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Cancer: Acute Leukemia

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Total 260 results found since Jan 2013.

Apoptosis repressor with caspase recruitment domain modulates second mitochondrial‐derived activator of caspases mimetic‐induced cell death through BIRC2/MAP3K14 signalling in acute myeloid leukaemia
Summary Overexpression of the apoptosis repressor with caspase recruitment domain (ARC, also termed NOL3) protein predicts adverse outcome in patients with acute myeloid leukaemia (AML) and confers drug resistance to AML cells. The second mitochondrial‐derived activator of caspases (SMAC, also termed DIABLO) mimetic, birinapant, promotes extrinsic apoptosis in AML cells. SMAC mimetics induce cleavage of cellular inhibitor of apoptosis (cIAP) proteins, leading to stabilization of the nuclear factor‐κB (NF‐κB)‐inducing kinase (MAP3K14, also termed NIK) and activation of non‐canonical NF‐κB signalling. To enhan...
Source: British Journal of Haematology - August 1, 2014 Category: Hematology Authors: Po Y. Mak, Duncan H. Mak, Vivian Ruvolo, Rodrigo Jacamo, Steven M. Kornblau, Hagop Kantarjian, Michael Andreeff, Bing Z. Carter Tags: Research Paper Source Type: research

Attenuated A20 expression of acute myeloid leukemia-derived dendritic cells increased the anti-leukemia immune response of autologous cytolytic T cells
In this study, A20 expression was up-regulated in AML-DCs activated with tumor necrosis factor (TNF)-α. Then, A20 attenuation with siRNA in AML-DC enhanced the expression of several co-stimulatory molecules and proinflammatory cytokines. Furthermore, after A20 attenuation in AML-DCs, the autologous cytolytic T cells (CTLs) induced by AML-DCs had higher killing capability and specificity for primary AML cells. Additionally, receptor-interacting protein (RIP) and the NF-κBp65 pathway were elevated in AML-DCs when A20 was reduced. Hence, this study identified A20 as a negative regulator for controlling AML-DC maturation and...
Source: Leukemia Research - April 7, 2014 Category: Hematology Authors: Xiaoying Zhang, Yongfeng Su, Haifeng Song, Zhiyong Yu, Bin Zhang, Hu Chen Tags: Clinical Studies Source Type: research

Increased 14-3-3ζ Expression in the Multidrug-Resistant Leukemia Cell Line HL-60/VCR as Compared to the Parental Line Mediates Cell Growth and Apoptosis in Part through Modification of Gene Expression.
Conclusions: Silencing of 14-3-3ζ increased the sensitivity of both sensitive and resistant HL-60 cells to TPT-induced apoptosis, possibly through altering the expression of apoptosis-associated proteins, suggesting that it may be a potential target for MDR AML. © 2014 S. Karger AG, Basel. PMID: 24603438 [PubMed - in process]
Source: Acta Haematologica - March 13, 2014 Category: Hematology Authors: Liang R, Chen XQ, Bai QX, Wang Z, Zhang T, Yang L, Dong BX, Gao GX, Gu HT, Zhu HF Tags: Acta Haematol Source Type: research

RNAi-mediated silencing of MLL-AF9 reveals leukemia-associated downstream targets and processes
Conclusion: Besides potential new therapeutic targets, the described transcription profile shaped by MLL-AF9 provides an information source into the molecular processes altered in MLL aberrant leukemia.
Source: Molecular Cancer - February 11, 2014 Category: Cancer & Oncology Authors: Katrin FleischmannPhilipp PagelIrene SchmidAdelbert Roscher Source Type: research

Upregulation of SOCS-1 by Nutlin-3 in acute myeloid leukemia cells but not in primary normal cells
CONCLUSION: Overall, our data suggest a potential role for the suppressor of cytokine signaling 1 as a therapeutic target of Nutlin-3 in p53 wild-type acute myeloid leukemias.
Source: Clinics - January 24, 2014 Category: Journals (General) Source Type: research

