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Artykuły w czasopismach na temat „Leukemia”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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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 (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

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2

Gilliland, D. Gary, Craig T. Jordan, and Carolyn A. Felix. "The Molecular Basis of Leukemia." Hematology 2004, no. 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

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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 (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

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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 (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

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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 (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 patient

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6

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 (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 ne

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7

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 (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

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8

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 (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 karyoty

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9

Kogan, Scott C., Diane E. Brown, David B. Shultz та ін. "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, № 4 (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 marke

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10

Wang, Wei, Magdalena Czader, and Sa A. Wang. "Blood- and bone marrow–based mature T-cell and natural killer cell leukemias and lymphomas: a summary in the series of the 2023 SH/EAHP Workshop." American Journal of Clinical Pathology 164, no. 1 (2025): 7–25. https://doi.org/10.1093/ajcp/aqaf009.

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Abstract This session included 51 cases submitted to the workshop “Progress in T- and NK-cell Lymphomas and Leukemias” by the Society for Hematopathology and European Association for Haematopathology under “Blood/Bone Marrow–Based Mature T- and NK-Cell Leukemias/Lymphomas” or “T/NK-cell neoplasms with a Leukemic Presentation.” Entities encompassed T-cell prolymphocytic leukemia, T-cell large granular lymphocytic leukemia (LGLL), natural killer (NK)-LGLL/chronic lymphoproliferative disorder of NK cells, adult T-cell leukemia/lymphoma, aggressive NK-cell leukemia, and their mimics. Submitted cas

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11

Buss, Eike C., Alexander Kalinkovich, Amir Schajnovitz, et al. "In Vivo Mobilization of Leukemic Human Precursor-B-ALL Cells by the CXCR4-Antagonist AMD3100 Is Via Secretion of SDF-1 and Synergistically by Catecholamine Action." Blood 112, no. 11 (2008): 1920. http://dx.doi.org/10.1182/blood.v112.11.1920.1920.

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Abstract Introduction Mobilization of leukemic cells from the bone marrow (BM) to the circulation in order to better kill them with DNA damaging chemotherapy agents is emerging as a new experimental therapeutic intervention, however the mechanism is not entirely clear. Currently CXCR4-antagonists such as the mobilizing agent AMD3100 (AMD) are becoming available for clinical usage. The aim of this study is to explore mechanisms of human precursor-B-ALL cell mobilization from the BM in a functional, pre-clinical immune deficient mouse model. Methodology Immunodeficient mice were stably engrafted

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12

Granados Romero, Francisco Fabian, and Enma maría Guadamud Lorenti. "Acute lymphoblastic leukemia." Journal of America health 1, no. 1 (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 w

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13

Swatler, Julian, Laura Turos-Korgul, Marta Brewinska-Olchowik, et al. "4-1BBL–containing leukemic extracellular vesicles promote immunosuppressive effector regulatory T cells." Blood Advances 6, no. 6 (2022): 1879–94. http://dx.doi.org/10.1182/bloodadvances.2021006195.

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Abstract Chronic and acute myeloid leukemia evade immune system surveillance and induce immunosuppression by expanding proleukemic Foxp3+ regulatory T cells (Tregs). High levels of immunosuppressive Tregs predict inferior response to chemotherapy, leukemia relapse, and shorter survival. However, mechanisms that promote Tregs in myeloid leukemias remain largely unexplored. Here, we identify leukemic extracellular vesicles (EVs) as drivers of effector proleukemic Tregs. Using mouse model of leukemia-like disease, we found that Rab27a-dependent secretion of leukemic EVs promoted leukemia engraftm

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14

Paiva, Aldair Sousa, Hugo Diogenes De Oliveira Paiva, Geraldo Barroso Cavalcanti, et al. "Contribution of Flow Cytometry Immunophenotyping in Diagnostic of Acute and Chronic Leukemias." Blood 132, Supplement 1 (2018): 5198. http://dx.doi.org/10.1182/blood-2018-99-118923.

