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https://www.readbyqxmd.com/read/27894958/poly-adp-ribose-polymerase-inhibitors-selectively-induce-cytotoxicity-in-tcf3-hlf-positive-leukemic-cells
#1
Jinhua Piao, Shiori Takai, Takahiro Kamiya, Takeshi Inukai, Kanji Sugita, Kazuma Ohyashiki, Domenico Delia, Mitsuko Masutani, Shuki Mizutani, Masatoshi Takagi
Poly (ADP-ribose) polymerase (PARP) is an indispensable component of the DNA repair machinery. PARP inhibitors are used as cutting-edge treatments for patients with homologous recombination repair (HRR)-defective breast cancers harboring mutations in BRCA1 or BRCA2. Other tumors defective in HRR, including some hematological malignancies, are predicted to be good candidates for treatment with PARP inhibitors. Screening of leukemia-derived cell lines revealed that lymphoid lineage-derived leukemia cell lines, except for those derived from mature B cells and KMT2A (MLL)-rearranged B-cell precursors, were relatively sensitive to PARP inhibitors...
November 25, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27888632/ventx-induces-expansion-of-primitive-erythroid-cells-and-contributes-to-the-development-of-acute-myeloid-leukemia-in-mice
#2
Eva Gentner, Naidu M Vegi, Medhanie A Mulaw, Tamoghna Mandal, Shiva Bamezai, Rainer Claus, Alpaslan Tasdogan, Leticia Quintanilla-Martinez, Alexander Grunenberg, Konstanze Döhner, Hartmut Döhner, Lars Bullinger, Torsten Haferlach, Christian Buske, Vijay P S Rawat, Michaela Feuring-Buske
Homeobox genes are key regulators in normal and malignant hematopoiesis. The human Vent-like homeobox gene VENTX, a putative homolog of the Xenopus laevis Xvent-2 gene, was shown to be highly expressed in normal myeloid cells and in patients with acute myeloid leukemia. We now demonstrate that constitutive expression of VENTX suppresses expression of genes responsible for terminal erythroid differentiation in normal CD34+ stem and progenitor cells. Transplantation of bone marrow progenitor cells retrovirally engineered to express VENTX caused massive expansion of primitive erythroid cells and partly acute erythroleukemia in transplanted mice...
November 24, 2016: Oncotarget
https://www.readbyqxmd.com/read/27855054/-pcr-detection-of-relevant-translocations-in-pediatric-acute-lymphoblastic-leukemia
#3
Francisco Xavier Guerra-Castillo, María Teresa Ramos-Cervantes, Cecilia Rosel-Pech, Elva Jiménez-Hernández, Vilma Carolina Bekker-Méndez
BACKGROUND: In Mexico, leukemia represents the most common type of cancer in the population under 15 years old with a high incidence rate when compared with developed countries. The etiology of leukemia may be unknown, however different factors are involve such as chromosomal translocations. The aim of this work is to detect the molecular alterations: TEL-AML1, MLL-AF4, BCR-ABL minor and E2A-PBX1 in pediatric patients with acute lymphoblastic leukemia. METHODS: 91 bone marrow samples were collected from pediatric patients with acute lymphoblastic leukemia from january 2012 to march 2013 at the Pediatric Hematology Service, Hospital General "Gaudencio González Garza"...
2016: Revista Médica del Instituto Mexicano del Seguro Social
https://www.readbyqxmd.com/read/27851970/the-hematopoietic-transcription-factors-runx1-and-erg-prevent-aml1-eto-oncogene-overexpression-and-onset-of-the-apoptosis-program-in-t-8-21-amls
#4
Amit Mandoli, Abhishek A Singh, Koen H M Prange, Esther Tijchon, Marjolein Oerlemans, Rene Dirks, Menno Ter Huurne, Albertus T J Wierenga, Eva M Janssen-Megens, Kim Berentsen, Nilofar Sharifi, Bowon Kim, Filomena Matarese, Luan N Nguyen, Nina C Hubner, Nagesha A Rao, Emile van den Akker, Lucia Altucci, Edo Vellenga, Hendrik G Stunnenberg, Joost H A Martens
The t(8;21) acute myeloid leukemia (AML)-associated oncoprotein AML1-ETO disrupts normal hematopoietic differentiation. Here, we have investigated its effects on the transcriptome and epigenome in t(8,21) patient cells. AML1-ETO binding was found at promoter regions of active genes with high levels of histone acetylation but also at distal elements characterized by low acetylation levels and binding of the hematopoietic transcription factors LYL1 and LMO2. In contrast, ERG, FLI1, TAL1, and RUNX1 bind at all AML1-ETO-occupied regulatory regions, including those of the AML1-ETO gene itself, suggesting their involvement in regulating AML1-ETO expression levels...
