scholarly journals Correction to Targeted Co-delivery of the Iron Chelator Deferoxamine and a HIF1α Inhibitor Impairs Pancreatic Tumor Growth

ACS Nano ◽  
2020 ◽  
Vol 14 (1) ◽  
pp. 1211-1211 ◽  
Author(s):  
Jiayan Lang ◽  
Xiao Zhao ◽  
Xiuchao Wang ◽  
Ying Zhao ◽  
Yiye Li ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Pancreatic Tumor ◽  
Iron Chelator ◽  
Iron Chelator Deferoxamine

scholarly journals Synergistic inhibition of lymphoid tumor growth in vitro by combined treatment with the iron chelator deferoxamine and an immunoglobulin G monoclonal antibody against the transferrin receptor

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 991-995 ◽  
Author(s):  
JD Kemp ◽  
KM Smith ◽  
LJ Kanner ◽  
F Gomez ◽  
JA Thorson ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Immunoglobulin G ◽  
Transferrin Receptor ◽  
Picolinic Acid ◽  
Combined Treatment ◽  
Iron Chelator ◽  
Response Analysis ◽  
Synergistic Inhibition ◽  
Iron Chelator Deferoxamine

Abstract Data are presented indicating that the growth of 5 out of 5 murine lymphoid tumors can be inhibited in a synergistic fashion in vitro by combined treatment with the iron chelator deferoxamine (DFO) and an immunoglobulin G (IgG) monoclonal anti-transferrin receptor antibody (ATRA). A two-way dose/response analysis shows that the ATRA becomes more efficient as an inhibitor with increasing doses of DFO. Flow cytometric studies further support the view that IgG ATRAS impair transferrin receptor (TR) function by causing TR down-modulation and degradation, even when the presence of DFO acts to promote increased cell surface TR expression. It is also shown that an IgG ATRA is nearly as effective as an IgM ATRA in inhibiting tumor cell growth when used in combination with DFO. Finally, studies with the iron chelator picolinic acid show that it produces only additive, or very slightly supra-additive, effects when used in combination with the ATRA. Therefore, these studies not only continue to suggest that combination chelator/ATRA therapy warrants further investigation as a tool in the therapy of hematopoietic malignancies, but also make the following new points: (1) the clinically familiar iron chelator deferoxamine, but not all iron chelators, produces synergistic inhibition of tumor growth in vitro with ATRAS; and (2) IgG ATRAS, which may be clinically more attractive reagents than IgA or IgM ATRAS because of better access to extra vascular tissue spaces, have unexpectedly been found to function as powerful growth inhibitors when used in combination with DFO.

scholarly journals Synergistic inhibition of lymphoid tumor growth in vitro by combined treatment with the iron chelator deferoxamine and an immunoglobulin G monoclonal antibody against the transferrin receptor

Blood ◽  
1990 ◽  
Vol 76 (5) ◽  
pp. 991-995
Author(s):  
JD Kemp ◽  
KM Smith ◽  
LJ Kanner ◽  
F Gomez ◽  
JA Thorson ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Immunoglobulin G ◽  
Transferrin Receptor ◽  
Picolinic Acid ◽  
Combined Treatment ◽  
Iron Chelator ◽  
Response Analysis ◽  
Synergistic Inhibition ◽  
Iron Chelator Deferoxamine

Data are presented indicating that the growth of 5 out of 5 murine lymphoid tumors can be inhibited in a synergistic fashion in vitro by combined treatment with the iron chelator deferoxamine (DFO) and an immunoglobulin G (IgG) monoclonal anti-transferrin receptor antibody (ATRA). A two-way dose/response analysis shows that the ATRA becomes more efficient as an inhibitor with increasing doses of DFO. Flow cytometric studies further support the view that IgG ATRAS impair transferrin receptor (TR) function by causing TR down-modulation and degradation, even when the presence of DFO acts to promote increased cell surface TR expression. It is also shown that an IgG ATRA is nearly as effective as an IgM ATRA in inhibiting tumor cell growth when used in combination with DFO. Finally, studies with the iron chelator picolinic acid show that it produces only additive, or very slightly supra-additive, effects when used in combination with the ATRA. Therefore, these studies not only continue to suggest that combination chelator/ATRA therapy warrants further investigation as a tool in the therapy of hematopoietic malignancies, but also make the following new points: (1) the clinically familiar iron chelator deferoxamine, but not all iron chelators, produces synergistic inhibition of tumor growth in vitro with ATRAS; and (2) IgG ATRAS, which may be clinically more attractive reagents than IgA or IgM ATRAS because of better access to extra vascular tissue spaces, have unexpectedly been found to function as powerful growth inhibitors when used in combination with DFO.