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Abstract BACKGROUND: Today immunophenotyping by flow cytometry is an useful adjunct to cytomorphologyc analysis to correct diagnostic of leukemias. It provides objective and quantitative data allowing for a high level of sensitivity detection and better characterization of acute and chronic leukemias. The purpose of this study was to demonstrate the contribution of the immunophenotyping by monoclonal antibodies (Mo.Ab.) in leukemic cells from patients with acute and chronic leukemias. METHODS: Analyzed 76 patients with leukemias before the treatment. The diagnostic of leukemias was based on th

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15

Kogan, Scott C., Suk-hyun Hong, David B. Shultz, Martin L. Privalsky та J. Michael Bishop. "Leukemia initiated by PMLRARα: the PML domain plays a critical role while retinoic acid–mediated transactivation is dispensable". Blood 95, № 5 (2000): 1541–50. http://dx.doi.org/10.1182/blood.v95.5.1541.005k28_1541_1550.

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The most common chromosomal translocation in acute promyelocytic leukemia (APL), t15;17(q22;q21), creates PMLRAR andRARPML fusion genes. We previously developed a mouse model of APL by expressing PMLRAR in murine myeloid cells. In order to examine the mechanisms by which PMLRAR can initiate leukemia, we have now generated transgenic mice expressingPMLRARm4 and RARm4, proteins that are unable to activate transcription in response to retinoic acid.PMLRARm4 transgenic mice developed myeloid leukemia, demonstrating that transcriptional activation by PMLRAR is not required for leukemic tran

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16

Kettyle, Laura M., Charles-Étienne Lebert-Ghali, Ivan V. Grishagin, et al. "Pathways, Processes, and Candidate Drugs Associated with a Hoxa Cluster-Dependency Model of Leukemia." Cancers 11, no. 12 (2019): 2036. http://dx.doi.org/10.3390/cancers11122036.

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High expression of the HOXA cluster correlates with poor clinical outcome in acute myeloid leukemias, particularly those harboring rearrangements of the mixed-lineage-leukemia gene (MLLr). Whilst decreased HOXA expression acts as a readout for candidate experimental therapies, the necessity of the HOXA cluster for leukemia maintenance has not been fully explored. Primary leukemias were generated in hematopoietic stem/progenitor cells from Cre responsive transgenic mice for conditional deletion of the Hoxa locus. Hoxa deletion resulted in reduced proliferation and colony formation in which surv

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17

Shvachko, L. P. "EMT-mechanizm induces the leukemic stemness phenotype in myeloid leukemias." Faktori eksperimental'noi evolucii organizmiv 23 (September 9, 2018): 256–60. http://dx.doi.org/10.7124/feeo.v23.1024.

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

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18

Santoro, E. Y., I. V. Kinchina, and V. I. Vetsega. "Leukemic optic disc infiltration in a patient with chronic myeloid leukemia: a clinical case." Modern technologies in ophtalmology, no. 1 (March 28, 2023): 354–57. http://dx.doi.org/10.25276/2312-4911-2023-1-354-357.

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Chronic myeloid leukemia is a malignant blood disease characterized by malignant transformation of hematopoetic progenitor cells, damage to the bone marrow, and other organs and systems. One of the rare manifestations of chronic myeloid leukemia is leukemiс infiltration of the optic disc. This process is characterized by damage to the optic nerve and nervous system by blast cells, which is an unfavorable prognosis for patients. It is important for an ophthalmologist to detect the disease and differentiate leukemic infiltration from other diseases accompanied by hemorrhages and optic disc edema

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19

Ahuja, HG, PS Jat, A. Foti, M. Bar-Eli, and MJ Cline. "Abnormalities of the retinoblastoma gene in the pathogenesis of acute leukemia." Blood 78, no. 12 (1991): 3259–68. http://dx.doi.org/10.1182/blood.v78.12.3259.3259.

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Abstract The retinoblastoma-susceptibility (Rb) gene is an antioncogene that is frequently altered in retinoblastomas, sarcomas, and some epithelial tumors. We examined the structure of the Rb gene by Southern blotting in 215 cases of leukemias and lymphomas of diverse phenotype and in 15 leukemic cell lines. In selected cases Rb protein expression was examined with specific monoclonal antibodies. Structural abnormalities of the Rb gene with absent protein expression were frequent in all types of human acute leukemia, but were particularly common (27% incidence) in M4 and M5 myeloid leukemia w

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Ahuja, HG, PS Jat, A. Foti, M. Bar-Eli, and MJ Cline. "Abnormalities of the retinoblastoma gene in the pathogenesis of acute leukemia." Blood 78, no. 12 (1991): 3259–68. http://dx.doi.org/10.1182/blood.v78.12.3259.bloodjournal78123259.