November 15, 2016: Cell Reports
https://www.readbyqxmd.com/read/27819671/protease-activated-receptor-1-inhibits-proliferation-but-enhances-leukemia-stem-cell-activity-in-acute-myeloid-leukemia
#5
S Goyama, M Shrestha, J Schibler, L Rosenfeldt, W Miller, E O'Brien, B Mizukawa, T Kitamura, J S Palumbo, J C Mulloy
Eradication of leukemia stem cells (LSCs) is the ultimate goal of treating acute myeloid leukemia (AML). We recently showed that the combined loss of Runx1/Cbfb inhibited the development of MLL-AF9-induced AML. However, c-Kit(+)/Gr-1(-) cells remained viable in Runx1/Cbfb-deleted cells, indicating that suppressing RUNX activity may not eradicate the most immature LSCs. In this study, we found upregulation of several hemostasis-related genes, including the thrombin-activatable receptor PAR-1 (protease-activated receptor-1), in Runx1/Cbfb-deleted MLL-AF9 cells...
November 7, 2016: Oncogene
https://www.readbyqxmd.com/read/27784352/-clinical-efficacy-of-decitabine-combined-with-modified-cag-regimen-for-relapse-refractory-acute-myeloid-leukemia-with-aml1-eto
#6
Qiang Liu, Xiao-Ming Fei
OBJECTIVE: To investigate the clinical characteristics of patients with relapse-refractory acute myeloid leukemia(AML) with AML1-ETO(+), and therapeutic effcacy and side effects of decitabine combined with modified CAG regimen. METHODS: Clinical data of 8 cases of AML with AML1-ETO(+) from June 2015 to January 2016 were analyzed retrospectively, including age, sex, initial symptoms, peripheral blood and bone marrow characteristics and so on. at the same time, the therapeutic effcacy and side effects of decitabine combined with modified CAG regimen were evaluated...
October 2016: Zhongguo Shi Yan Xue Ye Xue za Zhi
https://www.readbyqxmd.com/read/27766833/kinetic-and-thermodynamic-analyses-of-interaction-between-a-high-affinity-rna-aptamer-and-its-target-protein
#7
Ryo Amano, Kenta Takada, Yoichiro Tanaka, Yoshikazu Nakamura, Gota Kawai, Tomoko Kozu, Taiichi Sakamoto
AML1 (RUNX1) protein is an essential transcription factor involved in the development of hematopoietic cells. Several genetic aberrations that disrupt the function of AML1 have been frequently observed in human leukemia. AML1 contains a DNA-binding domain known as the Runt domain (RD), which recognizes the RD-binding double-stranded DNA element of target genes. In this study, we identified high-affinity RNA aptamers that bind to RD by SELEX. The binding assay using surface plasmon resonance indicated that a shortened aptamer retained the ability to bind to RD when 1 M potassium acetate was used...
October 21, 2016: Biochemistry
https://www.readbyqxmd.com/read/27725192/aml1-eto-promotes-sirt1-expression-to-enhance-leukemogenesis-of-t-8-21-acute-myeloid-leukemia
#8
Lei Zhou, Qian Wang, Xiaosu Chen, Lin Fu, Xiaodong Zhang, Lijun Wang, Ailing Deng, Dandan Li, Jing Liu, Na Lv, Lili Wang, Yonghui Li, Daihong Liu, Li Yu, Liping Dou
Recently, SIRT1 was found to play an important role in a variety of solid and hematologic malignancies. The expression and function of SIRT1 may differ completely depending on cell type and gene subtype, and it can act as a tumor suppressor or oncogene. We describe how SIRT1 mRNA and protein levels are overexpressed in t(8;21) AML cells. AML1-ETO triggers the activation of SIRT1 by binding at AML1 binding sites on the SIRT1 promoter. Pharmacologic targeting or RNAi-mediated inhibition of SIRT1 induces G1 arrest, apoptosis, and proliferation inhibition that is more sensitive in AML1-ETO-positive than AML1-ETO-negative cell lines...
