Relevant bibliographies by topics / Leukemia

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Leukemia'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Leukemia"

1

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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2

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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3

Horton, Sarah J., Vanessa Walf-Vorderwülbecke, Steve J. Chatters, Neil J. Sebire, Jasper de Boer, and Owen Williams. "Acute myeloid leukemia induced by MLL-ENL is cured by oncogene ablation despite acquisition of complex genetic abnormalities." Blood 113, no. 20 (May 14, 2009): 4922–29. http://dx.doi.org/10.1182/blood-2008-07-170480.

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Abstract Chromosomal translocations involving 11q23 are frequent in infant acute leukemia and give rise to the formation of MLL fusion genes. The mechanism of leukemic transformation by these fusions has been the subject of numerous investigations. However, the dependence of acute leukemia on MLL fusion activity in vivo and the efficacy of targeting this activity to eliminate disease have not been established. We have developed a model for conditional expression of MLL-ENL in hematopoietic progenitor cells, in which expression of the fusion oncogene is turned off by doxycycline. Conditionally immortalized myeloblast cells derived from these progenitors were found to induce leukemia in vivo. Leukemic cells isolated from primary recipient mice were shown to have acquired additional genetic abnormalities and, when transplanted into secondary recipients, induced leukemia with shortened latencies. However, the leukemic cells remained dependent on MLL-ENL expression in vitro and in vivo, and its ablation resulted in regression of established leukemias. This study demonstrates that even genetically complex leukemias can be reversed on inactivation of the initiating MLL fusion and has important implications for the design of novel leukemia therapies.
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4

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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5

Jones, RJ, SJ Sharkis, CB Miller, EK Rowinsky, PJ Burke, and WS May. "Bryostatin 1, a unique biologic response modifier: anti-leukemic activity in vitro." Blood 75, no. 6 (March 15, 1990): 1319–23. http://dx.doi.org/10.1182/blood.v75.6.1319.1319.

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Abstract Bryostatin 1, a macrocyclic lactone isolated from the marine bryozoan Bugula neritina, has demonstrated both antineoplastic activity against the murine P388 leukemia line in vivo and stimulatory activity against mouse and human hematopoietic progenitors. We studied the effects of bryostatin 1 on the growth of human leukemias in vitro. Bryostatin 1 inhibited 1 to 4 logs of clonogenic leukemia cell growth from three of four leukemia cell lines. Bryostatin 1 also inhibited, by at least 1 log, the proliferation of clonogenic acute nonlymphocytic leukemia (ANLL) cells from 10 to 12 patients with newly diagnosed or relapsed ANLL. Maximal inhibition of leukemic growth occurred at 10(-9) to 10(- 7) mol/L bryostatin 1. Interestingly, bryostatin 1 also inhibited the growth of hematopoietic progenitors from eight patients with myelodysplastic syndromes (MDS). Leukemia cells exposed to bryostatin 1 for up to 96 hours and then washed, demonstrated no substantial inhibition of clonogenic growth, indicating that the anti-leukemic effect of bryostatin 1 is cytostatic. The phorbol ester 12–0- tetradecanoylphorbol-13-acetate (TPA) produced more potent inhibition of clonogenic leukemia growth, and this inhibition was blocked by bryostatin 1. Thus, the anti-leukemic activity of bryostatin 1 may be mediated through activation of protein kinase C. Bryostatin 1 inhibits clonogenic leukemia cells at concentrations that stimulate normal hematopoietic progenitors. The differential effects of bryostatin 1 on normal and abnormal hematopoiesis suggest that bryostatin 1 may have value in the treatment of leukemias and MDS.
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Jones, RJ, SJ Sharkis, CB Miller, EK Rowinsky, PJ Burke, and WS May. "Bryostatin 1, a unique biologic response modifier: anti-leukemic activity in vitro." Blood 75, no. 6 (March 15, 1990): 1319–23. http://dx.doi.org/10.1182/blood.v75.6.1319.bloodjournal7561319.