NF-kappa B mediated Up-regulation of CCCTC-binding factor in pediatric acute lymphoblastic leukemia
Conclusions: Our results indicate that CTCF serves as both an anti-apoptotic factor and a proliferative factor in leukemic cells. It potentially contributes to leukemogenesis through the NF-kappaB pathway in pediatric ALL patients.
Source: Molecular Cancer - January 7, 2014 Category: Cancer & Oncology Authors: Han ZhangLin ZhuHuacheng HeShanshan ZhuWei ZhangXiao LiuXiaoxi ZhaoChao GaoMei MeiShilai BaoHuyong Zheng Source Type: research

Leukemia cell-targeted STAT3 silencing and TLR9 triggering generate systemic antitumor immunity
Signal transducer and activator of transcription 3 (STAT3) is an oncogene and immune checkpoint commonly activated in cancer cells and in tumor-associated immune cells. We previously developed an immunostimulatory strategy based on targeted Stat3 silencing in Toll-like receptor 9 (TLR9)-positive hematopoietic cells using CpG-small interfering RNA (siRNA) conjugates. Here, we assessed the therapeutic effect of systemic STAT3 blocking/TLR9 triggering in disseminated acute myeloid leukemia (AML). We used mouse Cbfb-MYH11/Mpl-induced leukemia model, which mimics human inv(16) AML. Our results demonstrate that intravenously del...
Source: Blood - January 2, 2014 Category: Hematology Authors: Hossain, D. M. S., Dos Santos, C., Zhang, Q., Kozlowska, A., Liu, H., Gao, C., Moreira, D., Swiderski, P., Jozwiak, A., Kline, J., Forman, S., Bhatia, R., Kuo, Y.-H., Kortylewski, M. Tags: Plenary Papers, Myeloid Neoplasia, Gene Therapy Source Type: research

Rothia dentocariosa induces TNF‐alpha production in a TLR2‐dependent manner
This article is protected by copyright. All rights reserved.
Source: FEMS Immunology and Medical Microbiology - November 25, 2013 Category: Microbiology Authors: Hideo Kataoka, Makoto Taniguchi, Haruka Fukamachi, Takafumi Arimoto, Hirobumi Morisaki, Hirotaka Kuwata Tags: Short Communication Source Type: research

Distinct poor prognostic subgroups of acute myeloid leukaemia, FLT3-ITD and P-glycoprotein-positive, have contrasting levels of FOXO1
Abstract: Regulation of ABCB1 (P-glycoprotein/Pgp) in AML was investigated. In a historical cohort with Pgp and transcriptional regulator expression profiling data available (n=141), FOXO1 correlated with Pgp protein expression. This was confirmed in an independent cohort (n=204). Down-regulation (siRNA) or hyperactivation (nicotinamide) of FOXO1 led to corresponding changes in Pgp. Low FOXO1 expression correlated with FLT3-ITDs (p
Source: Leukemia Research - November 25, 2013 Category: Hematology Authors: Claire H. Seedhouse, Ken I. Mills, Sophie Ahluwalia, Martin Grundy, Shili Shang, Alan K. Burnett, Nigel H. Russell, Monica Pallis Tags: Laboratory Studies Source Type: research

ERK5 Pathway Regulates Transcription Factors Important for Monocytic Differentiation of Human Myeloid Leukemia Cells
This study was performed using established cell lines HL60 and U937, and primary cultures of blasts from 10 patients with ML. We found that ERK5 and its direct downstream target transcription factor MEF2C are upregulated by 1,25D in parallel with monocytic differentiation. Further, inhibition of ERK5 activity by specific pharmacological agents BIX02189 and XMD8‐92 alters the phenotype of these cells by reducing the abundance of the VDD‐induced surface monocytic marker CD14, and concomitantly increasing surface expression of the general myeloid marker CD11b. Similar results were obtained when the expression of ERK5 was ...
Source: Journal of Cellular Physiology - November 22, 2013 Category: Cytology Authors: Xuening Wang, Stella Pesakhov, Jonathan S Harrison, Michael Danilenko, George P Studzinski Tags: Original Research Article Source Type: research

