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Cancer: Acute Lymphoblastic Leukemia

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Total 33 results found since Jan 2013.

Effect of siRNA-mediated silencing of p53R2 gene on sensitivity of T-ALL cellsto Daunorubicin
CONCLUSION: The results of the present study showed that silencing of p53R2 using siRNA can significantly increase the antitumor effects of Daunorubicin on T-ALL cells. Therefore, p53R2 siRNA has the potential to be used as an adjuvant therapy in combination with Daunorubicin in T-ALL.PMID:37419428 | DOI:10.1016/j.gene.2023.147622
Source: Gene - July 7, 2023 Category: Genetics & Stem Cells Authors: Omid KianiGhalesardi Farhad Zaker Abbas Ghotaslou Hassan Boustani Mohammad Reza Rezvani Jafar Kiani Minoo Shahidi Source Type: research

Targeted therapy with MXD3 siRNA, anti‐CD22 antibody and nanoparticles for precursor B‐cell acute lymphoblastic leukaemia
In this study, we hypothesize that an effective siRNA therapy for preB ALL can be developed using antiCD22 antibody (αCD22 Ab) and nanoparticles. We composed nanocomplexes with super paramagnetic iron oxide nanoparticles (SPIO NPs), αCD22 Abs and MXD3 siRNA molecules based on physical interactions between the molecules. We demonstrated that the MXD3 siRNA‐αCD22 Ab‐SPIO NP complexes entered leukaemia cells and knocked down MXD3, leading the cells to undergo apoptosis and resulting in decreased live cell counts in the cell line Reh and in primary preB ALL samples in vitro. Furthermore, the cytotoxic effects of the MXD...
Source: British Journal of Haematology - September 8, 2014 Category: Hematology Authors: Noriko Satake, Connie Duong, Cathy Chen, Gustavo A. Barisone, Elva Diaz, Joseph Tuscano, David M. Rocke, Jan Nolta, Nitin Nitin Tags: Research Paper Source Type: research

Inhibition of SMYD2 Sensitized Cisplatin to Resistant Cells in NSCLC Through Activating p53 Pathway
In conclusion, the present study elucidated that the activity of SMYD2 in NSCLC may affect the cell sensitivity to chemotherapeutic agents, especially to CDDP. The elevated SMYD2 mediated CDDP resistance and malignant phenotype in NSCLC, indicating that SMYD2 may be a useful biomarker of CDDP resistance in NSCLC. Inhibition of SMYD2 contributes to the methylation-related activation of p53 and thus results in cell apoptosis. Furthermore, combination treatment with CDDP and an SMYD2 inhibitor had a synergistically antitumor effects in a xenograft model in vivo. Given that SMYD2 has reversible effects and is a targetable prot...
Source: Frontiers in Oncology - April 25, 2019 Category: Cancer & Oncology Source Type: research

Non-canonical Notch Signaling Regulates Actin Remodeling in Cell Migration by Activating PI3K/AKT/Cdc42 Pathway
In conclusion, our research results indicate that DAPT activates PI3K/AKT/Cdc42 signaling by non-canonical Notch pathway, and the activated Cdc42 promotes the filopodia formation and inhibits lamellipodia assembly, resulting in reduced migration of breast cancer cells. The results imply that non-canonical Notch signaling may play a very important role in the rapid response of cells to the extracellular signals. Author Contributions LG, JD, and LL designed the study and wrote and revised the manuscript. LL and LZ performed most of the experiments and data analysis. SZ, X-YZ, P-XM, Y-DM, Y-YW, YC, S-JT, and Y-JZ assisted i...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

HMGB1 Interacts with the MLL-AF4 Fusion Complex to Regulate Pro-Leukemic Gene Transcription in Infant Acute Lymphoblastic Leukemia
In this study, we generated an HMGB1 siRNA knockdown in primary MLL-ALL cells from 3 infants to test our hypothesis that HMGB1-MLL interactions regulate pro-leukemic gene expression and represent a rational therapeutic target.CD19-selected leukemic blasts were isolated from the cryopreserved bone marrow or peripheral blood specimens of 3 infants with cytogenetically confirmed MLL-AF4 rearrangements. HMGB1 knockdown was confirmed by comparing HMGB1 mRNA and protein expression, by qPCR and Western Blot, in cells transfected with HMGB1 vs. control sequence siRNA. First, determined whether HMGB1 knockdown affected expression o...
Source: Blood - November 21, 2018 Category: Hematology Authors: Toia, L. M., Braverman, E. L., Magno, J. A., Shand, J. C. Tags: 602. Disordered Gene Expression in Hematologic Malignancy, including Disordered Epigenetic Regulation: Poster II Source Type: research

Decreased expression of the augmenter of liver regeneration results in growth inhibition and increased chemosensitivity of acute T lymphoblastic leukemia cells.
In conclusion, the results of this study demonstrated that targeted inhibition of the ALR expression in Jurkat cells triggered cell growth inhibition and sensitized cells to VCR via promoting apoptosis and regulating the cell cycle. PMID: 29048676 [PubMed - as supplied by publisher]
Source: Oncology Reports - October 20, 2017 Category: Cancer & Oncology Tags: Oncol Rep Source Type: research