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Bryostatin 1, a macrocyclic lactone isolated from the marine bryozoan Bugula neritina, has demonstrated both antineoplastic activity against the murine P388 leukemia line in vivo and stimulatory activity against mouse and human hematopoietic progenitors. We studied the effects of bryostatin 1 on the growth of human leukemias in vitro. Bryostatin 1 inhibited 1 to 4 logs of clonogenic leukemia cell growth from three of four leukemia cell lines. Bryostatin 1 also inhibited, by at least 1 log, the proliferation of clonogenic acute nonlymphocytic leukemia (ANLL) cells from 10 to 12 patients with newly diagnosed or relapsed ANLL. Maximal inhibition of leukemic growth occurred at 10(-9) to 10(- 7) mol/L bryostatin 1. Interestingly, bryostatin 1 also inhibited the growth of hematopoietic progenitors from eight patients with myelodysplastic syndromes (MDS). Leukemia cells exposed to bryostatin 1 for up to 96 hours and then washed, demonstrated no substantial inhibition of clonogenic growth, indicating that the anti-leukemic effect of bryostatin 1 is cytostatic. The phorbol ester 12–0- tetradecanoylphorbol-13-acetate (TPA) produced more potent inhibition of clonogenic leukemia growth, and this inhibition was blocked by bryostatin 1. Thus, the anti-leukemic activity of bryostatin 1 may be mediated through activation of protein kinase C. Bryostatin 1 inhibits clonogenic leukemia cells at concentrations that stimulate normal hematopoietic progenitors. The differential effects of bryostatin 1 on normal and abnormal hematopoiesis suggest that bryostatin 1 may have value in the treatment of leukemias and MDS.
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Dias, Sergio, Margaret Choy, Kari Alitalo, and Shahin Rafii. "Vascular endothelial growth factor (VEGF)–C signaling through FLT-4 (VEGFR-3) mediates leukemic cell proliferation, survival, and resistance to chemotherapy." Blood 99, no. 6 (March 15, 2002): 2179–84. http://dx.doi.org/10.1182/blood.v99.6.2179.

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Abstract Similar to solid tumors, growth of leukemias may also be angiogenesis dependent. Furthermore, tyrosine kinase receptors specific to endothelial cells are expressed on certain subsets of leukemias. We have previously demonstrated the existence of a VEGF/VEGFR-2 autocrine loop on leukemic cells that supports their growth and migration. Here, we demonstrate that in response to leukemia-derived proangiogenic and proinflammatory cytokines such as basic fibroblast growth factor and IL-1, endothelial cells release increasing amounts of another vascular endothelial growth factor (VEGF) family member, VEGF-C. In turn, interaction of VEGF-C with its receptor VEGFR-3 (FLT-4) promotes leukemia survival and proliferation. We demonstrate in 2 cell lines and 5 FLT-4+ leukemias that VEGF-C and a mutant form of the molecule that lacks the KDR-binding motif induce receptor phosphorylation, leukemia proliferation, and increased survival, as determined by increased Bcl-2/Bax ratios. Moreover, VEGF-C protected leukemic cells from the apoptotic effects of 3 chemotherapeutic agents. Because most leukemic cells release proangiogenic as well as proinflammatory cytokines, our data suggest that the generation of a novel paracrine angiogenic loop involving VEGF-C and FLT-4 may promote the survival of a subset of leukemias and protect them from chemotherapy-induced apoptosis. These results identify the VEGF-C/FLT-4 pathway as a novel therapeutic target for the treatment of subsets of acute leukemia.
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Adamaki, Maria, Spiros Vlahopoulos, George I. Lambrou, Athanasios G. Papavassiliou, and Maria Moschovi. "Aberrant AML1 gene expression in the diagnosis of childhood leukemias not characterized by AML1-involved cytogenetic abnormalities." Tumor Biology 39, no. 3 (March 2017): 101042831769430. http://dx.doi.org/10.1177/1010428317694308.

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The AML1 ( acute myeloid leukemia 1) gene, a necessary prerequisite of embryonic hematopoiesis and a critical regulator of normal hematopoietic development, is one of the most frequently mutated genes in human leukemia, involving over 50 chromosome translocations and over 20 partner genes. In the few existing studies investigating AML1 gene expression in childhood leukemias, aberrant upregulation seems to specifically associate with AML1 translocations and amplifications. The aim of this study was to determine whether overexpression also extends to other leukemic subtypes than the ones karyotypically involving AML1. We use quantitative real-time polymerase chain reaction methodology to investigate gene expression in 100 children with acute leukemias and compare them to those of healthy controls. We show that in childhood acute lymphoblastic leukemia, AML1 gene overexpression is associated with a variety of leukemic subtypes, both immunophenotypically and cytogenetically. Statistically significantly higher transcripts of the gene were detected in the acute lymphoblastic leukemia group as compared to the acute myeloid leukemia group, where AML1 overexpression appeared to associate with cytogenetic abnormalities additional to those that engage the AML1 gene, or that are reported as showing a “normal” karyotype. Collectively, our study shows that AML1 gene overexpression characterizes a broader range of leukemic subtypes than previously thought, including various maturation stages of B-cell acute lymphoblastic leukemia and cytogenetic types additional to those involving the AML1 gene.
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Kogan, Scott C., Diane E. Brown, David B. Shultz, Bao-Tran H. Truong, Valerie Lallemand-Breitenbach, Marie-Claude Guillemin, Eric Lagasse, Irving L. Weissman, and J. Michael Bishop. "Bcl-2 Cooperates with Promyelocytic Leukemia Retinoic Acid Receptor α Chimeric Protein (Pmlrarα) to Block Neutrophil Differentiation and Initiate Acute Leukemia." Journal of Experimental Medicine 193, no. 4 (February 19, 2001): 531–44. http://dx.doi.org/10.1084/jem.193.4.531.