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The retinoblastoma-susceptibility (Rb) gene is an antioncogene that is frequently altered in retinoblastomas, sarcomas, and some epithelial tumors. We examined the structure of the Rb gene by Southern blotting in 215 cases of leukemias and lymphomas of diverse phenotype and in 15 leukemic cell lines. In selected cases Rb protein expression was examined with specific monoclonal antibodies. Structural abnormalities of the Rb gene with absent protein expression were frequent in all types of human acute leukemia, but were particularly common (27% incidence) in M4 and M5 myeloid leukemia with monoc

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21

Namikawa, R., R. Ueda, and S. Kyoizumi. "Growth of human myeloid leukemias in the human marrow environment of SCID-hu mice." Blood 82, no. 8 (1993): 2526–36. http://dx.doi.org/10.1182/blood.v82.8.2526.2526.

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Abstract It has been shown previously that multilineage human hematopoiesis is maintained within human fetal bone marrow (BM) fragments implanted into severe combined immunodeficient (SCID) mice. We describe here an application of this animal model, the SCID-hu mouse, to the study of human myeloid leukemias. BM cells from 8 patients with various types of myeloid leukemias were injected directly into human bone grafts in the SCID-hu mouse. Cells from 7 patients grew in the human marrow without spreading to the mouse marrow. Cells from 6 of these patients were successfully transferred in vivo to

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22

Namikawa, R., R. Ueda, and S. Kyoizumi. "Growth of human myeloid leukemias in the human marrow environment of SCID-hu mice." Blood 82, no. 8 (1993): 2526–36. http://dx.doi.org/10.1182/blood.v82.8.2526.bloodjournal8282526.

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It has been shown previously that multilineage human hematopoiesis is maintained within human fetal bone marrow (BM) fragments implanted into severe combined immunodeficient (SCID) mice. We describe here an application of this animal model, the SCID-hu mouse, to the study of human myeloid leukemias. BM cells from 8 patients with various types of myeloid leukemias were injected directly into human bone grafts in the SCID-hu mouse. Cells from 7 patients grew in the human marrow without spreading to the mouse marrow. Cells from 6 of these patients were successfully transferred in vivo to secondar

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23

Heumann, D., G. Losa, C. Barras, A. Morell, and V. von Fliedner. "Characterization of acute undifferentiated leukemia by combined analysis of plasma membrane-associated gamma-glutamyltranspeptidase and soluble terminal transferase." Blood 66, no. 2 (1985): 255–58. http://dx.doi.org/10.1182/blood.v66.2.255.bloodjournal662255.

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gamma-Glutamyltranspeptidase (gamma-GT) is a plasma membrane-associated enzyme present in blasts of certain acute leukemias. We analyzed 90 cases of undifferentiated and differentiated acute leukemias for gamma- GT, using a colorimetric assay. Blasts of all patients with common acute lymphoblastic leukemia (ALL) and T-ALL were negative for gamma-GT (less than 5 units). In contrast, gamma-GT was significantly elevated in acute myeloblastic or monoblastic leukemia blasts (P less than .001). In 16 cases of acute undifferentiated leukemia (AUL) studied, the levels of gamma-GT ranged from 0 to 93 u

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Liao, Aijun, Kathleen Broeg, Todd Fox, et al. "Therapeutic efficacy of FTY720 in a rat model of NK-cell leukemia." Blood 118, no. 10 (2011): 2793–800. http://dx.doi.org/10.1182/blood-2011-01-331447.

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Abstract NK-cell leukemia is a clonal expansion of NK cells. The illness can occur in an aggressive or chronic form. We studied cell lines from human and rat NK-cell leukemias (aggressive NK-cell leukemia) as well as samples from patients with chronic NK-cell leukemia to investigate pathogenic mechanisms. Here we report that Mcl-1 was overexpressed in leukemic NK cells and that knockdown of Mcl-1 induced apoptosis in these leukemic cells. In vitro treatment of human and rat NK leukemia cells with FTY720 led to caspase-dependent apoptosis and decreased Mcl-1 expression in a time- and-dose-depen

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25

Venugopalan, Radhika K., Neha Singh, Michael L. Anthony, et al. "Leukemia-associated aberrant immunophenotype: A flow cytometry-based experience of 110 cases from a tertiary care center in Northern India." Journal of Cancer Research and Therapeutics 19, no. 5 (2023): 1335–39. http://dx.doi.org/10.4103/jcrt.jcrt_809_21.