Abstract 3964: NVP-BEZ235 enhances dexamethasone-induced BIM expression and apoptosis in models of T-ALL with PTEN dysfunction and increased PI3K/AKT activity
Introduction: Glucocorticoid (GC) resistance presents a major challenge in pediatric acute lymphoblastic leukemia (ALL) treatment. Increased activation of the PI3K/AKT pathway, which may occur following loss of PTEN function, may be a possible mechanism of GC resistance. We therefore investigated the effects of inhibiting the PI3K/AKT pathway with the dual PI3K/mTOR inhibitor NVP-BEZ235 on the enhancement of dexamethasone activity in in vitro and in vivo models of ALL and the role the PI3K/AKT pathway plays in resistance to GCs. Methods: Cytotoxicity of NVP-BEZ235, dexamethasone, and the combination were evaluated using DI...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Hall, C., Kang, M. Tags: Tumor Biology Source Type: research

Silencing of LSD1 gene modulates histone methylation and acetylation and induces the apoptosis of JeKo-1 and MOLT-4 cells.
In this study, we evaluated LSD1, and histone H3 lysine 4 (H3K4)me1 and H3K4me2 expression in patients with MCL and silenced LSD1 in JeKo‑1 and MOLT‑4 cells, in order to define its role in JeKo‑1 and MOLT‑4 cell proliferation and apoptosis. We retrospectively analyzed the protein expression of LSD1, and mono- and dimethylated H3K4 (H3K4me1 and H3K4me2), and cyclin D1 and Ki67 in 30 cases of MCL by immunohistochemistry. The correlation of LSD1, H3K4me1 and H3K4me2 with Ki67 was determined by statistical analysis. LSD1 was silenced by small interfering RNA (siRNA). Cell apoptosis and cell proliferation were d...
Source: International Journal of Molecular Medicine - June 19, 2017 Category: Molecular Biology Authors: Zou ZK, Huang YQ, Zou Y, Zheng XK, Ma XD Tags: Int J Mol Med Source Type: research

L-Tetrahydropalmatine Induces Apoptosis in EU-4 Leukemia cells by Down-Regulating X-linked inhibitor of apoptosis protein and increases the sensitivity towards Doxorubicin.
CONCLUSION: Findings of the study confirm that L-THP resulted in p53 independent apoptosis via down-regulating XIAP protein by inhibiting MDM2 associated with proteasome-dependent pathway and increased sensitivity of EU-4 cells against doxorubicin. L-THP caused activation of caspase and resulted in apoptosis, L-THP may be a novel molecule for inducing apoptosis specifically in p53 null leukemia EU-4 cells. PMID: 28721806 [PubMed - as supplied by publisher]
Source: Current Molecular Medicine - July 18, 2017 Category: Molecular Biology Authors: Li S, Chen D, Pei R, Lu Y, Zhang P, Ma J, Liu X, Du X, Sha K, Chen L, Cao J, Zhuang X, Wu J, Li L, Fan Z, Ye P, Tang S, Zhang B, Shi X, Li K Tags: Curr Mol Med Source Type: research

Physcion blocks cell cycle and induces apoptosis in human B cell precursor acute lymphoblastic leukemia cells by downregulating HOXA5.
This study is aimed to investigate the anti-leukemia activity of physcion in ALL. Our results have showed that physcion could significantly suppress cell growth, induce apoptosis and blocked cell cycle progression in vitro. Mechanistically, we found that physcion downregulated the expression of HOXA5, which is responsible for the anti-leukemia activity of physcion. To verify this finding, siRNA targeting HOXA5 and overexpressing plasmid were used to repress HOXA5 expression and introduce ectopic overexpression of HOXA5 in ALL cell lines, respectively. Our results showed that overexpression of HOXA5 significantly abrogated ...
Source: Biomedicine and pharmacotherapy = Biomedecine and pharmacotherapie - August 10, 2017 Category: Drugs & Pharmacology Authors: Gao F, Liu W, Guo Q, Bai Y, Yang H, Chen H Tags: Biomed Pharmacother Source Type: research

Notch1 is required for hypoxia-induced proliferation, invasion and chemoresistance of T-cell acute lymphoblastic leukemia cells
Conclusions: Notch1 signalling is required for hypoxia/HIF-1alpha-induced proliferation, invasion and chemoresistance in T-ALL. Pharmacological inhibitors of HIF-1alpha or Notch1 signalling may be attractive interventions for T-ALL treatment.
Source: Journal of Hematology and Oncology - January 5, 2013 Category: Hematology Authors: Jie ZouPeng LiFei LuNa LiuJianjian DaiJingjing YeXun QuXiulian SunDaoxin MaJino ParkChunyan Ji 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

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