nisha S., Amarendra K. Neppalli, and Ajay K. Nooka. "Plasma Cell Leukemia." In Personalized Therapy for Multiple Myeloma, 121–29. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-61872-2_7.

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Ravandi, Farhad. "Hairy Cell Leukemia." In Leukemias: Principles and Practice of Therapy, 339–47. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444327359.ch28.

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Hayman, Suzanne R. "Plasma Cell Leukemia." In Hematologic Malignancies: Multiple Myeloma and Related Plasma Cell Disorders, 119–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-08885-2_5.

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Sena Teixeira Mendes, Larissa, and Andrew Wotherspoon. "Hairy Cell Leukemia." In Encyclopedia of Pathology, 181–91. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-95309-0_3849.

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Rübe, Claudia E., Bernadine R. Donahue, Jay S. Cooper, Caspian Oliai, Yan Yu, Laura Doyle, Rene Rubin, et al. "Hairy Cell Leukemia." In Encyclopedia of Radiation Oncology, 305. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_515.

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Mendes, Larissa Sena Teixeira, and Andrew Wotherspoon. "Hairy Cell Leukemia." In Encyclopedia of Pathology, 1–11. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28845-1_3849-1.

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Schwab, Manfred. "Hairy Cell Leukemia." In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2553-2.

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Conference papers on the topic "Leukemia cell"

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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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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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Falang, A., G. M. Alessio, M. Donati, and T. A. Barbui. "DISSEMINATED INTRAVASCULAR COAGULATION (DIC) AND ACUTE LEUKEMIA:IDENTIFICATION OF A NEW CELLULAR PROCOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643661.

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There is an enhanced incidence (>50%) of severe coagulopathy in association with several types of acute leukemias. Cell associated procoagulants are considered important in this context. So far only a Tissue Factor (TF)-type procoagulant has been described in leukemic cells. We have set up here the experimentalconditions to identify other possible cellular procoagulants in leukemia. We have tested blast cell extracts from 21 patients with 5 different cytological subtypes (from Ml to M5 of acute non lymphoid leukemia (ANLL), according to theFAB classification, in order to assay whether they express "cancer procoagulant" (CP), a F VH-independent FX activating cysteine proteinase (Falanga … Gordon, 1985; Donati, et al. 1986). All the samples shortened the recalcification time of normal human plasma, the effect being significantly greater (p<0.001) in the M3 group. The activity was 20% to 100% independent from the presence of FVII and was susceptible to 2 cysteine proteinase inhibitors (Iodoacetamide, 2 mM, and HgCl2 ,0.1 mM) in all of the extracts but the M5 type. In addition, M2 and M3 samples directly activated pure FX in a two stage clotting assay. Control cell extracts from 10 healthy donors did not show any procoagulant activity, under the same conditions. This study provides evidence for a new procoagulant expressed by cells of ANLL; the peculiar characteristics of this procoagulant (i.e. its confinement to the malignant phenotype, its shedding into the plasma, its possible modulation by vitamin K antagonists) make this observation of potential interest in the development of new diagnostic and therapeutic tools in ANLL.
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Kuttikrishnan, Shilpa, Kirti S. Prabhu, Tamam Elimat, Ashraf Khalil, Nicholas H. Oberlies, Feras Q. Alali, and Shahab Uddin. "Anticancer Activity of Neosetophomone B, An Aquatic Fungal Secondary Metabolite, Against Hematological Malignancie S." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0106.

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Cancer is one of the most life threatening diseases, causing nearly 13% death in the worldwide. Leukemia, cancer of the hematopoetic cells is the main cause of cancer death in adults and children. Therapeutic agents used in treatment of cancer are known to have narrow therapeutic window and tendency to develop resistance against some cancer cell lines thus, proposing a need to discover some novel agents to treat cancer. In the present study we investigated the anticancer activity of Neosetophomone B(NSP-B), an aquatic fungal metabolite isolated from Neosetophoma sp against leukemic cells (K562 and U937). MTT results demonstrated a dose dependent inhibition of cell proliferation in K562 and U937 cell lines. Annexin staining using flow cytometry indicated that NSP-B treatment cause a dose dependent apoptosis in leukemic cells.Western blot analysis showed that NSP-B mediated apoptosis involves sequential activation of caspase 9, 3 and poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore NSP-B treatment of leukemic cells resulted in upregulation of pro-apoptotic proteins (Bax) with downregulation of anti-apoptotic proteins ( Bcl-2 ).Thus, present study focuses on exploring the mechanism of anticancer activity of NSP-B on leukemic cells, raising the possibility of its use as a novel therapeutic agent for hematological malignancies. Results: We sought to determine whether NSP-B suppresses the growth of leukemic cell lines. We tested a panel of leukemic cell lines with different doses of NSP-B. Cell viability decreased in a concentration-dependent manner in K562 and U937 cell lines. NSP-B induced apoptosis in K562 and U937 cell lines via downregulation of anti-apoptotic proteins and enhancement of pro-apoptotic proteins. NSP-B induced the activation of caspase cascade signaling pathway. Altogether our results suggest that the NSP-B plays an important role in apoptosis in leukemic cell lines .Conclusions: Our data provides insight on anticancer activities of NSP-B in leukemic cell lines (K562 and U937). NSP-B inhibit cell viability via inducing apoptosis. The NSP-B mediated apoptosis occurs via downregulation of anti-apoptotic proteins and enhancement of pro-apototic proteins, thereby activating the caspase-cascade signaling. Further studies are required to elicit role of NSP-B in regulating molecular pathway involved in the progression of cancer. Taken together, above results suggest that NSP-B may have a future therapeutic role in leukemia and possibly other hematological malignancies.
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Gopakumar, G., Gorthi R. K. Sai Subrahmanyam, and Gorthi Sai Siva. "Morphology based Classification of Leukemia Cell lines." In the 2014 Indian Conference. New York, New York, USA: ACM Press, 2014. http://dx.doi.org/10.1145/2683483.2683517.