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The promyelocytic leukemia retinoic acid receptor α (PMLRARα) chimeric protein is associated with acute promyelocytic leukemia (APL). PMLRARα transgenic mice develop leukemia only after several months, suggesting that PMLRARα does not by itself confer a fully malignant phenotype. Suppression of apoptosis can have a central role in tumorigenesis; therefore, we assessed whether BCL-2 influenced the ability of PMLRARα to initiate leukemia. Evaluation of preleukemic animals showed that whereas PMLRARα alone modestly altered neutrophil maturation, the combination of PMLRARα and BCL-2 caused a marked accumulation of immature myeloid cells in bone marrow. Leukemias developed more rapidly in mice coexpressing PMLRARα and BCL-2 than in mice expressing PMLRARα alone, and all mice expressing both transgenes succumbed to leukemia by 7 mo. Although both preleukemic, doubly transgenic mice and leukemic animals had abundant promyelocytes in the bone marrow, only leukemic mice exhibited thrombocytopenia and dissemination of immature cells. Recurrent gain of chromosomes 7, 8, 10, and 15 and recurrent loss of chromosome 2 were identified in the leukemias. These chromosomal changes may be responsible for the suppression of normal hematopoiesis and dissemination characteristic of the acute leukemias. Our results indicate that genetic changes that inhibit apoptosis can cooperate with PMLRARα to initiate APL.
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Granados Romero, Francisco Fabian, and Enma maría Guadamud Lorenti. "Acute lymphoblastic leukemia." Journal of America health 1, no. 1 (January 2, 2018): 1–5. http://dx.doi.org/10.37958/jah.v1i1.1.

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Acute lymphoblastic leukemia is the most common hematologic neoplasm in pediatric age. Acute lymphoblastic leukemia (ALL) comprises 80% of all acute leukemias in this age group. Although the etiology is unknown, some genetic, viral and environmental predisposing factors have been detailed. The clinical manifestations are usually the result of bone marrow by leukemic cells (anemia, thrombopenia and neutropenia). The diagnosis is made by morphological, cytogenetic and molecular analysis of bone marrow aspirate. The treatment lasts about two years. The prognosis of children with acute lymphoblastic leukemia has improved brilliantly in recent decades thanks to new drugs and treatment tailored to patients' risk.
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Dissertations / Theses on the topic "Leukemia"

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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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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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Dutta, Sayantanee. "CALM/AF10 leukemia." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-174268.

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Bagacean, Cristina. "Epigenetics in leukemia." Thesis, Brest, 2018. http://www.theses.fr/2018BRES0012.