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ABSTRACT Background: Leukemic cells express a characteristic set of “cluster of differentiation” (CD) markers, which forms the basis of the current WHO classification. Leukemia-associated aberrant immunophenotype (LAIP) refers to expression of unusual CD markers by leukemic cells, which are not normally expressed by their respective lineage. The incidence of LAIP varies considerably, and its clinical implications, prognostic relevance, and sensitivity to therapy are still debatable. This study was conducted to identify the immunophenotypic aberrancies in newly diagnosed leukemias in our Instit

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Bernt, Kathrin M., and Scott A. Armstrong. "Targeting Epigenetic Programs in MLL-Rearranged Leukemias." Hematology 2011, no. 1 (2011): 354–60. http://dx.doi.org/10.1182/asheducation-2011.1.354.

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Abstract Rearrangements of the Mixed-Lineage Leukemia (MLL) gene are found in > 70% of infant leukemia, ∼ 10% of adult acute myelogenous leukemia (AML), and many cases of secondary acute leukemias. The presence of an MLL rearrangement generally confers a poor prognosis. There are more than 60 known fusion partners of MLL having some correlation with disease phenotype and prognosis. The most common fusion proteins induce the inappropriate expression of homeotic (Hox) genes, which, during normal hematopoiesis, are maintained by wild-type MLL. MLL-rearranged leukemias display remarkable genomi

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Pandey, Sony, Mustafa Moazam, Kurtis Eisermann, Jeffrey Hord, Gail Fraizer, and Steven J. Kuerbitz. "The Importance of WT1 in Leukemia." Blood 118, no. 21 (2011): 4645. http://dx.doi.org/10.1182/blood.v118.21.4645.4645.

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Abstract Abstract 4645 Acute leukemias collectively comprise the most common group of malignancies in the pediatric age group. Increasingly, therapeutic approach and prognosis are influenced by leukemia-specific cytogenetic abnormalities and genetic alterations, thus highlighting the importance of identifying novel prognostic markers. The Wilms’ tumor suppressor gene WT1 is expressed in leukemic blasts and is found to be mutated in approximately 10 percent of leukemia cases. Although it is unclear whether WT1 acts as an oncogene or a tumor suppressor gene in leukemia, it is known to regulate g

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Longo, Giuseppe S. A., Richard Gorlick, William P. Tong, Emine Ercikan, and Joseph R. Bertino. "Disparate Affinities of Antifolates for Folylpolyglutamate Synthetase From Human Leukemia Cells." Blood 90, no. 3 (1997): 1241–45. http://dx.doi.org/10.1182/blood.v90.3.1241.

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Abstract Previous work showed that acute myelocytic leukemia blasts accumulate less long chain polyglutamates of methotrexate (MTX) than acute lymphocytic leukemia blasts when incubated with this radiolabeled antifolate. This difference likely explains the increased sensitivity of lymphoid leukemias to short-term exposure of MTX as compared with myeloid leukemias. In this study, we examined the basis for differences between long chain MTX polyglutamate accumulation between different leukemia cell types using both leukemia cell lines and blasts freshly isolated from blood of leukemic patients.

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Longo, Giuseppe S. A., Richard Gorlick, William P. Tong, Emine Ercikan, and Joseph R. Bertino. "Disparate Affinities of Antifolates for Folylpolyglutamate Synthetase From Human Leukemia Cells." Blood 90, no. 3 (1997): 1241–45. http://dx.doi.org/10.1182/blood.v90.3.1241.1241_1241_1245.

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Previous work showed that acute myelocytic leukemia blasts accumulate less long chain polyglutamates of methotrexate (MTX) than acute lymphocytic leukemia blasts when incubated with this radiolabeled antifolate. This difference likely explains the increased sensitivity of lymphoid leukemias to short-term exposure of MTX as compared with myeloid leukemias. In this study, we examined the basis for differences between long chain MTX polyglutamate accumulation between different leukemia cell types using both leukemia cell lines and blasts freshly isolated from blood of leukemic patients. The major

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Tsuruta-Kishino, Takako, Keisuke Kataoka, Hiroshi Kobayashi, et al. "Loss Of p53 Induces Leukemic Transformation In a Murine Model Of JAK2V617F-Induced Polycythemia Vera." Blood 122, no. 21 (2013): 269. http://dx.doi.org/10.1182/blood.v122.21.269.269.

