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Journal articles on the topic 'Myeloid leukemia'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

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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2

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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3

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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4

Aue, Georg, Yang Du, Susan M. Cleveland, et al. "Sox4 cooperates with PU.1 haploinsufficiency in murine myeloid leukemia." Blood 118, no. 17 (2011): 4674–81. http://dx.doi.org/10.1182/blood-2011-04-351528.

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Abstract Cooperation of multiple mutations is thought to be required for cancer development. In previous studies, murine myeloid leukemias induced by transducing wild-type bone marrow progenitors with a SRY sex determining region Y-box 4 (Sox4)–expressing retrovirus frequently carried proviral insertions at Sfpi1, decreasing its mRNA levels, suggesting that reduced Sfpi1 expression cooperates with Sox4 in myeloid leukemia induction. In support of this hypothesis, we show here that mice receiving Sox4 virus-infected Sfpi1ko/+ bone marrow progenitors developed myeloid leukemia with increased pen

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5

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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6

Jamieson, Catriona, Sidd Jaiswal, David Traver, Jason Gotlib, Mark Chao, and Irving L. Weissman. "Increased Expression of CD47 Is a Constant Marker in Mouse and Human Myeloid Leukemias." Blood 106, no. 11 (2005): 3260. http://dx.doi.org/10.1182/blood.v106.11.3260.3260.

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Abstract CD47, also known as integrin associated protein, is a ubiquitously expressed cell surface glycoprotein that interacts with a number of integrins, modulating leukocyte adhesion, migration, cell motility and platelet activation. CD47 is also the ligand for the macrophage inhibitory receptor signal regulatory protein α (SIRP α) and thus, impairs macrophage-mediated phagocytosis. Recent reports suggest that increased CD47 expression may play a role in the pathogenesis of lymphoproliferative disorders such as CLL (Mateo et al, Nat Med.1999; 5:1277) and multiple myeloma, and that a bivalent

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7

Войцеховский, Валерий, Valeriy Voytsekhovskiy, Татьяна Заболотских, et al. "DAMAGE OF THE BRONCHOPULMONARY SYSTEM IN PATIENTS WITH CHRONIC HEMOBLASTOSIS." Bulletin physiology and pathology of respiration 1, no. 69 (2018): 25–35. http://dx.doi.org/10.12737/article_5b975083a62278.59044240.

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In 185 patients with chronic hemoblastosis (chronic lymphocytic leukemia, chronic myeloid leukemia, idiopathic myelofibrosis, multiple myeloma) after autopsy, the pathology of the bronchopulmonary system was studied. It was found out that in addition to immunodeficiency, an important role in the occurrence of respiratory diseases in chronic lymphocytic leukemia, as well as in chronic myeloid leukemia and idiopathic myelofibrosis in the stage of blast crisis is played by specific leukemic infiltration of the lungs, bronchi, pleura and diaphragm; the presence of leukostasis in the vessels of med

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8

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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9

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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10

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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11

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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12

Pietsch, T., U. Kyas, U. Steffens, et al. "Effects of human stem cell factor (c-kit ligand) on proliferation of myeloid leukemia cells: heterogeneity in response and synergy with other hematopoietic growth factors." Blood 80, no. 5 (1992): 1199–206. http://dx.doi.org/10.1182/blood.v80.5.1199.1199.

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Abstract A novel hematopoietic growth factor, the stem cell factor (SCF), for primitive hematopoietic progenitor cells has recently been purified and its gene has been cloned. In this study we tested the mitogenic activity of recombinant human SCF on myeloid leukemia cells as well as the expression of its receptor. We have investigated the proliferation of 31 myeloid leukemia cell lines as well as fresh myeloid leukemic blasts from 17 patients in a 72-hour 3H-thymidine uptake assay in the presence of various concentrations of recombinant human (rh) SCF alone or in combination with saturating c

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13

Pietsch, T., U. Kyas, U. Steffens, et al. "Effects of human stem cell factor (c-kit ligand) on proliferation of myeloid leukemia cells: heterogeneity in response and synergy with other hematopoietic growth factors." Blood 80, no. 5 (1992): 1199–206. http://dx.doi.org/10.1182/blood.v80.5.1199.bloodjournal8051199.

