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Cancer: Acute Leukemia

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Total 260 results found since Jan 2013.

Carbon monoxide decreases interleukin-1β levels in the lung through the induction of pyrin.
In this report, we show that the CO-releasing molecule (CORM-2) can stimulate the expression of pyrin, a negative regulator of the NLRP3 inflammasome. CORM-2 increased the transcription of pyrin in the human leukemic cell line (THP-1) in the absence and presence of lipopolysaccharide (LPS). In THP-1 cells, CORM-2 treatment dose-dependently reduced the activation of caspase-1 and the secretion of IL-1β, and increased the levels of IL-10, in response to LPS and adenosine 5'-triphosphate (ATP), an NLRP3 inflammasome activation model. Genetic interference of IL-10 by small interfering RNA (siRNA) reduced the effectiveness of ...
Source: Cellular and Molecular Immunology - October 5, 2015 Category: Molecular Biology Authors: Kim SK, Joe Y, Chen Y, Ryu J, Lee JH, Cho GJ, Ryter SW, Chung HT Tags: Cell Mol Immunol Source Type: research

Reversal of chemoresistance with small interference RNA (siRNA) in etoposide resistant acute myeloid leukemia cells (HL-60).
CONCLUSIONS: Our results indicate that product of the ABCB1 gene have effective role in resistance to etoposide in acute myeloid leukemia cells. PMID: 26463638 [PubMed - in process]
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - October 1, 2015 Category: Drugs & Pharmacology Authors: Kachalaki S, Baradaran B, Majidi J, Yousefi M, Shanehbandi D, Mohammadinejad S, Mansoori B Tags: Biomed Pharmacother Source Type: research

Reversal of chemoresistance with small interference RNA (siRNA) in etoposide resistant acute myeloid leukemia cells (HL-60)
Conclusions Our results indicate that product of the ABCB1 gene have effective role in resistance to etoposide in acute myeloid leukemia cells.
Source: Biomedicine and Pharmacotherapy - September 26, 2015 Category: Drugs & Pharmacology Source Type: research

Rapamycin restores p14, p15 and p57 expression and inhibits the mTOR/p70S6K pathway in acute lymphoblastic leukemia cells.
Abstract The aim of the present study was to investigate the effects of rapamycin and its underlying mechanisms on acute lymphoblastic leukemia (ALL) cells. We found that the p14, p15, and p57 genes were not expressed in ALL cell lines (Molt-4 and Nalm-6) and adult ALL patients, whereas mTOR, 4E-BP1, and p70S6K were highly expressed. In Molt-4 and Nalm-6 cells exposed to rapamycin, cell viability decreased and the cell cycle was arrested at the G1/S phase. Rapamycin restored p14, p15, and p57 gene expression through demethylation of the promoters of these genes. As expected, rapamycin also increased p14 and p15 pr...
Source: International Journal of Hematology - September 11, 2015 Category: Hematology Authors: Li H, Kong X, Cui G, Ren C, Fan S, Sun L, Zhang Y, Cao R, Li Y, Zhou J Tags: Int J Hematol Source Type: research

Abstract 4997: Phosphorylation of SLAP by the KIT-D816V oncogenic mutant suppresses SLAP-mediated negative regulation of KIT signaling
The SRC-like-adaptor protein (SLAP) is a negative regulator of mitogenic signaling. SLAP shares considerable structural homology with SRC, apart from lacking a kinase domain. SLAP is known to be expressed in a variety of cells and regulates cell surface receptor signaling by direct association. Here we show that SLAP interacts with the type III receptor tyrosine kinase KIT and also with its oncogenic mutant KIT-D816V. This mutant has been described as a driving mutant in several cancers including mastocytosis and certain types of acute myeloid leukemia. The association is mediated through phosphotyrosine residues in KIT an...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Kazi, J. U., Sun, J., Ronnstrand, L. Tags: Molecular and Cellular Biology Source Type: research