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Les dérivés de la cytosine sont d’importantes modifications épigénétiques dont le rôle dans l’évolution de la leucémie lymphoïde chronique (LLC) n’est pas totalement exploré. Dans ce contexte, notre première étude vise à examiner le niveau global de la 5-methylcytosine (5-mCyt), 5-hydroxymethylcytosine (5-hmCyt), 5-carboxylcytosine (5-CaCyt) et 5-hydroxymethyluridine (5-hmU) dans des lymphocytes B purifiés de patients LLC (n=56) et d’individus sains (n=17). Les principaux acteurs de la régulation épigénétique (DNMT1/3A/3B, MBD2/4, TET1/2/3, SAT1) ont été évalués par PCR quantitative en temps réel. L’analyse a permis de mettre en exergue trois groupes de patients. En premier lieu, un groupe de patients stables (délai médian de progression [PFS] et délai au premier traitement [TFT] >120 mois), avec un profil épigénétique similaire au groupe contrôle. Deuxièmement, un groupe intermédiaire (PFS=84; TFT=120 mois) qui présente une augmentation de la déméthylation de l’ADN expliquée par l'induction SAT1 / TET2 pendant la progression de la maladie. Troisièmement, un groupe de patients avec une forme active de la maladie (PFS=52; TFT=112 mois) qui présentent une hyperlymphocytose, une réduction du temps de doublement des lymphocytes et des modifications épigénétiques majeures. Au sein de ce groupe, une réduction est observée pour la 5-mCyt, 5-hmCyt, 5-CaCyt et serait associée à une diminution des DNMTs, TETs et MBDs au cours de la progression de la maladie. Les profils épigénétiques mis en évidence sont indépendants du statut mutationnel IGHV mais sont associés avec les anomalies cytogénétiques. Nous nous sommes également intéressés à cette association et nous avons montré dans la deuxième étude que les modifications des dérivées de la cytosine peuvent affiner le pouvoir pronostic des anomalies cytogénétiques. En conclusion, nos résultats suggèrent que les variations de la méthylation ainsi que des intermédiaires de la déméthylation de l’ADN sont impliqués dans la progression de la LLC
Cytosine derivatives are important epigenetic modifications whose role in the pathogenesis and evolution of chronic lymphocytic leukemia (CLL) is not fully explored. In this context, our first study aims to examine the global DNA level of 5-methylcytosine (5-mCyt), 5-hydroxymethylcytosine (5-hmCyt), 5-carboxylcytosine (5-CaCyt) and 5-hydroxymethyluridine (5-hmU) in purified B lymphocytes of CLL patients (n = 56) and healthy individuals (n = 17). The main actors in epigenetic regulation (DNMT1 / 3A / 3B, MBD2 / 4, TET1 / 2/3, SAT1) were evaluated by quantitative real time PCR. The analysis highlighted three groups of patients. First, a group of patients with stable disease (median time to progression [PFS] and time to first treatment [TFT]> 120 months), with an epigenetic profile similar to the control group. Secondly, an intermediate group (PFS = 84, TFT = 120 months) which shows an increase in DNA demethylation explained by SAT1 / TET2 induction during disease progression. Third, a group of patients with an active form of the disease (PFS = 52, TFT = 112 months) who have hyperlymphocytosis, a short lymphocyte doubling time, and major epigenetic changes. Within this group, a reduction is observed for 5-mCyt, 5-hmCyt, 5-CaCyt which is associated with a decrease in DNMTs, TETs and MBDs during disease progression. The identified epigenetic profiles are independent of IGHV mutational status but are associated with cytogenetic abnormalities. We were also interested in this association and we showed in the second study that modifications of cytosine derivatives levels can refine the prognostic power of cytogenetic abnormalities.In conclusion, our results suggest that methylation variations as well as DNA demethylation intermediates are involved in the progression of CLL
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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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8

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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Xue, Liting. "Oncogene Function in Pre-Leukemia Stage of INV(16) Acute Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/740.

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The CBFbeta-SMMHC fusion protein is expressed in acute myeloid leukemia (AML) samples with the chromosome inversion inv(16)(p13;q22). This fusion protein binds the transcription factor RUNX with higher affinity than its physiological partner CBFbeta and disrupts the core binding factor (CBF) activity in hematopoietic stem and progenitor cells. Studies in the Castilla laboratory have shown that CBFbeta-SMMHC expression blocks differentiation of hematopoietic progenitors, creating a pre-leukemic progenitor that progresses to AML in cooperation with other mutations. However, the combined function of cumulative cooperating mutations in the pre-leukemic progenitor cells that enhance their expansion to induce leukemia is not known. The standard treatment for inv(16) AML is based on the use of non-selective cytotoxic chemotherapy, resulting in a good initial response, but with limited long-term survival. Therefore, there is a need for developing targeted therapies with improved efficacy in leukemic cells and minimal toxicity for normal cells. Here, we used conditional Nras+/LSL-G12D; Cbfb+/56M; Mx1Cre knock-in mice to show that allelic expression of oncogenic N-RasG12D expanded the multi-potential progenitor (MPP) compartment by 8 fold. Allelic expression of Cbfbeta-SMMHC increased the MPPs and short-term hematopoietic stem cells (ST-HSCs) by 2 to 4 fold both alone and in combination with N-RasG12D expression. In addition, allelic expression of oncogenic N-RasG12D and Cbfbeta-SMMHC increases survival of pre-leukemic stem and progenitor cells. Differential analysis of bone marrow cells determined that Cbfb+/MYH11 and Nras+/G12D; vii Cbfb+/MYH11 cells included increased number of blasts, myeloblasts and promyelocytes and a reduction in immature granulocytes, suggesting that expression of N-RasG12D cannot bypass Cbfbeta-SMMHC driven differentiation block. N-RasG12D and Cbfbeta-SMMHC synergized in leukemia, in which Nras+/G12D; Cbfb+/MYH11 mice have a shorter median latency than Cbfb+/MYH11 mice. In addition, the synergy in leukemogenesis was cell autonomous. Notably, leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC showed higher (over 100 fold) leukemia-initiating cell activity in vivo than leukemic cells expressing Cbfbeta-SMMHC (L-IC activity of 1/4,000 and 1/528,334, respectively). Short term culture and biochemical assays revealed that pre-leukemic and leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC have reduced levels of pro-apoptotic protein Bim compared to control. The Nras+/G12D; CbfbMYH11 pre-leukemic and leukemic cells were sensitive to pharmacologic inhibition of MEK/ERK signaling pathway with increasing apoptosis and Bim protein levels but not sensitive to PI3K inhibitors. In addition, knock-down of Bcl2l11 (Bim) expression in Cbfbeta-SMMHC pre-leukemic progenitors decreased their apoptosis levels. In collaboration with Dr. John Bushweller’s and other research laboratories, we recently developed a CBFbeta-SMMHC inhibitor named AI-10-49, which specifically binds to CBFbeta-SMMHC, prevents its binding to RUNX proteins and restores CBF function. Biochemical analysis in human leukemic cells showed that AI-10-49 has significant specificity in reducing the viability of leukemic cells expressing CBFbeta-SMMHC (IC50= 0.83μM), and negligible toxicity in normal cells. Likewise, mouse Nras+/G12D; viii Cbfb+/MYH11 leukemic cells were sensitive to AI-10-49 (IC50= 0.93μM). By using the NrasLSL-G12D; Cbfb56M mouse model, we also show that AI-10-49 significantly prolongs the survival of mice bearing the leukemic cells. Preliminary mechanistic analysis of AI-10-49 activity has shown that AI-10-49 increased BCL2L11 transcript levels in a dose and time dependent manner in murine and human leukemic cells, suggesting that the viability through BIM-mediated apoptosis may be targeted by both oncogenic signals. My thesis study demonstrates that Cbfbeta-SMMHC and N-RasG12D promote the survival of pre-leukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define NrasLSL-G12D; Cbfb56M mice as a valuable genetic model for the study of inv(16) AML targeted therapies. For instance, the novel CBFbeta-SMMHC inhibitor AI-10-49 shows a significant efficacy in this mouse model. This small molecule will serve as a promising first generation drug for targeted therapy of inv(16) leukemia and also a very useful tool to understand mechanisms of leukemogenesis driving by CBFbeta-SMMHC.
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Xue, Liting. "Oncogene Function in Pre-Leukemia Stage of INV(16) Acute Myeloid Leukemia: A Dissertation." eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/740.