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A novel hematopoietic growth factor, the stem cell factor (SCF), for primitive hematopoietic progenitor cells has recently been purified and its gene has been cloned. In this study we tested the mitogenic activity of recombinant human SCF on myeloid leukemia cells as well as the expression of its receptor. We have investigated the proliferation of 31 myeloid leukemia cell lines as well as fresh myeloid leukemic blasts from 17 patients in a 72-hour 3H-thymidine uptake assay in the presence of various concentrations of recombinant human (rh) SCF alone or in combination with saturating concentrat

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14

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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15

Takimoto, Rishu, Junji Kato, Koichi Takada, Takuya Matsunaga, and Yoshiro Niitsu. "Impaired Expression of the DNA Repair Factor DDB2 in Human Myeloid Leukemias." Blood 104, no. 11 (2004): 2046. http://dx.doi.org/10.1182/blood.v104.11.2046.2046.

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Abstract Recent studies have suggested that chromosomal deletions might represent a mechanism of inactivation of DNA repair system in various hematological malignancies, including myeloid leukemias. However, the precise mechanisms remain unclear. Damaged DNA binding protein-2 (DDB2), a DNA repair factor induced by tumor suppressor p53, plays an important role in the nucleotide excision repair of UV-damaged DNA. Despite frequent mutations of p53 in human leukemic cells, the role of DDB2 on the leukemogenesis is unkown. In this study, we examined expression of DDB2 mRNA in four human myeloid leu

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16

Kumari, Uma, and K. Sreenath Yadav. "Proteomics and NGS Analysis of Induced Myeloid Leukemia Cells." International Journal for Research in Applied Science and Engineering Technology 11, no. 9 (2023): 105–12. http://dx.doi.org/10.22214/ijraset.2023.55614.

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Abstract: Induced myeloid leukemia cells have emerged as critical models for unraveling intricate molecular mechanisms of leukemogenesis. Integration of proteomics and Next-Generation Sequencing (NGS) analyses has yielded profound insights. Mcl1's significance in tumorigenesis and therapeutic resistance highlights Mcl-1 inhibitors' promise as anticancer agents. A selectively designed macrocyclic compound for Mcl-1 with high affinity, currently in clinical development, signifies a milestone in precision therapy. Activation of the Bak-dependent mitochondrial apoptotic pathway in acute myeloid le

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17

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

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Acute leukemias are a group of hematopoietic stem cell malignancies characterized by the proliferation and accumulation of immature cell (blasts) clones that associate medullary insufficiency syndrome (anemia, neutropenia, thrombocytopenia). Depending on the origin of the malignant clone, two major categories of acute leukemias are: acute lymphocytic leukemia (ALL) and acute myeloid leukemia (AML). Studies show an annual incidence of acute leukemias in European adults of 5-6 cases per 100,000 people with an increase in over 70 years of age, reaching an incidence of about 15-20 / 100,000 people

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18

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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19

Narayanan, Geetha, M. T. Sugeeth, and Lali V. Soman. "Mixed Phenotype Acute Leukemia Presenting as Leukemia Cutis." Case Reports in Medicine 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/1298375.

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Leukemia cutis (LC) is defined as infiltration of the skin by leukemic cells resulting in clinically recognizable cutaneous lesions. It is common in congenital leukemia and acute myeloid leukemia. However, LC has rarely been reported with mixed phenotypic acute leukemia (MPAL). We report the case of a lady who presented with erythematous papular and nodular lesions all over the body. Skin biopsy showed leukemic infiltration and bone marrow aspiration showed MPAL of the T/myeloid with monocytic differentiation lineage. This is the first report of an adult patient with MPAL of the T/myeloid with

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20

Oakley, Kevin, Yufen Han, Bandana A. Vishwakarma, et al. "Setbp1 promotes the self-renewal of murine myeloid progenitors via activation of Hoxa9 and Hoxa10." Blood 119, no. 25 (2012): 6099–108. http://dx.doi.org/10.1182/blood-2011-10-388710.