October 8, 2016: Experimental Hematology
https://www.readbyqxmd.com/read/27713544/aml1-eto-accelerates-cell-migration-and-impairs-cell-to-cell-adhesion-and-homing-of-hematopoietic-stem-progenitor-cells
#9
Marco Saia, Alberto Termanini, Nicoletta Rizzi, Massimiliano Mazza, Elisa Barbieri, Debora Valli, Paolo Ciana, Alicja M Gruszka, Myriam Alcalay
The AML1/ETO fusion protein found in acute myeloid leukemias functions as a transcriptional regulator by recruiting co-repressor complexes to its DNA binding site. In order to extend the understanding of its role in preleukemia, we expressed AML1/ETO in a murine immortalized pluripotent hematopoietic stem/progenitor cell line, EML C1, and found that genes involved in functions such as cell-to-cell adhesion and cell motility were among the most significantly regulated as determined by RNA sequencing. In functional assays, AML1/ETO-expressing cells showed a decrease in adhesion to stromal cells, an increase of cell migration rate in vitro, and displayed an impairment in homing and engraftment in vivo upon transplantation into recipient mice...
October 7, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27709797/homoharringtonine-combined-with-aclarubicin-and-cytarabine-synergistically-induces-apoptosis-in-t-8-21-leukemia-cells-and-triggers-caspase-3-mediated-cleavage-of-the-aml1-eto-oncoprotein
#10
Jiang Cao, Hao Feng, Ning-Ning Ding, Qing-Yun Wu, Chong Chen, Ming-Shan Niu, Wei Chen, Ting-Ting Qiu, Hong-Hu Zhu, Kai-Lin Xu
Homoharringtonine combined with aclarubicin and cytarabine (HAA) is a highly effective treatment for acute myeloid leukemia (AML), especially for t(8;21) AML. However, the underlying mechanisms by which HAA kills t(8;21) AML cells remain unclear. In this study, SKNO-1 and Kasumi-1 cells with t(8;21) were used. Compared with individual or pairwise administration of homoharringtonine, aclarubicin, or cytarabine, HAA showed the strongest inhibition of growth and induction of apoptosis in SKNO-1 and Kasumi-1 cells...
November 2016: Cancer Medicine
https://www.readbyqxmd.com/read/27690235/dnmt3a-is-a-haploinsufficient-tumor-suppressor-in-cd8-peripheral-t-cell-lymphoma
#11
Staci L Haney, G Michael Upchurch, Jana Opavska, David Klinkebiel, Ryan A Hlady, Sohini Roy, Samikshan Dutta, Kaustubh Datta, Rene Opavsky
DNA methyltransferase 3A (DNMT3A) is an enzyme involved in DNA methylation that is frequently mutated in human hematologic malignancies. We have previously shown that inactivation of Dnmt3a in hematopoietic cells results in chronic lymphocytic leukemia in mice. Here we show that 12% of Dnmt3a-deficient mice develop CD8+ mature peripheral T cell lymphomas (PTCL) and 29% of mice are affected by both diseases. 10% of Dnmt3a+/- mice develop lymphomas, suggesting that Dnmt3a is a haploinsufficient tumor suppressor in PTCL...