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The CBFbeta-SMMHC fusion protein is expressed in acute myeloid leukemia (AML) samples with the chromosome inversion inv(16)(p13;q22). This fusion protein binds the transcription factor RUNX with higher affinity than its physiological partner CBFbeta and disrupts the core binding factor (CBF) activity in hematopoietic stem and progenitor cells. Studies in the Castilla laboratory have shown that CBFbeta-SMMHC expression blocks differentiation of hematopoietic progenitors, creating a pre-leukemic progenitor that progresses to AML in cooperation with other mutations. However, the combined function of cumulative cooperating mutations in the pre-leukemic progenitor cells that enhance their expansion to induce leukemia is not known. The standard treatment for inv(16) AML is based on the use of non-selective cytotoxic chemotherapy, resulting in a good initial response, but with limited long-term survival. Therefore, there is a need for developing targeted therapies with improved efficacy in leukemic cells and minimal toxicity for normal cells. Here, we used conditional Nras+/LSL-G12D; Cbfb+/56M; Mx1Cre knock-in mice to show that allelic expression of oncogenic N-RasG12D expanded the multi-potential progenitor (MPP) compartment by 8 fold. Allelic expression of Cbfbeta-SMMHC increased the MPPs and short-term hematopoietic stem cells (ST-HSCs) by 2 to 4 fold both alone and in combination with N-RasG12D expression. In addition, allelic expression of oncogenic N-RasG12D and Cbfbeta-SMMHC increases survival of pre-leukemic stem and progenitor cells. Differential analysis of bone marrow cells determined that Cbfb+/MYH11 and Nras+/G12D; vii Cbfb+/MYH11 cells included increased number of blasts, myeloblasts and promyelocytes and a reduction in immature granulocytes, suggesting that expression of N-RasG12D cannot bypass Cbfbeta-SMMHC driven differentiation block. N-RasG12D and Cbfbeta-SMMHC synergized in leukemia, in which Nras+/G12D; Cbfb+/MYH11 mice have a shorter median latency than Cbfb+/MYH11 mice. In addition, the synergy in leukemogenesis was cell autonomous. Notably, leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC showed higher (over 100 fold) leukemia-initiating cell activity in vivo than leukemic cells expressing Cbfbeta-SMMHC (L-IC activity of 1/4,000 and 1/528,334, respectively). Short term culture and biochemical assays revealed that pre-leukemic and leukemic cells expressing N-RasG12D and Cbfbeta-SMMHC have reduced levels of pro-apoptotic protein Bim compared to control. The Nras+/G12D; CbfbMYH11 pre-leukemic and leukemic cells were sensitive to pharmacologic inhibition of MEK/ERK signaling pathway with increasing apoptosis and Bim protein levels but not sensitive to PI3K inhibitors. In addition, knock-down of Bcl2l11 (Bim) expression in Cbfbeta-SMMHC pre-leukemic progenitors decreased their apoptosis levels. In collaboration with Dr. John Bushweller’s and other research laboratories, we recently developed a CBFbeta-SMMHC inhibitor named AI-10-49, which specifically binds to CBFbeta-SMMHC, prevents its binding to RUNX proteins and restores CBF function. Biochemical analysis in human leukemic cells showed that AI-10-49 has significant specificity in reducing the viability of leukemic cells expressing CBFbeta-SMMHC (IC50= 0.83μM), and negligible toxicity in normal cells. Likewise, mouse Nras+/G12D; viii Cbfb+/MYH11 leukemic cells were sensitive to AI-10-49 (IC50= 0.93μM). By using the NrasLSL-G12D; Cbfb56M mouse model, we also show that AI-10-49 significantly prolongs the survival of mice bearing the leukemic cells. Preliminary mechanistic analysis of AI-10-49 activity has shown that AI-10-49 increased BCL2L11 transcript levels in a dose and time dependent manner in murine and human leukemic cells, suggesting that the viability through BIM-mediated apoptosis may be targeted by both oncogenic signals. My thesis study demonstrates that Cbfbeta-SMMHC and N-RasG12D promote the survival of pre-leukemic myeloid progenitors primed for leukemia by activation of the MEK/ERK/Bim axis, and define NrasLSL-G12D; Cbfb56M mice as a valuable genetic model for the study of inv(16) AML targeted therapies. For instance, the novel CBFbeta-SMMHC inhibitor AI-10-49 shows a significant efficacy in this mouse model. This small molecule will serve as a promising first generation drug for targeted therapy of inv(16) leukemia and also a very useful tool to understand mechanisms of leukemogenesis driving by CBFbeta-SMMHC.
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Books on the topic "Leukemia"