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Abstract Acquisition of self-renewal capability by myeloid progenitors to become leukemic stem cells during myeloid leukemia development is poorly understood. Here, we show that Setbp1 overexpression efficiently confers self-renewal capability to myeloid progenitors in vitro, causing their immortalization in the presence of stem cell factor and IL-3. Self-renewal after immortalization requires continuous Setbp1 expression. We also found that Hoxa9 and Hoxa10 mRNA are present at dramatically higher levels in Setbp1-immortalized cells compared with other immortalized cells, and are induced short

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21

Parasole, Rosanna, Laura Vicari, Fara Petruzziello, et al. "Trisomy of Chromosome 7: a Novel Cytogenetic Abnormality in a Paediatric Case of Mixed Acute Leukemia." Blood 114, no. 22 (2009): 4121. http://dx.doi.org/10.1182/blood.v114.22.4121.4121.

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Abstract Abstract 4121 Background Mixed acute leukemias are an heterogeneous category of poorly differentiated leukemias, affecting people of all ages. These forms of leukemias are very rare, 3-5% of all acute leukemias, and are characterized by co-expression of myeloid and lymphoid associated-antigens on the same leukemic cells. The therapeutic approach is not defined because, often, mixed leukemias switch their lineage of origin during treatment and the prognosis is very poor. We describe a novel, never reported before, cytogenetic abnormality in a child with a mixed acute leukemia. Methods

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22

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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23

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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24

Shi, Yang, and Endi Wang. "Blastic Plasmacytoid Dendritic Cell Neoplasm: A Clinicopathologic Review." Archives of Pathology & Laboratory Medicine 138, no. 4 (2014): 564–69. http://dx.doi.org/10.5858/arpa.2013-0101-rs.

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Blastic plasmacytoid dendritic cell neoplasm is a rare entity grouped with the acute myeloid leukemia–related precursor neoplasms in the 2008 World Health Organization classification. It was previously postulated to originate from natural killer cells, T cells, or monocytes but is now believed to arise from the plasmacytoid dendritic cell. The pathogenesis of blastic plasmacytoid dendritic cell neoplasm is not well understood, although the neoplasm demonstrates frequent deletion of tumor suppressor genes, including RB1, CDKN1B, CDKN2A, and TP53. Blastic plasmacytoid dendritic cell neoplasm is

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25

Pavlova, T. Yu, and T. T. Valiev. "Priapism as the first symptom of chronic myeloid leukemia: literature review and own clinical case report." Oncohematology 17, no. 4 (2022): 88–93. http://dx.doi.org/10.17650/1818-8346-2022-17-4-88-93.

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Chronic myeloid leukemia is a ph-positive myeloproliferative disease, which is usually manifested by hyperleukocytosis and massive splenomegaly. Chronic myeloid leukemia is rare in childhood and adolescence, it accounts for 2 to 3 % of all leukemias cases. priapism is a rare manifestation of chronic myeloid leukemia and is an urgent urological condition that requires timely treatment to prevent long-term complications, in particular, erectile dysfunction.This review presents the literature information about priapism as the first sign of chronic myeloid leukemia, as well as the first descriptio

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26

Jianbiao Zhou, Jessie Yiying Quah, Yvonne Ng, et al. "ASLAN003, a potent dihydroorotate dehydrogenase inhibitor for differentiation of acute myeloid leukemia." Haematologica 105, no. 9 (2019): 2286–97. http://dx.doi.org/10.3324/haematol.2019.230482.