The role of epigenetics in the regulation of apoptosis in myelodysplastic syndromes and acute myeloid leukemia
Abstract: Disordered stem cell epigenetics and apoptosis-regulating mechanisms contribute essentially to the pathogenesis of myelodysplastic syndromes (MDS) and may trigger disease-progression to secondary acute myeloid leukemia (AML).Expression of apoptosis-mediators FAS (CD95) and DAPK1 the latter being also known for its association with autophagy are upregulated in neoplastic cells in patients with low-risk MDS and epigenetically silenced and downregulated in high-risk MDS and AML as confirmed by a study 50 MDS and 30 AMLs complementing this review. 5-Azacytidine (AZA) and 5-aza-2′deoxycytidine (DAC), promoted FAS an...
Source: Critical Reviews in Oncology Hematology - November 1, 2013 Category: Cancer & Oncology Authors: Heidrun Karlic, Harald Herrmann, Franz Varga, Roman Thaler, Rene Reitermaier, Silvia Spitzer, Viviane Ghanim, Katharina Blatt, Wolfgang R. Sperr, Peter Valent, Michael Pfeilstöcker Source Type: research

Bryostatin 5 induces apoptosis in acute monocytic leukemia cells by activating PUMA and caspases.
Abstract Acute leukemia is a malignant clonal hematopoietic stem cell disease. In the current study, we examined the effects of bryostatin 5 on acute monocytic leukemia cells in vitro and in vivo. We also explored the mechanisms and pathways underlying the increase in apoptosis induced by bryostatin 5. Bryostatin 5 inhibited the growth of primary acute monocytic leukemia cells and U937 cells in a dose- and time-dependent manners. Bryostatin 5 also induced an increase in apoptosis and a decrease in the mitochondrial membrane potential (MMP) in U937 cells. Transmission electron microscopy (TEM) revealed that bryosta...
Source: European Journal of Pharmacology - September 11, 2013 Category: Drugs & Pharmacology Authors: Wang Y, Zhang J, Wang Q, Zhang T, Yang Y, Yang F, Gao G, Dong H, Zhu H, Li Y, Lin H, Tang H, Chen X Tags: Eur J Pharmacol Source Type: research

Gfi-1 is the transcriptional repressor of SOCS1 in acute myeloid leukemia cells.
In this study, we explored the role of histone methylation in SOCS1 expression in AML cells. By ChIP assay, we demonstrated that G9a and SUV39H1, two enzymes catalyzing H3K9 methylation, were physically associated with the SOCS1 promoter, and treatment with chaetocin, a histone methyltransferase inhibitor, suppressed H3K9 methylation on the SOCS1 promoter and enhanced SOCS1 expression. Furthermore, knockdown of G9a and SUV39H1 by siRNA could also induce SOCS1 expression. On the other hand, SOCS1 knockdown by shRNA eliminated chaetocin-induced cell apoptosis. To investigate further whether any transcription factor was invol...
Source: Journal of Leukocyte Biology - September 9, 2013 Category: Hematology Authors: Lee MC, Kuo YY, Chou WC, Hou HA, Hsiao M, Tien HF Tags: J Leukoc Biol Source Type: research

The expression of histone deacetylase 4 is associated with prednisone poor-response in childhood acute lymphoblastic leukemia
In conclusion, our data point to HDAC4 as drug target in childhood ALL, especially in prednisone poor-responders.
Source: Leukemia Research - August 14, 2013 Category: Hematology Authors: Bernd Gruhn, Thomas Naumann, Dorothee Gruner, Mario Walther, Susan Wittig, Sabine Becker, James F. Beck, Jürgen Sonnemann Tags: Clinical Studies Source Type: research