1

William, Dameshek, Gunz Frederick, and Henderson Edward S, eds. Leukemia. 6th ed. Philadelphia: Saunders, 1996.

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Peacock, Judith. Leukemia. Mankato, Mn: LifeMatters, 2000.

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Wilmoth, Lerner Adrienne, ed. Leukemia. Detroit: Greenhaven Press, 2009.

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Eric So, Chi Wai, ed. Leukemia. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6.

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Weissman, I. L., ed. Leukemia. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-69722-7.

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Goldsmith, Connie. Leukemia. Minneapolis: Twenty-First Century Books, 2012.

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Parks, Peggy J. Leukemia. San Diego, CA: Daniel A. Leone, Publisher, 2009.

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B, Silverstein Virginia, and Nunn Laura Silverstein, eds. Leukemia. Berkeley Heights, NJ, USA: Enslow Publishers, 2000.

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National Institutes of Health (U.S.), ed. Leukemia. [Bethesda, Md.?]: National Institutes of Health, 1985.

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Chamberlain, Joan. Leukemia. [Bethesda, MD]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, 1987.

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Book chapters on the topic "Leukemia"

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Jamieson, Catriona H. M., Emmanuelle Passegué, and Irving L. Weissman. "Leukemia and Leukemic Stem Cells." In Stem Cells in the Nervous System: Functional and Clinical Implications, 157–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18883-1_12.

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So, Chi Wai Eric. "An Overview: From Discovery of Candidate Mutations to Disease Modeling and Transformation Mechanisms of Acute Leukemia." In Leukemia, 1–5. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_1.

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Zeisig, Bernd B., and Chi Wai Eric So. "Retroviral/Lentiviral Transduction and Transformation Assay." In Leukemia, 207–29. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_10.

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Krivtsov, Andrei V., Yingzi Wang, Zhaohui Feng, and Scott A. Armstrong. "Gene Expression Profiling of Leukemia Stem Cells." In Leukemia, 231–46. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_11.

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Bonnet, Dominique. "Humanized Model to Study Leukemic Stem Cells." In Leukemia, 247–62. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_12.

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Wunderlich, Mark, and James C. Mulloy. "Model Systems for Examining Effects of Leukemia Associated Oncogenes in Primary Human CD34+ Cells via Retroviral Transduction." In Leukemia, 263–85. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_13.

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Schuringa, Jan Jacob, and Hein Schepers. "Ex Vivo Assays to Study Self-Renewal and Long-Term Expansion of Genetically Modified Primary Human Acute Myeloid Leukemia Stem Cells." In Leukemia, 287–300. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_14.

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Yeung, Jenny, and and Chi Wai Eric So. "Identification and Characterization of Hematopoietic Stem and Progenitor Cell Populations in Mouse Bone Marrow by Flow Cytometry." In Leukemia, 301–15. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_15.