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Differentiation therapies achieve remarkable success in acute promyelocytic leukemia, a subtype of acute myeloid leukemia. However, excluding acute promyelocytic leukemia, clinical benefits of differentiation therapies are negligible in acute myeloid leukemia except for mutant isocitrate dehydrogenase 1/2. Dihydroorotate dehydrogenase catalyses the fourth step of the de novo pyrimidine synthesis pathway. ASLAN003 is a highly potent dihydroorotate dehydrogenase inhibitor that induces differentiation, as well as reduces cell proliferation and viability, of acute myeloid leukemia cell lines and p

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27

Kurtzberg, J., TA Waldmann, MP Davey, et al. "CD7+, CD4-, CD8- acute leukemia: a syndrome of malignant pluripotent lymphohematopoietic cells." Blood 73, no. 2 (1989): 381–90. http://dx.doi.org/10.1182/blood.v73.2.381.381.

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Abstract Following our initial observation of in vivo conversion of CD7+, CD4-, CD8- acute lymphoblastic leukemia (ALL) cells from lymphoid to myeloid lineages (Proc Natl Acad Sci (USA) 81:253, 1984) we have studied eight additional cases of ALL with this leukemic cell phenotype. The CD7+, CD4-, CD8- phenotype was associated with a distinct clinical entity with those affected predominantly male (either less than 35 years or greater than 65 years of age), with frequent mediastinal and/or thymic masses, skin and CNS disease, high peripheral WBC counts, and bone marrow blasts that were morphologi

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Kurtzberg, J., TA Waldmann, MP Davey, et al. "CD7+, CD4-, CD8- acute leukemia: a syndrome of malignant pluripotent lymphohematopoietic cells." Blood 73, no. 2 (1989): 381–90. http://dx.doi.org/10.1182/blood.v73.2.381.bloodjournal732381.

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Following our initial observation of in vivo conversion of CD7+, CD4-, CD8- acute lymphoblastic leukemia (ALL) cells from lymphoid to myeloid lineages (Proc Natl Acad Sci (USA) 81:253, 1984) we have studied eight additional cases of ALL with this leukemic cell phenotype. The CD7+, CD4-, CD8- phenotype was associated with a distinct clinical entity with those affected predominantly male (either less than 35 years or greater than 65 years of age), with frequent mediastinal and/or thymic masses, skin and CNS disease, high peripheral WBC counts, and bone marrow blasts that were morphologically L1

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29

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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30

Konopleva, Marina, Elena Elstner, Teresa J. McQueen та ін. "Peroxisome proliferator-activated receptor γ and retinoid X receptor ligands are potent inducers of differentiation and apoptosis in leukemias". Molecular Cancer Therapeutics 3, № 10 (2004): 1249–62. http://dx.doi.org/10.1158/1535-7163.1249.3.10.

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Abstract The peroxisome proliferator-activated receptor γ (PPARγ) is a member of the nuclear receptor family that forms heterodimers with retinoid X receptor. These heterodimers bind to DNA and activate the transcription of target genes. Here, we report that the PPARγ receptor protein is expressed in primary myeloid and lymphoid leukemias and in lymphoma and myeloma cell lines. In this study, we compared the activity of several PPARγ ligands including BRL49653 (rosiglitazone), 15-deoxy-Δ12,14-prostaglandin J2, and the novel triterpenoid 2-cyano-3,12-dioxooleana-1,9-dien-28-oic acid on leukemia

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Frankfurt, Olga, and Martin S. Tallman. "Growth Factors in Leukemia." Journal of the National Comprehensive Cancer Network 5, no. 2 (2007): 203–15. http://dx.doi.org/10.6004/jnccn.2007.0020.

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The role of myeloid growth factors, such as granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor, in the management of acute myeloid and acute lymphoblastic leukemias has been evaluated extensively in multiple clinical trials. Growth factors have been given before, concurrently, or sequentially with chemotherapy with the goal of reducing the duration of neutropenia and consequently the incidence and severity of infections, and improving the rate of remissions and overall survival. They also have been studied as chemotherapy-sensitizing agents in an effort

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32

Sultana, Sajeda, Md Selimuz zaman, and Md Abdul Wohab. "The Production of Colony-Stimulating Factor (CSF) by the Peripheral Blood Cells Factors by Leukemic Leukocytes." Scholars Journal of Applied Medical Sciences 13, no. 05 (2025): 1020–26. https://doi.org/10.36347/sjams.2025.v13i05.002.