Role of Protein kinase D2 in pancreatic tumor growth and tumor angiogenesis

2010 ◽  
Vol 48 (08) ◽  
Author(s):  
N Azoitei ◽  
GV Pusapati ◽  
A Kleger ◽  
C Brunner ◽  
F Genze ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Tumor Growth ◽  
Tumor Angiogenesis ◽  
Pancreatic Tumor

The Inhibition Effect of Caveolin-1 on PANC1 Human Pancreatic Tumor Growth In vitro and In vivo*

2012 ◽  
Vol 38 (12) ◽  
pp. 1121-1131
Author(s):  
Xiao-Hui WANG ◽  
Ya-Min ZHENG ◽  
Ye-Qing CUI ◽  
Shuang LIU ◽  
Hai-Chen SUN ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Pancreatic Tumor ◽  
Caveolin 1 ◽  
Inhibition Effect

scholarly journals Analysis of yggX and gshA Mutants Provides Insights into the Labile Iron Pool in Salmonella enterica

2008 ◽  
Vol 190 (23) ◽  
pp. 7608-7613 ◽  
Author(s):  
Michael P. Thorgersen ◽  
Diana M. Downs
Keyword(s):  
Salmonella Enterica ◽  
Iron Chelator ◽  
Fenton Chemistry ◽  
Labile Iron Pool ◽  
Growth Defects ◽  
Labile Iron ◽  
Iron Pool ◽  
Mutant Phenotypes ◽  
Permeable Iron ◽  
Iron Chelator Deferoxamine

ABSTRACT Strains of Salmonella enterica lacking YggX and the cellular reductant glutathione exhibit defects similar to those resulting from iron deficiency and oxidative stress. Mutant strains are sensitive to hydrogen peroxide and superoxide, deregulate the expression of the Fur-regulated gene entB, and fail to grow on succinate medium. Suppression of some yggX gshA mutant phenotypes by the cell-permeable iron chelator deferoxamine allowed the conclusion that increased levels of cellular Fenton chemistry played a role in the growth defects. The data presented are consistent with a scenario in which glutathione acts as a physiological chelator of the labile iron pool and in which YggX acts upstream of the labile iron pool by preventing superoxide toxicity.

Blocking gp130-mediated IL-6 and Oncostatin M signaling inhibits pancreatic tumor growth in vivo

2021 ◽  
Author(s):  
I Pozios ◽  
E Günzler ◽  
N Hering ◽  
M Arndt ◽  
C Kamphues ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Pancreatic Tumor ◽  
Oncostatin M

Oxygen free radical-mediated selective endothelial dysfunction in isolated coronary artery

1992 ◽  
Vol 262 (3) ◽  
pp. H806-H812 ◽  
Author(s):  
K. Todoki ◽  
E. Okabe ◽  
T. Kiyose ◽  
T. Sekishita ◽  
H. Ito
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Free Radicals ◽  
Free Radical ◽  
Coronary Artery ◽  
Iron Chelator ◽  
Oxygen Free Radical ◽  
Alpha Tocopherol ◽  
Endothelium Dependent Relaxation ◽  
Iron Chelator Deferoxamine

To understand the direct involvement of free radicals causing reduction in endothelium-dependent relaxation of isolated canine coronary ring preparations, this study was undertaken to examine the effect of free radicals generated from dihydroxy fumarate (DHF) plus Fe(3+)-ADP or from H2O2 plus FeSO4. The vasodilators (acetylcholine, bradykinin, A23187, and nitroglycerin) were given after DHF/Fe(3+)-ADP or H2O2/FeSO4 was removed from the organ chamber. The earlier DHF/Fe(3+)-ADP exposure produced an attenuation of the relaxation of the rings induced by acetylcholine, bradykinin, or A23187 but not of the relaxation induced by nitroglycerin. The observed effect of previous DHF/Fe(3+)-ADP exposure was significantly protected in the vessels isolated from the dogs treated with alpha-tocopherol. In the experiments for assessing the effect of various scavengers, 1O2 scavenger histidine or iron chelator deferoxamine effectively protected the attenuation induced by DHF/Fe(3+)-ADP exposure of the relaxation elicited by acetylcholine; superoxide dismutase (SOD), catalase, or dimethyl sulfoxide (DMSO) had no effect on this system. Furthermore, the relaxation elicited by acetylcholine, but not nitroglycerin, was significantly attenuated by the earlier exposure to .OH generated by Fenton's reagent (H2O2+FeSO4); the attenuation was significantly protected by DMSO. These results are consistent with the view that .OH, 1O2, and/or iron-dependent reactive species selectively damage endothelium-dependent relaxation as opposed to endothelium-independent relaxation in endothelium-intact coronary ring preparations. It is also postulated that lipid peroxidation may be responsible for this effect.

scholarly journals Methyl 2-Cyano-3,12-dioxooleana-1,9-dien-28-oate Decreases Specificity Protein Transcription Factors and Inhibits Pancreatic Tumor Growth: Role of MicroRNA-27a

2010 ◽  
Vol 78 (2) ◽  
pp. 226-236 ◽  
Author(s):  
Indira Jutooru ◽  
Gayathri Chadalapaka ◽  
Maen Abdelrahim ◽  
Md Riyaz Basha ◽  
Ismael Samudio ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Tumor Growth ◽  
Pancreatic Tumor ◽  
Specificity Protein ◽  
Protein Transcription
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