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Sroczynska, Patrycja, Christophe Lancrin, Stella Pearson, Valerie Kouskoff, and Georges Lacaud. "In Vitro Differentiation of Embryonic Stem Cells as a Model of Early Hematopoietic Development." In Leukemia, 317–34. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_16.

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Ottersbach, Katrin, and Elaine Dzierzak. "Analysis of the Mouse Placenta as a Hematopoietic Stem Cell Niche." In Leukemia, 335–46. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-59745-418-6_17.

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Conference papers on the topic "Leukemia"

1

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

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Leukemia is a kind of blood cancer that may cause significant damage to a person's general health. It is characterized by the production of an excessive number of white blood cells. To address leukemia quickly and effectively, it is important to have a diagnosis that is both correct and quick. Not too long ago, experts started using AI methods to help find cancer much earlier. One of the hardest parts of making a method to find leukemia is separating the nuclei from the rest of the picture. When medical staff use quick and accurate division methods, they can find patients faster and treat them more effectively. So far, hybrid clustering algorithms have been very helpful in the process of picture segmentation in the field of medical image processing. To find leukemias like chronic myeloid leukemia (CML) and chronic lymphocytic leukemia (CLL), this study looks into segmentation methods that use machine learning (ML) and deep learning (DL). The study looks at how many ML and DL algorithms can be used to automatically diagnose different types of leukemia. It is checked to see how well the ML and DL algorithms do at segmentation, pre-processing, feature extraction, selection, and total classification accuracy.
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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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Tanaka, H., N. Narahara, H. Sadakata, K. Andoh, N. Kobayashi, and T. Maekawa. "ANALYSIS OF LEUKEMIA PELT. TISSUE FACTOR BY WESTERN BLOTTING TECHNIQUE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643285.

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It has been reported that the tissue factor(TF) of monocytes and leukemic leukocytes is one of the trigger substances of disseminated intravascular coagulation(DIC) in leukemia patients. To assess the properties of TF of leukemia cells, their TF was analyzed by the method of Western blotting. Placenta TF was purified using Concanavalin-A affinity chromatography. Briefly, human placenta TF was extracted from placenta acetone powder using Triton X-100 extraction and purified by Concanavalin-A affinity chromatography and SDS-preparative PAGE. Hie final product of the purified placenta TF-apoprotein exhibited a molecular weight (MW) approximately 46 kD in non-reduced condition and 47 kD in reduced condition and showed single band on analytical SDS-PAGE. Activity of purified placenta apo-TF after relipidation with placenta phospholipid was 4500 units/mg and was 6300 times purified from the starting material. Serum IgG fraction was separated from rabbits after 8 times weekly injections of purified placenta TF. This anti-TF-IgG fraction showed single precipitin line against purified placenta apo-TF and inhibited procoagulant activity of saline extract of the placenta as well as those of homogenates of the endotoxin(LPS)-stimulated Molt-4 cells and U-937 cells. Using this antibody, analysis of TF of cultured leukemia cells(Molt-4 and U-937) and acute promyelocytic leukemia(APL) cells was done by the Western blotting technique as follows: LPS-stimulated Molt-4, U-937 or APL cells were homogenized, delipidated and solubilized with 1% SDS-PAGE. Thereafter, Western blotting was done by the method of Towbin and TF of the blotted protein was immunologically identified. The nitrocellulose paper was soaked with anti-TF-IgG for 18 hours’, then peroxidase-conjugated anti-rabbit-goat IgG was used as an indicator of the antibody and o-dianisidine as substrate. In either case of APL cells, LPS-stimulated Molt-4 or U-937, single band which showed procoagulant activity was detected and the MW of the protein was approximately 48 kD in non-reduced condition. These results indicate that TF of all these leukemic leukocytes has common antigenic determinant and equal MW to placenta TF.
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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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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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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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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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Pabinger, I., K. T. Lechner, P. Bettelheim, R. Dudczak, W. Hinterberger, C. Korninger, and I. Int Medicine. "COAGULATION ACTIVATION AND OCCURRENCE OF HYPOFIBRINOGENEMIA IN PATIENTS WITH ACUTE NONLYMPHOBLASTIC LEUKEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643672.

