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https://www.readbyqxmd.com/read/28299660/etv6-runx1-acute-lymphoblastic-leukaemia-in-identical-twins
#1
Anthony M Ford, Mel Greaves
Acute leukaemia is the major subtype of paediatric cancer with a cumulative risk of 1 in 2000 for children up to the age of 15 years. Childhood acute lymphoblastic leukaemia (ALL) is a biologically and clinically diverse disease with distinctive subtypes; multiple chromosomal translocations exist within the subtypes and each carries its own prognostic relevance. The most common chromosome translocation observed is the t(12;21) that results in an in-frame fusion between the first five exons of ETV6 (TEL) and almost the entire coding region of RUNX1 (AML1)...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28299657/runx1-eto-leukemia
#2
Shan Lin, James C Mulloy, Susumu Goyama
AML1-ETO leukemia is the most common cytogenetic subtype of acute myeloid leukemia, defined by the presence of t(8;21). Remarkable progress has been achieved in understanding the molecular pathogenesis of AML1-ETO leukemia. Proteomic surveies have shown that AML-ETO forms a stable complex with several transcription factors, including E proteins. Genome-wide transcriptome and ChIP-seq analyses have revealed the genes directly regulated by AML1-ETO, such as CEBPA. Several lines of evidence suggest that AML1-ETO suppresses endogenous DNA repair in cells to promote mutagenesis, which facilitates acquisition of cooperating secondary events...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28272704/a-minicircuitry-comprised-of-microrna-9-and-sirt1-contributes-to-leukemogenesis-in-t-8-21-acute-myeloid-leukemia
#3
L Zhou, L Fu, N Lv, X-S Chen, J Liu, Y Li, Q-Y Xu, S Huang, X-D Zhang, L-P Dou, L L Wang, Y-H Li, L Yu
OBJECTIVE: The AML1-ETO fusion protein (AE) resulting from the t(8;21) translocation is highly related to the pathogenesis and development of leukemia. microRNA-9 (miR-9) acts as a tumor suppressor gene in AE-positive acute myeloid leukemia (AML). Silent mating type information regulation 2 homolog-1 (SIRT1) is overexpressed in most cancer cells by increasing proliferation as a tumorigenic gene. The present study was performed to investigate the underlying interaction between miR-9 and SIRT1 in AE-positive AML...
February 2017: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/28261265/new-insights-into-transcriptional-and-leukemogenic-mechanisms-of-aml1-eto-and-e2a-fusion-proteins
#4
Jian Li, Chun Guo, Nickolas Steinauer, Jinsong Zhang
BACKGROUND: Nearly 15% of acute myeloid leukemia (AML) cases are caused by aberrant expression of AML1-ETO, a fusion protein generated by the t(8;21) chromosomal translocation. Since its discovery, AML1-ETO has served as a prototype to understand how leukemia fusion proteins deregulate transcription to promote leukemogenesis. Another leukemia fusion protein, E2A-Pbx1, generated by the t(1;19) translocation, is involved in acute lymphoblastic leukemias (ALLs). While AML1-ETO and E2A-Pbx1 are structurally unrelated fusion proteins, we have recently shown that a common axis, the ETO/E-protein interaction, is involved in the regulation of both fusion proteins, underscoring the importance of studying protein-protein interactions in elucidating the mechanisms of leukemia fusion proteins...
August 2016: Frontiers in Biology
https://www.readbyqxmd.com/read/28220038/phosphatase-prl2-promotes-aml1-eto-induced-acute-myeloid-leukemia
#5
M Kobayashi, S Chen, Y Bai, C Yao, R Gao, X-J Sun, C Mu, T A Twiggs, Z-H Yu, H S Boswell, M C Yoder, R Kapur, J C Mulloy, Z-Y Zhang, Y Liu
Leukemia accepted article preview online, 21 February 2017. doi:10.1038/leu.2017.67.
February 21, 2017: Leukemia: Official Journal of the Leukemia Society of America, Leukemia Research Fund, U.K
https://www.readbyqxmd.com/read/28129329/space-time-clustering-of-childhood-leukemia-evidence-of-an-association-with-etv6-runx1-tel-aml1-fusion
#6
Christian Kreis, Judith E Lupatsch, Felix Niggli, Matthias Egger, Claudia E Kuehni, Ben D Spycher
BACKGROUND: Many studies have observed space-time clustering of childhood leukemia (CL) yet few have attempted to elicit etiological clues from such clustering. We recently reported space-time clustering of CL around birth, and now aim to generate etiological hypotheses by comparing clustered and nonclustered cases. We also investigated whether the clustering resulted from many small aggregations of cases or from a few larger clusters. METHODS: We identified cases of persons born and diagnosed between 1985 and 2014 at age 0-15 years from the Swiss Childhood Cancer Registry...
