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Cancer: Burkitt Lymphoma

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Total 23 results found since Jan 2013.

Inhibition of JAK2/STAT3 Signaling Pathway Suppresses Proliferation of Burkitt's Lymphoma Raji Cells via Cell Cycle Progression, Apoptosis, and Oxidative Stress by Modulating HSP70.
CONCLUSIONS Blocking the JAK2/STAT3 signaling pathway may inhibit proliferation, induce cell cycle arrest, and promote oxidative stress and apoptosis in Raji cells via the down-regulation of HSP70. PMID: 30194286 [PubMed - in process]
Source: Medical Science Monitor - September 9, 2018 Category: Research Tags: Med Sci Monit Source Type: research

MiR-29 silencing modulates the expression of target genes related to proliferation, apoptosis and methylation in Burkitt lymphoma cells
ConclusionsOur results suggest a significant role for miR-29s in BL pathogenesis in altering the expression of targets involved in critical cancer pathways, such as cell cycle control, apoptosis inhibition and DNA methylation. Moreover, methylation-mediated miR-29 epigenetic silencing may occur during BL development.
Source: Journal of Cancer Research and Clinical Oncology - January 9, 2018 Category: Cancer & Oncology Source Type: research

EGF-Induced VEGF Exerts a PI3K-Dependent Positive Feedback on ERK and AKT through VEGFR2 in Hematological < i > In Vitro < /i > Models
This study investigated the crosstalk between EGFR and VEGFR2 signaling in two hematologicalin vitro models: THP1, a human monocytic leukemia, and Raji, a Burkitt ’s lymphoma, cell lines. Results showed that both cell lines express EGFR and VEGFR2 and responded to EGF stimulation by activating EGFR, triggering VEGF production and phosphorylating ERK, AKT, and p38 very early, with a peak of expression at 10–20min. Blocking EGFR using Tyrphostin resulted in inhibiting EGFR induced activation of ERK, AKT, and p38. In addition, EGF stimulation caused a significant and immediate increase, within 1min, in pVEGFR2 in both cel...
Source: PLoS One - November 1, 2016 Category: Biomedical Science Authors: Lilian Saryeddine Source Type: research

Abstract 3617: Inhibition of KLF4 expression in resistant B-NHL cell lines inhibited cell growth and sensitized the cells to drug-induced apoptosis
In conclusion, the overexpression of KLF4 may be responsible, in part, in the pathogenesis, malignancy, and drug resistance of B-NHL lymphomas. In addition, the present findings suggest that the chemical inhibition of KLF4 by Kenpaullone treatment or the inhibition of YY1 may be considered as targets for therapeutic intervention in the treatment of B-lymphoma overexpressing KLF4, when used alone or in combination with sub-toxic chemo/immune-drugs. Current studies are evaluating the role of KLF4 inhibition in vivo using B-NHL tumor xenografts models.Citation Format: Mayra R. Montecillo-Aguado, Gabriel G. Vega, Hector Mayani...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Montecillo–Aguado, M. R., Vega, G. G., Mayani, H., Huerta–Yepez, S., Hernandez–Pando, R., Martinez–Maza, O., Bonavida, B., Vega, M. I. Tags: Experimental and Molecular Therapeutics Source Type: research

Histone deacetylase 6 activity is critical for the metastasis of Burkitt’s lymphoma cells
Conclusions: We identified a critical role of HDAC6 in the metastasis of Burkitt?s lymphoma cells, suggesting that pharmacological inhibition of HDAC6 could be a promising strategy for the management of metastatic Burkitt?s lymphoma.
Source: BioMed Central - December 5, 2014 Category: Journals (General) Authors: Ning DingLingyan PingLixia FengXiaohui ZhengYuqin SongJun Zhu Source Type: research

Histone deacetylase 6 activity is critical for the metastasis of Burkitt¿s lymphoma cells
Conclusions: We identified a critical role of HDAC6 in the metastasis of Burkitt?s lymphoma cells, suggesting that pharmacological inhibition of HDAC6 could be a promising strategy for the management of metastatic Burkitt?s lymphoma.
Source: Cancer Cell International - December 5, 2014 Category: Cancer & Oncology Authors: Ning DingLingyan PingLixia FengXiaohui ZhengYuqin SongJun Zhu Source Type: research

Histone deacetylase inhibitor potentiated the ability of MTOR inhibitor to induce autophagic cell death in Burkitt leukemia/lymphoma
Conclusions: These findings confirmed the synergistic effect of the HDAC and MTOR inhibitors on Burkitt leukemia/lymphoma, and provided an insight into clinical application of targeting autophagy in treating MYC-associated lymphoid malignancies.
Source: Journal of Hematology and Oncology - July 18, 2013 Category: Hematology Authors: Li Hua DongShu ChengZhong ZhengLi WangYang ShenZhi Xiang ShenSai Juan ChenWei Li Zhao Source Type: research

Lentiviral Vector-Mediated siRNA Knockdown of c-MYC: Cell Growth Inhibition and Cell Cycle Arrest at G2/M Phase in Jijoye Cells.
Abstract Inhibition of c-MYC has been considered as a potential therapy for lymphoma treatment. We explored a lentiviral vector-mediated small interfering RNA (siRNA) expression vector to stably reduce c-MYC expression in B cell line Jijoye cells and investigated the effects of c-MYC downregulation on cell growth, cell cycle, and apoptosis in vitro. The expression of c-MYC mRNA and protein levels were inhibited significantly by c-MYC siRNA. The c-MYC downregulation resulted in the inhibition of cell proliferation and cell cycle arrest at G2/M phase, which was associated with decreased expression of cyclin B and cy...
Source: Biochemical Genetics - May 9, 2013 Category: Genetics & Stem Cells Authors: Song A, Ye J, Zhang K, Sun L, Zhao Y, Yu H Tags: Biochem Genet Source Type: research