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122 consecutive adult patients (pts) with acute nonlympho-blastic leukemia (ANLL) were studied for evidence of coagulation activation andoccurrence of hypofibrinogenemia. In 16 pts (13%) decreased fibrinogenlevels (< 1.5g/l) were found.Data on fibrinopeptide A levels (FPA), ethanol gelation test (EGT) andfibrin(ogen) degredation products(FDP) are listed in the table:The occurrence of hypofibrinogenemia was not correlated to the peripheral blast cell count. 10/18 pts with M3 (FAB-classifica-tion), 2/46pts with M2, 2/25 pts with M4 and 2/14 pts with M5 leukemia developed hypofibrinogenemia. Early death occurred in 31% of pts with hypofibrinogenemia (in most pts due to hemorrhage) and only in 10% without (in most pts due to septicemia). No significant difference in remission duration was found between the 2 groups. 48 patients were reinvestigated at the time of recurrence of disease. 5 of 7 patients with and 38 of 41 patients without initial hypofibrinogenemia had a coagulation pattern similar to the one observed at first presentation.The following conclusions can bedrawn:(1) In most patients with ANLL there is evidence of coagulation activation. (2) Hypofibrinogenemia in patients with ANLL appears to bethrombin mediated. Therefore the term disseminated intravascular coagulation (DIC) may be used. (3) DIC is strongly associated with the subtype M3 (promyelocytic L), but may as well occur in other ANLL subtypes.(4) The presence of DIC seems to be a specific property of certain leukemic clones. This assumption is supported by the coagulation studiesduring recurrence of ANLL. (5) Patients with low fibrinogen levels areat high risk of early death due to hemorrhagic complications.
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Lau, J., M. Cecchini, E. S. Yi, and H. R. Cajigas. "More Than Meets the Eye: Bronchopulmonary Leukemic Infiltrates in Chronic Lymphocytic 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.a5864.

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Gopigari, Niveditha, and Tripty Singh. "Comparision of Segmentation Techniques for Acute Lymphoblastic Leukemia in Leukemia Cancer." In 2022 13th International Conference on Computing Communication and Networking Technologies (ICCCNT). IEEE, 2022. http://dx.doi.org/10.1109/icccnt54827.2022.9984527.

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Reports on the topic "Leukemia"

1

Shlomchik, Warren D. Mechanisms of Graft-vs.-Leukemia Against a Novel Murine Model of Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, July 2005. http://dx.doi.org/10.21236/ada443726.

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Shlomchik, Warren D. Mechanisms of Graft-vs. -Leukemia Against a Novel Murine Model of Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada426337.

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Shlomchik, Warren D. Mechanisms of Graft-vs.-Leukemia against a Novel Murine Model of Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada464064.

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

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Ileal perforation peritonitis is a critical surgical emergency often encountered in developing countries, commonly associated with typhoid fever, tuberculosis, trauma, and non-specific enteritis. This case report presents a unique instance of nonspecific enteritis associated with chronic myeloid leukemia (CML). A 16-year-old girl with a history of pulmonary tuberculosis presented with symptoms, leading to the diagnosis of ileal perforations and CML. Surgical intervention involved ileal resection and double barrel ileostomy. The postoperative course included complications and chemotherapy with imatinib, demonstrating the challenges and management strategies in such cases. The discussion emphasizes the varied aetiologies of non-traumatic ileal perforation in different regions and sheds light on the rare gastrointestinal manifestations of CML. Notably, this report underscores the significance of prompt imatinib therapy in controlling CML while highlighting the need for vigilant monitoring and dose adjustments due to chemotherapy-related adverse effects.
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Untaaveesup, Suvijak, Sasinipa Trithiphen, Kamolchanok Kulchutisin, Tarinee Rungjirajittranon, Sujitra Panyoy, Thanapon Kaokunakorn, Nattawut Leelakanok, and Weerapat Owattanapanich. Genetic Alterations in Extramedullary Leukemia among Acute Myeloid Leukemia Patients: Insights from a Cohort Study and Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2023. http://dx.doi.org/10.37766/inplasy2023.8.0091.

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Davis, Jalin, Summer Hood, Alex Miller, Sam Stein, and Kaylee Stem. Effectiveness of Aerobic Exercise for Adults with Leukemia. University of Tennessee Health Science Center, May 2020. http://dx.doi.org/10.21007/chp.mot2.2020.0001.

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Shannon, Kevin M. Molecular Analysis of Preleukemic and Leukemic Bone Marrow from Children with Monosomy V Syndrome and Juvenile Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, October 1996. http://dx.doi.org/10.21236/ada324280.

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Wang, Jean Y. Pathogenic Mechanism of Malignant Progression in Chronic Myelogenous Leukemia. Fort Belvoir, VA: Defense Technical Information Center, September 2005. http://dx.doi.org/10.21236/ada446373.

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Haas, M. Radiation-induced leukemia: Comparative studies in mouse and man. Office of Scientific and Technical Information (OSTI), January 1991. http://dx.doi.org/10.2172/6053623.

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Hingley, Sally. Psycho-social Aspects of Acute Lymphocytic Leukemia in Children. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.1616.

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