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Abstract Myeloproliferative neoplasms (MPN) have an inherent tendency toward leukemic transformation, but its mechanisms remain largely unknown. Recently, TP53 mutation is reported to be frequently found in cases with post-MPN leukemia. Here, to address the contribution of p53 loss to leukemic transformation from MPN in vivo, we retrovirally transduced c-kit+ bone marrow (BM) cells from p53 knockout (p53-/-) and littermate mice (p53+/+) with either wild-type Jak2 (Jak2WT) or Jak2V617F respectively, and transplanted them into lethally irradiated mice. At 3 weeks after transplantation, both reci

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Ling, Di, Ralph B. Arlinghaus, and Xiaoyang Ling. "Vaccination with Leukemia Cell Expression Membrane Bound GM-CSF Overcomes the Host Immunosuppression Induced by Leukemia." Blood 112, no. 11 (2008): 5435. http://dx.doi.org/10.1182/blood.v112.11.5435.5435.

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Abstract Immunotherapy of leukemia involves stimulating host-cell mediated immunity by facilitating immune recognition of leukemia cells, which are normally weakly immunogenic. We previously showed that vaccination with membrane bound GM-CSF leukemic cells protects mice from leukemia challenge (Ling et al., Oncogene, 2007). In these studies, after addition of a transmembrane domain to the original GM-CSF coding sequence (tmGM-CSF), the construct was transduced into murine leukemia cells (WEHI-3B), which was shown to be more than 98% on the cell surface. Vaccination with lethally irradiated tmG

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Heumann, D., G. Losa, C. Barras, A. Morell, and V. von Fliedner. "Characterization of acute undifferentiated leukemia by combined analysis of plasma membrane-associated gamma-glutamyltranspeptidase and soluble terminal transferase." Blood 66, no. 2 (1985): 255–58. http://dx.doi.org/10.1182/blood.v66.2.255.255.

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Abstract gamma-Glutamyltranspeptidase (gamma-GT) is a plasma membrane-associated enzyme present in blasts of certain acute leukemias. We analyzed 90 cases of undifferentiated and differentiated acute leukemias for gamma- GT, using a colorimetric assay. Blasts of all patients with common acute lymphoblastic leukemia (ALL) and T-ALL were negative for gamma-GT (less than 5 units). In contrast, gamma-GT was significantly elevated in acute myeloblastic or monoblastic leukemia blasts (P less than .001). In 16 cases of acute undifferentiated leukemia (AUL) studied, the levels of gamma-GT ranged from

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Quere, Ronan, Silja Andradottir, Ann Brun, et al. "High Levels of the Adhesion Molecule CD44 on Leukemic Cells Generate Acute Myeloid Leukemia Relapse After Withdrawal of the Initial Transforming Event." Blood 116, no. 21 (2010): 3154. http://dx.doi.org/10.1182/blood.v116.21.3154.3154.

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Abstract Abstract 3154 Multiple genetic hits are detected in patients with acute myeloid leukemia (AML). To investigate this further, we developed a tetracycline inducible mouse model of AML, where the initial transforming event, overexpression of HOXA10, can be eliminated. Continuous overexpression of HOXA10 is required to generate AML in primary recipient mice, but is not essential for maintenance of the leukemia. Transplantation of AML to secondary recipients showed that in established leukemias, ∼80% of the leukemia-initiating cells (LICs) in bone marrow stopped proliferating upon withdraw

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Matulonis, UA, C. Dosiou, C. Lamont, et al. "Role of B7-1 in mediating an immune response to myeloid leukemia cells." Blood 85, no. 9 (1995): 2507–15. http://dx.doi.org/10.1182/blood.v85.9.2507.bloodjournal8592507.

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A costimulatory signal from B7–1 (CD80) to its counter-receptor CD28 is required for T-cell activation. Many tumors, including most human leukemias, lack expression of B7–1, and this has been suggested to contribute to the failure of immune recognition of these diseases. A murine leukemia model system was developed to assess the potential role of B7–1 in the induction immunity to leukemia cells. The nonleukemic 32Dc13 myeloid cell line was transformed by transfection of the BCR/ABL gene, generating a subline (32Dp210/clone 26) that was leukemic and rapidly lethal to syngeneic, immunocompetent

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Cantilena, Caroline R., Xin Zhao, Sachiko Kajigaya, et al. "Activity of the Telomerase Inhibitor GRN163L (Imetelstat) on Acute Myeloblastic Leukemia Blasts Is Enhanced By DNA Methyltransferase Inhibitors Irrespective of TERT Promoter Methylation Status." Blood 126, no. 23 (2015): 1267. http://dx.doi.org/10.1182/blood.v126.23.1267.1267.