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Aberrant production of colony-stimulating factors (CSFs) by leukemic leukocytes represents a critical mechanism in leukemia pathophysiology. This study investigated CSF production profiles across acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and chronic myeloid leukemia (CML) compared to healthy controls. Leukemic cells demonstrated significantly elevated spontaneous production of G-CSF, GM-CSF, and M-CSF, with distinct patterns characteristic of each leukemia subtype. This observational study was conducted over a two-year period (January 2022 to December 2023) in the Depar

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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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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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Miner, Samantha, Sawa Ito, Kazushi Tanimoto, et al. "Myeloid Leukemias Directly Suppress T Cell Proliferation Through STAT3 and Arginase Pathways." Blood 122, no. 21 (2013): 3885. http://dx.doi.org/10.1182/blood.v122.21.3885.3885.

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Abstract The immune-editing effect of myeloid leukemia has recently been reported in several studies. We previously demonstrated that the K562 leukemia-derived cell line suppresses T cell proliferation, which suggests that myeloid leukemia may function in a similar way to myeloid derived suppressor cells (MDSC). While the mechanism of suppression in leukemia is not fully understood, recent murine and human studies suggest that the STAT3 and arginase pathways play a key role in the immunosuppressive function of MDSC. We hypothesized that myeloid leukemia utilizes the MDSC STAT3 and arginase pat

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Fishman, Hila, Shreyas Madiwale, Ifat Geron, et al. "ETV6-NCOA2 fusion induces T/myeloid mixed-phenotype leukemia through transformation of nonthymic hematopoietic progenitor cells." Blood 139, no. 3 (2022): 399–412. http://dx.doi.org/10.1182/blood.2020010405.

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Abstract Mixed-phenotype acute leukemia is a rare subtype of leukemia in which both myeloid and lymphoid markers are co-expressed on the same malignant cells. The pathogenesis is largely unknown, and the treatment is challenging. We previously reported the specific association of the recurrent t(8;12)(q13;p13) chromosomal translocation that creates the ETV6-NCOA2 fusion with T/myeloid leukemias. Here we report that ETV6-NCOA2 initiates T/myeloid leukemia in preclinical models; ectopic expression of ETV6-NCOA2 in mouse bone marrow hematopoietic progenitors induced T/myeloid lymphoma accompanied

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Sharma, Sonali, Benjamin J. Rodems, Cameron D. Baker, et al. "Abstract 6653: Taurine Transporter SLC6A6 promotes myeloid leukemia progression by regulating glycolysis." Cancer Research 85, no. 8_Supplement_1 (2025): 6653. https://doi.org/10.1158/1538-7445.am2025-6653.

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Abstract Interactions of stem cells with their surrounding microenvironment are known to be essential for both normal development and for sustaining self-renewing adult stem cells, such as the hematopoietic stem cells (HSCs). Since cancers often hijack developmental signals for their progression, it is likely that niche-driven signals that sustain HSCs also influence the growth of leukemias arising from mutations in HSCs and early hematopoietic progenitors, such as acute myeloid leukemia (AML) and blast crisis chronic myeloid leukemia (bcCML). To identify candidate cell surface receptors essen

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

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Li, Shi-Wu, Dongqi Tang, Kim P. Ahrens, Jin-Xiong She, Raul C. Braylan, and Lijun Yang. "All-trans-retinoic acid induces CD52 expression in acute promyelocytic leukemia." Blood 101, no. 5 (2003): 1977–80. http://dx.doi.org/10.1182/blood-2002-05-1426.

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It is well known that all-trans-retinoic acid (ATRA) can induce myeloid cell differentiation in acute promyelocytic leukemia (APL) cells. In this study, we found that ATRA treatment of the APL cell line NB4 induced the expression of CD52, both at transcriptional and translational levels. CD52 is a 21- to 28-kDa nonmodulating cell surface glycosylphosphatidylinositol-linked glycoprotein expressed on lymphocytes and monocytes, but not in human myeloid cells. The ATRA-dependent induction of CD52 expression was not observed in non-promyelocytic leukemia cell lines such as K562, U937, and HL-60, su

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Maikut-Zabrodskaya, I. M. "Functional State of Liver in Patients with Progressing Chronic Myeloid Leukemia." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 6, no. 5 (2021): 193–98. http://dx.doi.org/10.26693/jmbs06.05.193.

