scholarly journals Aberrant nuclear factor-kappa B activity in acute myeloid Leukemia: from molecular pathogenesis to therapeutic target

Oncotarget ◽  
2015 ◽  
Vol 6 (8) ◽  
pp. 5490-5500 ◽  
Author(s):  
Jianbiao Zhou ◽  
Ying Qing Ching ◽  
Wee-Joo Chng
Keyword(s):  
Acute Myeloid Leukemia ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Nuclear Factor Kappa B ◽  
Molecular Pathogenesis ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Acute Myeloid

scholarly journals CXXC5 (Retinoid-Inducible Nuclear Factor, RINF) is a Potential Therapeutic Target in High-Risk Human Acute Myeloid Leukemia

Oncotarget ◽  
2013 ◽  
Vol 4 (9) ◽  
pp. 1438-1448 ◽  
Author(s):  
Audrey Astori ◽  
Hanne Fredly ◽  
Thomas Aquinas Aloysius ◽  
Lars Bullinger ◽  
Véronique Mansat-De Mas ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
High Risk ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Nuclear Factor ◽  
Potential Therapeutic Target ◽  
Human Acute Myeloid Leukemia ◽  
Acute Myeloid

scholarly journals Novel Targeted Nano-Parthenolide Molecule against NF-kB in Acute Myeloid Leukemia

Molecules ◽  
2019 ◽  
Vol 24 (11) ◽  
pp. 2103 ◽  
Author(s):  
Noureldien H. E. Darwish ◽  
Thangirala Sudha ◽  
Kavitha Godugu ◽  
Dhruba J. Bharali ◽  
Osama Elbaz ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Nuclear Factor Kappa B ◽  
Leukemic Cell ◽  
Leukemic Cells ◽  
Nuclear Factor ◽  
Normal Cells ◽  
Selective Targeting ◽  
Acute Myeloid

The targeted nano-encapsulation of anticancer drugs can improve drug delivery and the selective targeting of cancer cells. Nuclear factor kappa B (NF-kB) is a regulator for different biological responses, including cell proliferation and differentiation. In acute myeloid leukemia (AML), constitutive NF-κB has been detected in more than 50% of cases, enabling leukemic cells to resist apoptosis and stimulate uncontrolled proliferation. We evaluated NF-kB expression in bone marrow samples from 103 patients with AML using quantitative real time polymerase chain reaction (RT-PCR) and found that expression was increased in 80.5% (83 out 103) of these patients with AML in comparison to the control group. Furthermore, overexpressed transmembrane glycoprotein (CD44) on leukemic cells in comparison to normal cells is known to play an important role in leukemic cell engraftment and survival. We designed poly lactide co-glycolide (PLGA) nanoparticles conjugated with antiCD44 and encapsulating parthenolide (PTL), a nuclear factor kappa B (NF-kB) inhibitor, in order to improve the selectivity and targeting of leukemic cells and to spare normal cells. In vitro, in leukemic cell lines Kasumi-1, KG-1a, and THP-1, proliferation was decreased by 40% (** p < 0.01) with 5 µM PLGA-antiCD44-PTL nanoparticles in comparison to the same concentration of free PTL (~10%). The higher uptake of the nanoparticles by leukemic cells was confirmed with confocal microscopy. In conclusion, PLGA-antiCD44-PTL nanoparticles improved the bioavailability and selective targeting of leukemic cells, thus holding promise as a drug delivery system to improve the cure rate of AML.

scholarly journals HDAC8: A Promising Therapeutic Target for Acute Myeloid Leukemia

2020 ◽  
Vol 8 ◽  
Author(s):  
Marco Spreafico ◽  
Alicja M. Gruszka ◽  
Debora Valli ◽  
Mara Mazzola ◽  
Gianluca Deflorian ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Promising Therapeutic Target ◽  
Acute Myeloid

scholarly journals Arginine dependence of acute myeloid leukemia blast proliferation: a novel therapeutic target

Blood ◽  
2015 ◽  
Vol 125 (15) ◽  
pp. 2386-2396 ◽  
Author(s):  
Francis Mussai ◽  
Sharon Egan ◽  
Joseph Higginbotham-Jones ◽  
Tracey Perry ◽  
Andrew Beggs ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Leukemia Blast ◽  
Key Points ◽  
Acute Myeloid Leukemia Blast ◽  
Acute Myeloid ◽  
Novel Therapeutic

Key Points Arginase depletion with BCT-100 pegylated recombinant human arginase is cytotoxic to AML blasts.

scholarly journals The retinoic acid receptor co-factor NRIP1 is uniquely upregulated and represents a therapeutic target in acute myeloid leukemia with chromosome 3q rearrangements

Haematologica ◽  
2021 ◽  
Author(s):  
Sarah Grasedieck ◽  
Ariene Cabantog ◽  
Liam MacPhee ◽  
Junbum Im ◽  
Christoph Ruess ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Therapeutic Target ◽  
Myeloid Leukemia ◽  
Integration Site ◽  
Retinoic Acid Receptor ◽  
Aberrant Expression ◽  
Interacting Protein ◽  
Disease Subtype ◽  
Non Coding Rna ◽  
Acute Myeloid

Aberrant expression of Ecotropic Viral Integration Site 1 (EVI1) is a hallmark of acute myeloid leukemia (AML) with inv(3) or t(3;3), which is a disease subtype with especially poor outcome. In studying transcriptomes from AML patients with chromosome 3q rearrangements, we identified a significant upregulation of the Nuclear Receptor Interacting Protein 1 (NRIP1) as well as its adjacent non-coding RNA LOC101927745. Utilizing transcriptomic and epigenomic data from over 900 primary patient samples as well as genetic and transcriptional engineering approaches, we have identified several mechanisms that can lead to upregulation of NRIP1 in AML. We hypothesize that the LOC101927745 transcription start site harbors a context-dependent enhancer that is bound by EVI1, causing upregulation of NRIP1 in AML with chr3 abnormalities. Furthermore, we show that NRIP1 knockdown negatively affects the proliferation and survival of 3q-rearranged AML cells and increases their sensitivity towards ATRA, suggesting that NRIP1 is relevant for the pathogenesis of inv(3)/t(3;3) AML and could serve as a novel therapeutic target in myeloid malignancies with 3q abnormalities.

scholarly journals NMR-Based Metabolomic Analysis of the Molecular Pathogenesis of Therapy-Related Myelodysplasia/Acute Myeloid Leukemia

2011 ◽  
Vol 10 (6) ◽  
pp. 2873-2881 ◽  
Author(s):  
Kristin E. Cano ◽  
Liang Li ◽  
Smita Bhatia ◽  
Ravi Bhatia ◽  
Stephen J. Forman ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Molecular Pathogenesis ◽  
Metabolomic Analysis ◽  
Acute Myeloid
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