Abstract 3591: Inhibition of heme oxygenase 1 decreases proliferation and resensitizes TKI-resistant Flt3-ITD-positive AML cells
Acute myelogenous leukemia (AML) afflicts ∼12,330 new patients per year in the United States. Regrettably, only 25% of patients will survive five years past diagnosis. The most common mutation in AML is internal tandem duplication (ITD) of the juxtamembrane domain of the fms-like tyrosine kinase receptor-3 (Flt3), which renders it constitutively active. This mutation correlates with poor clinical prognosis and has been targeted therapeutically. Unfortunately, Flt3-directed tyrosine kinase inhibitors (TKI) have shown only modest benefit as single agents. Additionally, relapse and resistance are major factors in the treatm...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Irwin, M. E., Chandra, J. Tags: Experimental and Molecular Therapeutics Source Type: research

Abstract 2090: GLI3 repressor levels determine Hedgehog pathway activity and predict response to Smoothened antagonist in acute myeloid leukemia
The Hedgehog (Hh) signaling pathway is activated in most hematological and solid cancers and is a promising target for therapeutic development. Deletions in the receptor Patched (PTCH) or activating mutations in the upstream positive regulator Smoothened (SMO) have been reported in a few cancers such as basal cell carcinoma and medulloblastoma, but are largely absent in most tumor types; therefore, the mechanism of pathway activation in most cancers remains unknown. In normal tissues, Hh pathway activation via PTCH/SMO causes an increase in the downstream activating transcription factor GLI1 and a decrease in the transcr...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Chaudhry, P., Singh, M., Triche, T., Jorapur, A., Gill, P. S., Merchant, A. Tags: Molecular and Cellular Biology Source Type: research

Abstract 4381: High efficacy of T-LAK cell-originated protein kinase inhibitor in acute myeloid leukemia with FLT3-ITD mutation
The internal tandem duplication (FLT3-ITD) a gain-of-function mutation of FLT3, is associated with poor outcome in acute myeloid leukemia (AML). The use of FLT3 inhibitors currently undergoing clinical investigation has not yet improved overall survival. Therefore, novel therapies are needed. T-LAK cell-originated protein kinase (TOPK), a serine-threonine protein kinase, is highly expressed and associated with an aggressive cancer phenotype, but is hardly detectable in normal tissues. Here, we investigate TOPK in AML and demonstrate that it is highly expressed in most AML cell lines and some primary blasts, but is not dete...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Alachkar, H., Mutonga, M., Park, J.-H., Malnassy, G., Woods, A., Raca, G., Odenike, O. M., Takamatsu, N., Miyamoto, T., Hisada, S., Matsuo, Y., Stock, W., Nakamura, Y. Tags: Experimental and Molecular Therapeutics Source Type: research

Induction of cytosine arabinoside-resistant human myeloid leukemia cell death through autophagy regulation by hydroxychloroquine.
Abstract We investigated the effects of the autophagy inhibitor hydroxychloroquine (HCQ) on cell death of cytosine arabinoside (Ara-C)-resistant human acute myeloid leukemia (AML) cells. Ara-C-sensitive (U937, AML-2) and Ara-C-resistant (U937/AR, AML-2/AR) human AML cell lines were used to evaluate HCQ-regulated cytotoxicity, autophagy, and apoptosis as well as effects on cell death-related signaling pathways. We found that HCQ-induced dose- and time-dependent cell death in Ara-C-resistant cells compared to Ara-C-sensitive cell lines. The extent of cell death and features of HCQ-induced autophagic markers includin...
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - July 1, 2015 Category: Drugs & Pharmacology Authors: Kim Y, Eom JI, Jeung HK, Jang JE, Kim JS, Cheong JW, Kim YS, Min YH Tags: Biomed Pharmacother Source Type: research