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Abstract Introduction. The high telomerase activity in leukemia cells protects them from proliferation arrest, senescence, and apoptosis and may be driven by mutation or epigenetic alteration in the telomerase promoter. However, the mechanism of telomerase regulation and potential therapeutic application of telomerase inhibition in leukemia are not fully understood. We evaluated epigenetic methylation patterns in the telomerase promoter region in myeloid cell lines and primary acute myeloid leukemia (AML) blasts. These epigenetic patterns may serve as a biomarker for sensitivity to DNA methylt

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Wasfa Sana, Abid ur Rehman, Bisma Ahmed, Md Abu Sayeed, and Mashhood uz Zafar Farooq. "Association of DNA Repair XRCC1 Gene Polymorphism with Leukemia." Indus Journal of Bioscience Research 2, no. 2 (2024): 719–31. https://doi.org/10.70749/ijbr.v2i02.242.

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A group of cancerous diseases of the blood and bone marrow known as leukemias are life-threatening. It is crucial to recognize the leukemic cells lineage when making a diagnosis of leukemia because treatment for the disease depends on whether the cells are myeloid or lymphoid. As per the Observation There is total 300 blood samples in which 150 were leukemic patients and 150 were healthy person. The genotype distribution frequencies of the XRCC1 gene's SNP rs25487 results demonstrate a highly significant connection between heterozygous (GA) rs25487 of the XRCC1 gene and an increased risk of le

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Jacob, Bindya, Motomi Osato, Namiko Yamashita, et al. "Stem cell exhaustion due to Runx1 deficiency is prevented by Evi5 activation in leukemogenesis." Blood 115, no. 8 (2010): 1610–20. http://dx.doi.org/10.1182/blood-2009-07-232249.

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Abstract The RUNX1/AML1 gene is the most frequently mutated gene in human leukemia. Conditional deletion of Runx1 in adult mice results in an increase of hematopoietic stem cells (HSCs), which serve as target cells for leukemia; however, Runx1−/− mice do not develop spontaneous leukemia. Here we show that maintenance of Runx1−/− HSCs is compromised, progressively resulting in HSC exhaustion. In leukemia development, the stem cell exhaustion was rescued by additional genetic changes. Retroviral insertional mutagenesis revealed Evi5 activation as a cooperating genetic alteration and EVI5 overexp

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Gebbia, Vittorio, Pietro Citarrella, Vincenzo Miserendino, et al. "The Effects of the Macrocyclic Lactone Bryostatin-1 on Leukemic Cells in Vitro." Tumori Journal 78, no. 3 (1992): 167–71. http://dx.doi.org/10.1177/030089169207800304.

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The macrocyclic lactone bryostatin-1 was found to exert in vitro antineoplastic activity against several leukemic cell lines, including human K562 erythroleukemia, HL60 promyelocytic leukemia, REH and MOLT-4 lymphoblastic leukemias, CCRFCEM lymphoma, KG-1 myeloid leukemia, and murine P388 lymphocytic leukemia. No statistically significant difference in sensitivity to bryostatin-1 was found between adriamycin-resistant P388 and K526 subclones and their sensitive counterparts. Freshly explanted clonogenic leukemic cells showed a variable sensitivity to bryostatin-1 in 10/12 tested samples. The I

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

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Leukemia, a wide spectrum of diseases with altered proliferation and differentiation capacity of myeloid and lymphoid blood progenitors, is the most frequent type of cancer in children and one of the most common in adults. We discovered a covalent small-molecule “probe” for the treatment of acute myeloid and lymphoblastic leukemias that allows for post-translational modulation of the proteome in these leukemia cells. The probe dramatically induces apoptosis of leukemic cells at sub-toxic doses and consistently reduces proliferation, impairs cellular metabolism and promotes chemosensitization t

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40

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

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Hosen, Naoki, Haruo Sugiyama, and Irving L. Weissman. "The Wilms’ Tumor Gene WT1 Is Over-Expressed in Immature Leukemia Cells but Not Necessary for Leukemia Development in Mouse Leukemia Models." Blood 108, no. 11 (2006): 1429. http://dx.doi.org/10.1182/blood.v108.11.1429.1429.