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Chronic myeloid leukemia is found in approximately 20% of newly diagnosed cases of leukemia in adults. In Europe and North America, chronic myeloid leukemia ranks third among leukemias (after acute leukemias and chronic lymphoblastic leukemia). The problem of diagnosis, treatment, rehabilitation and adaptation of patients with chronic myeloid leukemia is relevant, as there is a gradual increase in the incidence of this disease both in the world and in our country. Some progress has been achieved in the treatment of patients with oncohematological diseases, in particular chronic myeloid leukemi

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Lee, Po-Shing, Ching-Nan Lin, Chientzu Liu, Chien-Tai Huang, and Wei-Shiou Hwang. "Acute Leukemia With Myeloid, B-, and Natural Killer Cell Differentiation." Archives of Pathology & Laboratory Medicine 127, no. 2 (2003): e93-e95. http://dx.doi.org/10.5858/2003-127-e93-alwman.

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Abstract Biphenotypic acute leukemias account for 4% to 8% of all acute leukemias. Most of these leukemias are of myeloid–B-cell or myeloid–T-cell lineage. Acute myeloid–natural killer cell leukemia has been recognized recently. We report the first case, to our knowledge, of CD56+ acute leukemia showing unequivocal myeloid and B-cell differentiation in a 20-year-old woman, whose blast cells were positive for myeloperoxidase, CD13, CD33, CD117, terminal deoxynucleotidyl transferase, CD19, CD20, CD22, CD34, HLA-DR, and CD56 but negative for CD3, CD5, CD7, and CD10. Rare Auer rods were identified

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James Ropa, Nirmalya Saha, Hsiangyu Hu, Luke F. Peterson, Moshe Talpaz, and Andrew G. Muntean. "SETDB1 mediated histone H3 lysine 9 methylation suppresses MLL-fusion target expression and leukemic transformation." Haematologica 105, no. 9 (2019): 2273–85. http://dx.doi.org/10.3324/haematol.2019.223883.

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Epigenetic regulators play a critical role in normal and malignant hematopoiesis. Deregulation, including epigenetic deregulation, of the HOXA gene cluster drives transformation of about 50% of acute myeloid leukemia. We recently showed that the Histone 3 Lysine 9 methyltransferase SETDB1 negatively regulates the expression of the pro-leukemic genes Hoxa9 and its cofactor Meis1 through deposition of promoter H3K9 trimethylation in MLL-AF9 leukemia cells. Here, we investigated the biological impact of altered SETDB1 expression and changes in H3K9 methylation on acute myeloid leukemia. We demons

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Ghosn, Youssef, Mohammed Hussein Kamareddine, Antonios Tawk, et al. "Inorganic Nanoparticles as Drug Delivery Systems and Their Potential Role in the Treatment of Chronic Myelogenous Leukaemia." Technology in Cancer Research & Treatment 18 (January 1, 2019): 153303381985324. http://dx.doi.org/10.1177/1533033819853241.

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Chronic myeloid leukemia is a myeloproliferative disease where cells of myeloid linage display a t(9;22) chromosomal translocation leading to the formation of the BCR/ABL fusion gene and the continuous activation of tyrosine kinases. This malignancy has a peak incidence at 45 to 85 years, accounting for 15% of all leukemias in adults. Controlling the activity of tyrosine kinase became the main strategy in chronic myeloid leukemia treatment, with imatinib being placed at the forefront of current treatment protocols. New approaches in future anticancer therapy are emerging with nanomedicine bein

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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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Birg, F., M. Courcoul, O. Rosnet, et al. "Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages." Blood 80, no. 10 (1992): 2584–93. http://dx.doi.org/10.1182/blood.v80.10.2584.2584.