2017: PloS One
https://www.readbyqxmd.com/read/28089879/clinical-outcome-of-autologous-hematopoietic-cell-transplantation-in-adult-patients-with-acute-myeloid-leukemia-who-may-benefit-from-autologous-hematopoietic-cell-transplantation
#7
Jae-Ho Yoon, Hee-Je Kim, Sung-Soo Park, Young-Woo Jeon, Sung-Eun Lee, Byung-Sik Cho, Ki-Seong Eom, Yoo-Jin Kim, Seok Lee, Chang-Ki Min, Seok-Goo Cho, Dong-Wook Kim, Jong-Wook Lee, Woo-Sung Min
The role of autologous hematopoietic cell transplantation (auto-HCT) for postremission therapy of acute myeloid leukemia is yet to be elucidated. We retrospectively analyzed 240 patients treated with auto-HCT in first remission. All patients were treated with standard induction chemotherapy, and CD34(+) stem cells were collected at each cycle of consolidation. Stem cells were infused after total body irradiation (1200 cGy), cytarabine (9 g/m(2)), and melphalan (100 mg/m(2)). Estimated 5-year overall survival, disease-free survival (DFS), cumulative incidence of relapse (CIR), and nonrelapse mortality were 58...
January 12, 2017: Biology of Blood and Marrow Transplantation
https://www.readbyqxmd.com/read/28043811/honokiol-induces-proteasomal-degradation-of-aml1-eto-oncoprotein-via-increasing-ubiquitin-conjugase-ubch8-expression-in-leukemia
#8
Bin Zhou, Haiying Li, Chongyun Xing, Haige Ye, Jianhua Feng, Jianbo Wu, Zhongqiu Lu, Jing Fang, Shenmeng Gao
AML1-ETO is the most common oncoprotein leading to acute myeloid leukemia (AML), in which 5-year survival rate is only about 30%. However, currently there are no specific therapies for AML patients with AML1-ETO. Here, we report that AML1-ETO protein is rapidly degraded by Honokiol (HNK), a natural phenolic compound isolated from the plant Magnolia officinalis. HNK induced the degradation of AML1-ETO in a concentration- and time-dependent manner in leukemic cell lines and primary AML blasts with t(8;21) translocation...
December 30, 2016: Biochemical Pharmacology
https://www.readbyqxmd.com/read/28030795/aml-associated-oncofusion-proteins-pml-rara-aml1-eto-and-cbfb-myh11-target-runx-ets-factor-binding-sites-to-modulate-h3ac-levels-and-drive-leukemogenesis
#9
Abhishek A Singh, Amit Mandoli, Koen H M Prange, Marko Laakso, Joost H A Martens
Chromosomal translocations are one of the hallmarks of acute myeloid leukemia (AML), often leading to gene fusions and expression of an oncofusion protein. Over recent years it has become clear that most of the AML associated oncofusion proteins molecularly adopt distinct mechanisms for inducing leukemogenesis. Still these unique molecular properties of the chimeric proteins converge and give rise to a common pathogenic molecular mechanism. In the present study we compared genome-wide DNA binding and transcriptome data associated with AML1-ETO, CBFB-MYH11 and PML-RARA oncofusion protein expression to identify unique and common features...
December 24, 2016: Oncotarget
https://www.readbyqxmd.com/read/27894958/poly-adp-ribose-polymerase-inhibitors-selectively-induce-cytotoxicity-in-tcf3-hlf-positive-leukemic-cells
#10
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...
February 1, 2017: 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
#11
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
#12
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
#13
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
#14
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
#15
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
#16
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 systematic evolution of ligands by exponential enrichment. 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...
November 15, 2016: Biochemistry
https://www.readbyqxmd.com/read/27725192/aml1-eto-promotes-sirt1-expression-to-enhance-leukemogenesis-of-t-8-21-acute-myeloid-leukemia
#17
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
#18
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
#19
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
#20
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
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