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Abstract The Wilms tumor gene WT1, which is over-expressed in almost all leukemia, is one of the most promising targets for immunotherapy. To clarify which cells express WT1, we generated a knock-in reporter GFP mice (WT1GFP/+) and assayed for WT1 expression in normal and leukemic hematopoietic cells. In normal hematopoietic cells, WT1 was expressed in none of the long-term hematopoietic stem cells (HSCs) and very few (<1%) of multipotent progenitor cells. WT1 was expressed in 17.4% of megakaryocyte-erythrocyte progenitor cells and 4.1% of common myeloid progenitor cells, while the frequenc

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Holden, JT, RB Geller, DC Farhi, et al. "Characterization of Thy-1 (CDw90) expression in CD34+ acute leukemia." Blood 86, no. 1 (1995): 60–65. http://dx.doi.org/10.1182/blood.v86.1.60.bloodjournal86160.

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Thy-1 (CDw90) is a phosphatidylinositol-anchored cell surface molecule which, when coexpressed with CD34 in normal human bone marrow, identifies a population of immature cells that includes putative hematopoietic stem cells. To date, the characterization of Thy-1 expression has been confined largely to normal tissues and cell lines. In this study, we evaluated the frequency and intensity of Thy-1 expression as defined by reactivity with the anti-Thy-1 antibody 5E10 in 38 cases of CD34+ acute leukemia (21 acute myelogenous leukemia [AML], 8 chronic myelogenous leukemia [CML] in blast crisis, an

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Gobessi, Stefania, Francesca Belfiore, Sara Bennardo, Brendan Doe, Luca Laurenti та Dimitar G. Efremov. "Expression of ZAP-70 Does Not Accelerate Leukemia Development and Progression in the Eμ-TCL1 Transgenic Mouse Model of Chronic Lymphocytic Leukemia". Blood 120, № 21 (2012): 925. http://dx.doi.org/10.1182/blood.v120.21.925.925.

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Abstract Abstract 925 One of the most relevant prognostic factors in chronic lymphocytic leukemia (CLL) is expression of the protein tyrosine kinase ZAP-70. Typically, patients whose leukemic cells express ZAP-70 at 30–100% of the levels in normal T cells have aggressive disease, whereas patients whose leukemic cells do not express ZAP-70 or express only low levels of this protein have indolent disease. Previously, we and others demonstrated that ZAP-70 modulates B-cell receptor signaling and thus affects the capacity of the leukemic cells to respond to antigen stimulation. However, a direct l

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Segawa, Hidekazu, Shinya Kimura, Junya Kuroda, Takeshi Yuasa, and Taira Maekawa. "Zoledronate Inhibits Leukemia Growth in Bone Marrow and Synergizes with Imatinib Mesylate Against Ph+ Primary Leukemic Cells." Blood 104, no. 11 (2004): 2096. http://dx.doi.org/10.1182/blood.v104.11.2096.2096.

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Abstract Imatinib mesylate has drastically changed Philadelphia chromosome positive (Ph+) leukemia treatment. However, remissions induced in advanced phase Ph+ leukemias tend to be short-lived even treated with imatinib. Combined therapy of imatinib with an agent which inhibits downstream signaling of BCR/ABL such as Ras is intriguing. Phase I studies of farnesyl transferase inhibitors (FTIs), which targeted farnesylation of Ras, with imatinib against Ph+ leukemias demonstrated limited combination effects. We previously reported that the third-generation bisphosphonates (BPs) zoledronate (ZOL)

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45

Kumar, Bijender, Marvin Orellana, Jamison Brooks, et al. "Leukemia Cells Remodel Adipocyte Niches and Their Progenitor Functions to Generate Leukemia Favoring Niche." Blood 132, Supplement 1 (2018): 1294. http://dx.doi.org/10.1182/blood-2018-99-115689.