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Harun, Nor Hazlyna, Nur Azzah Abu Bakar, Uvaghesvary AP Mohan, Maslinda Mohd Nadzir, Mohamad Ghozali Hassan, and Robiyanti Adollah. "Automated Cell Counting System For Chronic Leukemia." In 2019 IEEE Jordan International Joint Conference on Electrical Engineering and Information Technology (JEEIT). IEEE, 2019. http://dx.doi.org/10.1109/jeeit.2019.8717500.

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Rejintal, Ashwini, and N. Aswini. "Image processing based leukemia cancer cell detection." In 2016 IEEE International Conference on Recent Trends in Electronics, Information & Communication Technology (RTEICT). IEEE, 2016. http://dx.doi.org/10.1109/rteict.2016.7807865.

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Blackburn, Jessica, Sali Liu, Sarah Martinez, Kimberly Dobrinski, Finola Moore, Riadh Lobbardi, and David Langenau. "Abstract PR05: Clonal evolution enhances leukemia-propagating cell activity in T-cell acutelymphoblastic leukemia through AKT/mTORC1 pathway activation." In Abstracts: AACR Special Conference: Pediatric Cancer at the Crossroads: Translating Discovery into Improved Outcomes; November 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.pedcan-pr05.

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Blackburn, Jessica, Sali Liu, Kimberly Dobrinski, Sarah Martinez, Finola Moore, Riadh Lobbardi, and David Langenau. "Abstract A08: Clonal evolution enhances leukemia propagating cell activity in T-cell acutelymphoblastic leukemia through AKT/mTORC1 pathway activation." In Abstracts: AACR Special Conference: The Translational Impact of Model Organisms in Cancer; November 5-8, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.modorg-a08.

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Blackburn, Jessica, Sali Liu, Kimberly Dobrinski, Sarah Martinez, Finola Moore, Riadh Lobbardi, and David Langenau. "Abstract PR06: Clonal evolution enhances leukemia propagating cell activity in T-cell acutelymphoblastic leukemia through AKT/mTORC1 pathway activation." In Abstracts: AACR Special Conference: The Translational Impact of Model Organisms in Cancer; November 5-8, 2013; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1557-3125.modorg-pr06.

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Velu, Chinavenmeni S., Aditya Chaubey, James D. Phelan, Sara Meyer, Shane R. Horman, Mark Wunderlich, Monica L. Guzman, et al. "Abstract 979: microRNA-mediated leukemia-initiating cell activity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-979.

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Reports on the topic "Leukemia cell"

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Cooper, Laurence, and Rita Young. Development of Augmented Leukemia/Lymphoma-Specific T-Cell Immunotherapy for Deployment with Haploidentical, Hematompoietic Progenitor-Cell Transplant. Fort Belvoir, VA: Defense Technical Information Center, May 2008. http://dx.doi.org/10.21236/ada487262.

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Cooper, Laurence. Development of Augmented Leukemia/Lymphoma-Specific T-Cell Immunotherapy for Deployment with Haploidentical, Hematompoietic Progenitor-Cell Transplant. Fort Belvoir, VA: Defense Technical Information Center, May 2011. http://dx.doi.org/10.21236/ada560655.

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Ferrando, Adolfo A. Targeting Class I PI3Ks in the Treatment of T-cell Acute Lymphoblastic Leukemia. Fort Belvoir, VA: Defense Technical Information Center, August 2013. http://dx.doi.org/10.21236/ada591435.

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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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Lundgren, D. L., W. C. Griffith, and F. F. Hahn. Inverse relationship of tumors and mononuclear cell leukemia infiltration in the lungs of F344 rats. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381384.

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Splitter, Gary, Zeev Trainin, and Yacov Brenner. Lymphocyte Response to Genetically Engineered Bovine Leukemia Virus Proteins in Persistently Lymphocytic Cattle from Israel and the U.S. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570556.bard.