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Abstract FLT3, a receptor belonging to the FMS/KIT family and localized to 13q12, could play a role in the biology of early hematopoietic progenitor cells. Because FMS and KIT are expressed in both normal progenitors and myeloid leukemias, we looked for FLT3 expression in fresh human leukemic cells using Northern blot analysis. High levels of FLT3 expression were detected in 92% of the cases of acute myeloid leukemia (AML) tested, ranging from the M1 to the M5 stages of differentiation assessed in the French-American-British classification. Immature (MO) AML cells, biphenotypic leukemias, and

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47

Birg, F., M. Courcoul, O. Rosnet, et al. "Expression of the FMS/KIT-like gene FLT3 in human acute leukemias of the myeloid and lymphoid lineages." Blood 80, no. 10 (1992): 2584–93. http://dx.doi.org/10.1182/blood.v80.10.2584.bloodjournal80102584.

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FLT3, a receptor belonging to the FMS/KIT family and localized to 13q12, could play a role in the biology of early hematopoietic progenitor cells. Because FMS and KIT are expressed in both normal progenitors and myeloid leukemias, we looked for FLT3 expression in fresh human leukemic cells using Northern blot analysis. High levels of FLT3 expression were detected in 92% of the cases of acute myeloid leukemia (AML) tested, ranging from the M1 to the M5 stages of differentiation assessed in the French-American-British classification. Immature (MO) AML cells, biphenotypic leukemias, and AML with

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48

Gluzman, D. F., L. M. Sklyarenko, M. P. Zavelevich, S. V. Koval, and T. S. Ivanivskaya. "LEUKEMIC BLAST CELLS AND CONTROVERSIES IN MODELS OF HEMATOPOIESIS." Experimental Oncology 37, no. 1 (2015): 2–4. http://dx.doi.org/10.31768/2312-8852.2015.37(1):2-4.

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Classical and up-to-date models of hematopoietic lineage determination are briefly reviewed with the focus on myeloid-based models challenging the existence of the common progenitor for T cells, B cells and NK cells. The analysis of immunophenotype of leukemic blast cells seems to be a promising approach for interpreting some controversies in the schemes of normal hematopoiesis. The liter ature data as well as our own findings in the patients with various types of acute leukemias are in favor of the concept postulating that common myeloid-lymphoid progenitors giving rise to T and B cell branch

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Dinndorf, PA, and GH Reaman. "Acute lymphoblastic leukemia in infants: evidence for B cell origin of disease by use of monoclonal antibody phenotyping." Blood 68, no. 4 (1986): 975–78. http://dx.doi.org/10.1182/blood.v68.4.975.975.

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Abstract Since the prognosis of infants with acute lymphoblastic leukemia (ALL) is so poor, it has been suggested that these leukemias may not be lymphoid in origin, but may originate from stem cell, myeloid, or megakaryocytic progenitors. Alternately it has been hypothesized that these leukemias originate in lymphoid cells at the earliest stages of B cell development. Another possibility is that these leukemias may be of more than one lineage. Therefore we examined leukemic blasts from 12 infants with ALL using monoclonal antibodies to myeloid and lymphoid differentiation antigens. The majori

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50

Dinndorf, PA, and GH Reaman. "Acute lymphoblastic leukemia in infants: evidence for B cell origin of disease by use of monoclonal antibody phenotyping." Blood 68, no. 4 (1986): 975–78. http://dx.doi.org/10.1182/blood.v68.4.975.bloodjournal684975.

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Since the prognosis of infants with acute lymphoblastic leukemia (ALL) is so poor, it has been suggested that these leukemias may not be lymphoid in origin, but may originate from stem cell, myeloid, or megakaryocytic progenitors. Alternately it has been hypothesized that these leukemias originate in lymphoid cells at the earliest stages of B cell development. Another possibility is that these leukemias may be of more than one lineage. Therefore we examined leukemic blasts from 12 infants with ALL using monoclonal antibodies to myeloid and lymphoid differentiation antigens. The majority of spe

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