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Abstract Increasing evidence suggests that the cancer cells take shelter in different osteoblastic and adipocytic niches, where they hide from chemotherapy and continue to survive. As yet, how leukemia cells alter the bone marrow (BM) adipocytic niches to facilitate their expansion and assist them in evading chemotherapy is unclear. We have previously shown that the acute myeloid leukemia (AML) cells directly or through their exosomes, reprogram BM osteoblastic niche which facilitates their expansion and suppress normal hematopoiesis(Kumar B et al, Leukemia 2018,32(3):575-587). In this study ,

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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 112, no. 11 (2008): 3109. http://dx.doi.org/10.1182/blood.v112.11.3109.3109.

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Abstract Chromosomal translocations involving the Mixed-Lineage-Leukemia (MLL) gene on chromosome 11q23 are frequent in infant acute leukemia and give rise to the formation of MLL-fusion genes. Several studies have addressed the importance of MLL-fusion activity for the initiation and maintenance of hematopoietic transformation. However, the dependence of established leukemias on MLL-fusion activity has not been previously addressed. 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 dox

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Caudell, David, David P. Harper, Rachel L. Novak, et al. "Retroviral insertional mutagenesis identifies Zeb2 activation as a novel leukemogenic collaborating event in CALM-AF10 transgenic mice." Blood 115, no. 6 (2010): 1194–203. http://dx.doi.org/10.1182/blood-2009-04-216184.

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AbstractThe t(10;11) translocation results in a CALM-AF10 fusion gene in a subset of leukemia patients. Expression of a CALM-AF10 transgene results in leukemia, with prolonged latency and incomplete penetrance, suggesting that additional events are necessary for leukemic transformation. CALM-AF10 mice infected with the MOL4070LTR retrovirus developed acute leukemia, and ligation-mediated polymerase chain reaction was used to identify retroviral insertions at 19 common insertion sites, including Zeb2, Nf1, Mn1, Evi1, Ift57, Mpl, Plag1, Kras, Erg, Vav1, and Gata1. A total of 26% (11 of 42) of th

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Dinndorf, PA, RG Andrews, D. Benjamin, D. Ridgway, L. Wolff, and ID Bernstein. "Expression of normal myeloid-associated antigens by acute leukemia cells." Blood 67, no. 4 (1986): 1048–53. http://dx.doi.org/10.1182/blood.v67.4.1048.1048.

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Abstract Monoclonal antibodies that react with hematopoietic cells and their precursors in a stage and lineage restricted fashion were used in indirect immunofluorescence assays to examine leukemic cells from 105 pediatric age patients. The differentiative states of blasts from 42 patients with acute nonlymphocytic leukemia (ANLL) were defined by these antibodies. When these were compared to their morphologic and histochemical levels of differentiation as defined by the French- American-British (FAB) classification, no direct relationship was found. The reactivity of these antibodies with leuk

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Dinndorf, PA, RG Andrews, D. Benjamin, D. Ridgway, L. Wolff, and ID Bernstein. "Expression of normal myeloid-associated antigens by acute leukemia cells." Blood 67, no. 4 (1986): 1048–53. http://dx.doi.org/10.1182/blood.v67.4.1048.bloodjournal6741048.

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Monoclonal antibodies that react with hematopoietic cells and their precursors in a stage and lineage restricted fashion were used in indirect immunofluorescence assays to examine leukemic cells from 105 pediatric age patients. The differentiative states of blasts from 42 patients with acute nonlymphocytic leukemia (ANLL) were defined by these antibodies. When these were compared to their morphologic and histochemical levels of differentiation as defined by the French- American-British (FAB) classification, no direct relationship was found. The reactivity of these antibodies with leukemic cell

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Jones, Letetia, Sabina Sevcikova, Vernon Phan, et al. "Myc Drives Chromosomal Gain in Acute Myeloid Leukemia." Blood 112, no. 11 (2008): 792. http://dx.doi.org/10.1182/blood.v112.11.792.792.

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Abstract Acute Myeloid Leukemia (AML) is a disease characterized by diverse genetic pathogenesis, including both balanced and unbalanced chromosomal aberrations. Much is known regarding the pathogenic effects of balanced rearrangements in AML, whereas our understanding of how unbalanced aberrations contribute to leukemia is more limited. The balanced t(15;17) chromosomal rearrangement is a nearly constant feature of acute promyeloctyic leukemia (APL), a subtype AML. The translocation fuses the promyelocytic leukemia gene (PML) to the retinoic acid receptor α gene (RARA). Trisomy 8 is the most

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