September 2016: PLoS Genetics
https://www.readbyqxmd.com/read/27620872/genome-wide-repression-of-erna-and-target-gene-loci-by-the-etv6-runx1-fusion-in-acute-leukemia
#12
Susanna Teppo, Saara Laukkanen, Thomas Liuksiala, Jessica Nordlund, Mikko Oittinen, Kaisa Teittinen, Toni Grönroos, Pascal St-Onge, Daniel Sinnett, Ann-Christine Syvänen, Matti Nykter, Keijo Viiri, Merja Heinäniemi, Olli Lohi
Approximately 20%-25% of childhood acute lymphoblastic leukemias carry the ETV6-RUNX1 (E/R) fusion gene, a fusion of two central hematopoietic transcription factors, ETV6 (TEL) and RUNX1 (AML1). Despite its prevalence, the exact genomic targets of E/R have remained elusive. We evaluated gene loci and enhancers targeted by E/R genome-wide in precursor B acute leukemia cells using global run-on sequencing (GRO-seq). We show that expression of the E/R fusion leads to widespread repression of RUNX1 motif-containing enhancers at its target gene loci...
November 2016: Genome Research
https://www.readbyqxmd.com/read/27587249/-frequency-and-clinical-features-of-asxl2-gene-mutation-in-acute-myeloid-leukemia-patients-with-aml1-eto-fusion-gene-positive
#13
J X Zhao, X H Chen, J L Li, J Pan, Y H Tan, Z F Xu, F G Ren, Y F Zhang, J Xu, M Q Li, J Li, N Zhang, J M Chang, X J Wang, H W Wang
OBJECTIVE: To investigate frequency and clinical features of additional sex combs-like 2 (ASXL2) gene mutation in acute myeloid leukemia (AML) patients with AML1-ETO fusion gene and to analyze the relationship between ASXL2 gene mutation and c- kit gene mutation. METHODS: Mutation analysis of exon 11 and 12 of ASXL2 gene in 59 de novo AML patients was performed by using polymerase chain reaction (PCR) followed by sequence analysis. The clinical features, survival curve and c-kit gene mutation in ASXL2 gene mutation positive and negative patients were compared...
August 14, 2016: Zhonghua Xue Ye Xue za Zhi, Zhonghua Xueyexue Zazhi
https://www.readbyqxmd.com/read/27576335/silver-nanoparticles-exhibit-size-dependent-differential-toxicity-and-induce-expression-of-syncytin-1-in-fa-aml1-and-molt-4-leukaemia-cell-lines
#14
Sultan Alqahtani, Pawika Promtong, Anthony W Oliver, Xiaotong T He, Thomas D Walker, Andrew Povey, Lynne Hampson, Ian N Hampson
Human endogenous retrovirus (HERV) sequences make up ~8% of the human genome and increased expression of some HERV proteins has been observed in various pathologies including leukaemia and multiple sclerosis. However, little is known about the function of these HERV proteins or environmental factors which regulate their expression. Silver nanoparticles (AgNPs) are used very extensively as antimicrobials and antivirals in numerous consumer products although their effect on the expression of HERV gene products is unknown...
November 2016: Mutagenesis
https://www.readbyqxmd.com/read/27554046/action-mechanisms-of-histone-deacetylase-inhibitors-in-the-treatment-of-hematological-malignancies
#15
Yoichi Imai, Yoshiro Maru, Junji Tanaka
Histone deacetylases (HDACs) critically regulate gene expression by determining the acetylation status of histones. In addition, studies have increasingly focused on the activities of HDACs, especially involving non-histone proteins, and their various biological effects. Aberrant HDAC expression observed in several kinds of human tumors makes HDACs potential targets for cancer treatment. Several preclinical studies have suggested that HDAC inhibitors exhibit some efficacy in the treatment of acute myelogenous leukemia (AML) with AML1-ETO, which mediates transcriptional repression through its interaction with a complex including HDAC1...
August 24, 2016: Cancer Science
https://www.readbyqxmd.com/read/27540136/clic5-a-novel-etv6-target-gene-in-childhood-acute-lymphoblastic-leukemia
#16
Benjamin Neveu, Jean-François Spinella, Chantal Richer, Karine Lagacé, Pauline Cassart, Mathieu Lajoie, Silvana Jananji, Simon Drouin, Jasmine Healy, Gilles R X Hickson, Daniel Sinnett
The most common rearrangement in childhood precursor B-cell acute lymphoblastic leukemia is the t(12;21)(p13;q22) translocation resulting in the ETV6-AML1 fusion gene. A frequent concomitant event is the loss of the residual ETV6 allele suggesting a critical role for the ETV6 transcriptional repressor in the etiology of this cancer. However, the precise mechanism through which loss of functional ETV6 contributes to disease pathogenesis is still unclear. To investigate the impact of ETV6 loss on the transcriptional network and to identify new transcriptional targets of ETV6, we used whole transcriptome analysis of both pre-B leukemic cell lines and patients combined with chromatin immunoprecipitation...