Autocrine motility factor receptor promotes the proliferation of human acute monocytic leukemia THP-1 cells.
In conclusion, AMFR appears to be crucial for the proliferation of the THP‑1 acute monocytic leukemia cell line. Therefore, AMFR may represent a potential target for the treatment of acute monocytic leukemia. PMID: 26136223 [PubMed - as supplied by publisher]
Source: International Journal of Molecular Medicine - June 30, 2015 Category: Molecular Biology Authors: Wang Y, Ma L, Wang C, Sheng G, Feng L, Yin C Tags: Int J Mol Med Source Type: research

Induction of cytosine arabinoside-resistant human myeloid leukemia cell death through autophagy regulation by hydroxychloroquine
Publication date: Available online 30 May 2015 Source:Biomedicine & Pharmacotherapy Author(s): Yundeok Kim , Ju-In Eom , Hoi-Kyung Jeung , Ji Eun Jang , Jin Seok Kim , June-Won Cheong , Young Sam Kim , Yoo Hong Min We investigated the effects of the autophagy inhibitor hydroxychloroquine (HCQ) on cell death of cytosine arabinoside (Ara-C)-resistant human acute myeloid leukemia (AML) cells. Ara-C (cytosine arabinoside)-sensitive (U937, AML-2) and Ara-C-resistant (U937/AR, AML-2/AR) human myeloid leukemia cell lines were used to evaluate HCQ-regulated cytotoxicity, autophagy, and apoptosis, as well as effects on ce...
Source: Biomedicine and Pharmacotherapy - June 20, 2015 Category: Drugs & Pharmacology Source Type: research

Modulation of glucocorticoid resistance in pediatric T-cell Acute Lymphoblastic Leukemia by increasing BIM expression with the PI3K/mTOR inhibitor BEZ235.
CONCLUSIONS: Our data support the further investigation of agents targeting the PI3K/mTOR pathway to modulate glucocorticoid resistance in T-ALL. PMID: 26080839 [PubMed - as supplied by publisher]
Source: Clinical Cancer Research - June 16, 2015 Category: Cancer & Oncology Authors: Hall CP, Reynolds CP, Kang MH Tags: Clin Cancer Res Source Type: research

The Association between p38 MAPK‐Mediated TNF‐α/TNFR2 Up‐Regulation and 2‐(4‐Aminophenyl)‐7‐Methoxybenzothiazole‐Induced Apoptosis in Human Leukemia U937 Cells
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Physiology - June 8, 2015 Category: Cytology Authors: Chia‐Hui Huang, Ying‐Jung Chen, Tzu‐Yu Chao, Wen‐Hsin Liu, Jung‐Jung Changchien, Wan‐Ping Hu, Long‐Sen Chang Tags: Original Research Article Source Type: research

WEHI-3 cells inhibit adipocyte differentiation in 3T3-L1 cells.
Abstract By investigating the anti-adipogenic effects of WEHI-3 cells - a murine acute myelomonocytic leukemia cell line - we sought to improve the efficiency of hematopoietic stem cell transplantation (HSCT). Analysis of Oil Red O staining and the expression of adipogenic genes, including PPARγ, C/EBPα, FAS and LPL, indicated that WEHI-3 cells significantly inhibited 3T3-L1 mouse preadipocyte cells from differentiating into adipocytes. In vivo, fat vacuoles in mice injected with WEHI-3 cells were also remarkably reduced in the murine bone marrow pimelosis model. Moreover, the key gene in the Rho signaling path...
Source: Biochemical and Biophysical Research communications - April 21, 2015 Category: Biochemistry Authors: Lai J, Liu G, Yan G, He D, Zhou Y, Chen S Tags: Biochem Biophys Res Commun Source Type: research

Haploinsufficiency of the c-myc transcriptional repressor FIR, as a dominant negative-alternative splicing model, promoted p53-dependent T-cell acute lymphoblastic leukemia progression by activating Notch1.
In conclusion, the alternative splicing of FIR, which generates FIRΔexon2, may contribute to both colorectal carcinogenesis and leukemogenesis. PMID: 25671302 [PubMed - as supplied by publisher]
Source: Oncotarget - February 13, 2015 Category: Cancer & Oncology Tags: Oncotarget Source Type: research