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The goal of this proposal was to identify proteins of BLV recognized by lymphocyte subpopulations and determine the contribution of these proteins to viral pathogenesis. Our hypothesis was that BLV pathogenesis is governed by the T-cell response and that the immune system likely plays an important role in controlling the utcome of infection. Our studies presented in ths final report demonstrate that T cell competency declines with advancing stages of infection. Dramatic differences were observed in lymphocyte proliferation to recombinant proteins encoded by BLV gag (p12, p15, and p24) and env (gp30 and gp15) genes in different disease stages. Because retroviruses are known to mutate frequently, examinatin of infected cattle from both Israel and the United States will likely detect variability in the immune response. This combined research approach provides the first opportunity to selectively address the importance of T-cell proliferation to BLV proteins and cytokines produced during different stages of BLV infection. Lack of this information regarding BLV infection has hindered understanding lympocyte regulation of BLV pathogenesis. We have developed the essential reagents necessary to determine the prominence of different lymphocyte subpopulations and cytokines produced during the different disease stages within the natural host. We found that type 1 cytokines (IL-2 and IFN-g) increased in PBMCs from animals in early disease, and decreasd in PBMCs from animals in late disease stages of BLV infection, while IL-10, increased with disease progression. Recently, a dichotomy between IL-12 and IL-10 has emerged in regards to progression of a variety of diseases. IL-12 activates type 1 cytokine production and has an antagonistic effect on type 2 cytokines. Here, using quantitative competitive PCR, we show that peripheral blood mononuclear cells from bovine leukemia virus infected animals in the alymphocytotic disease stage express increased amount of IL-12 p40 mRNA. In contrast, IL-12 p40 mRNA expression by PL animals was significantly decreased compared to normal and alymphocytotic animals. To examine the functions of these cytokines on BLV expression, BLV tax and pol mRNA expression and p24 protein production were quantified by competitive PCR, and by immunoblotting, respectively. IL-10 inhibited BLV tax and pol mRNA expression by BLV-infected PBMCs. In addition, we determined that macrophages secret soluble factor(s) that activate BLV expression, and that secretion of the soluble factor(s) could be inhibited by IL-10. In contrast, IL-2 increased BLV tax and pol mRNA, and p24 protein production. These findings suggest that macrophages have a key role in regulating BLV expression, and IL-10 produced by BLV-infected animals in late disease stages may serve to control BLV expression, while IL-2 in the early stage of disease may activate BLV expression. PGE2 is an important immune regulator produced only by macrophages, and is known to facilitate HIV replication. We hypothesized that PGE2 may regulate BLV expression. Here, we show that cyclooxygenase-2 (COX-2) mRNA expression was decreased in PBMCs treated with IL-10, while IL-2 enhanced COX-2 mRNA expression. In contrast, addition of PGE2 stimulated BLV tax and pol mRNA expression. In addition, the specific COX-2 inhibitor, NS-398, inhibited BLV expression, while addition of PGE2 increased BLV tax expression regardless of NS-398. These findings suggest that macrophage derived cyclooxygenase -2 products, such as PGE2, may regulate virus expression and disease rogression in BLV infection, and that cytokines (IL-2 and IL-10) may regulate BLV expression through PGE2 production.
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Kungwankiattichai, Smith, Ben Ponvilawa, Claudie Roy, Pattaraporn Tunsing, Florian Kuchenbauer, and Weerapat Owattanapanich. Maintenance with Hypomethylating Agents after Allogeneic Stem Cell Transplantation in Acute Myeloid Leukemia and Myelodysplastic Syndrome: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0078.

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Review question / Objective: P: Patients with AML or MDS after allo-SCT; I: Hypomethylating agents after allo-SCT; C: Observation after allo-SCT; O: Overall survival rates. Condition being studied: Hypomethylating agents (HMAs) seem to have a range of properties favorable to post-allogeneic hematopoietic stem cell transplantation (allo-SCT) maintenance in acute myeloid leukemia (AML) patients. This meta-analysis was performed to review all relevant studies to compare the outcomes of patients undergoing allo-SCT for AML or MDS receiving HMA maintenance therapy with observation only. Information sources: The systematic search of the Embase and MEDLINE databases identified 4,416 articles, from which 512 duplicates were removed. This resulted in 3,904 articles available for title and abstract review. Subsequently, 3,875 articles were excluded as the article type and study design did not fulfill the inclusion criteria, or there was no report on a primary outcome of interest. The remaining 29 articles underwent full-length review and 18 of those were excluded for the aforementioned reasons. Ultimately, the eligibility criteria for our meta-analysis were met by 11 studies: 2 RCTs, 1 prospective cohort study, and 8 retrospective cohort studies.
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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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Lee, Byeong-Chel. Purinergic Receptors in Quiescence and Localization of Leukemic Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2012. http://dx.doi.org/10.21236/ada564468.

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Lee, Byeong-Chel. Purinergic Receptors in Quiescence and Localization of Leukemic Stem Cells. Fort Belvoir, VA: Defense Technical Information Center, May 2013. http://dx.doi.org/10.21236/ada581409.

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