December 2016: Haematologica
https://www.readbyqxmd.com/read/27531762/-clinical-features-and-prognosis-of-227-cases-of-acute-myeloid-leukemia-with-cross-lineage-antigen-expression
#17
Fang Fang, Ping Zhu, Ying Zhang, Xu-Zhen Lu, Yu-Jun Dong, Yu-Hua Sun, Li-Hong Wang, Ding-Fang Bu, Xi-Nan Cen, Mang-Ju Wang
OBJECTIVE: To analyse the clinical features and prognostic significance of cross-lineage antigen expression in patients with acute myeloid leukemia(AML) in order to establish individualized treatment for a better outcome and prognosis. METHODS: A total of 227 cases (exduding M3) were detected by flow cytometry for immune phenotype. The CD7(-)CD56(-)CD19(-) AML served as control. The clinical features, treatment response and prognosis of CD7(+) group, CD56(+) group and CD19(+) group were compared...
August 2016: Zhongguo Shi Yan Xue Ye Xue za Zhi
https://www.readbyqxmd.com/read/27512117/bpr1j373-an-oral-multiple-tyrosine-kinase-inhibitor-targets-c-kit-for-the-treatment-of-c-kit-driven-myeloid-leukemia
#18
Li-Tzong Chen, Chiung-Tong Chen, Weir-Torn Jiaang, Tsai-Yun Chen, Joseph H Butterfield, Neng-Yao Shih, John Tsu-An Hsu, Hui-You Lin, Sheng-Fung Lin, Hui-Jen Tsai
Acute myelogenous leukemia (AML) carrying t(8;21)(q22;q22) or inv(16)/t(16;16)(p13;q22) is classified as core binding factor (CBF)-AML and accounts for approximately 15% of AML. c-KIT mutation can be detected in 17%∼46% of CBF-AML and is associated with poor prognosis. c-KIT mutation is a crucial hit and cooperates with AML1-ETO resulting from t(8;21)(q22;q22) to cause overt AML. Tyrosine kinase inhibitors (TKI) targeting c-KIT, such as imatinib, has been used successfully to treat c-KIT driven gastrointestinal stromal tumors...
October 2016: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/27509060/immortalization-of-human-ae-pre-leukemia-cells-by-htert-allows-leukemic-transformation
#19
Shan Lin, Junping Wei, Mark Wunderlich, Fu-Sheng Chou, James C Mulloy
Human CD34+ hematopoietic stem and progenitor cells (HSPC) expressing fusion protein AML1-ETO (AE), generated by the t(8;21)(q22;q22) rearrangement, manifest enhanced self-renewal and dysregulated differentiation without leukemic transformation, representing a pre-leukemia stage. Enabling replicative immortalization via telomerase reactivation is a crucial step in cancer development. However, AE expression alone is not sufficient to maintain high telomerase activity to immortalize human HSPC cells, which may hamper transformation...
August 5, 2016: Oncotarget
https://www.readbyqxmd.com/read/27486062/tle4-regulation-of-wnt-mediated-inflammation-underlies-its-role-as-a-tumor-suppressor-in-myeloid-leukemia
#20
Thomas H Shin, Christopher Brynczka, Farshid Dayyani, Miguel N Rivera, David A Sweetser
The presence of AML1-ETO (RUNX1-CBF2T1), a fusion oncoprotein resulting from a t(8;21) chromosomal translocation, has been implicated as a necessary but insufficient event in the development of a subset of acute myeloid leukemias (AML). While AML1-ETO prolongs survival and inhibits differentiation of hematopoietic stem cells (HSC), other contributory events are needed for cell proliferation and leukemogenesis. We have postulated that specific tumor suppressor genes keep the leukemic potential of AML1-ETO in check...
September 2016: Leukemia Research
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