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Seyedhossein Aharinejad

Researcher at Medical University of Vienna

Publications -  140
Citations -  3910

Seyedhossein Aharinejad is an academic researcher from Medical University of Vienna. The author has contributed to research in topics: Vascular endothelial growth factor & Transplantation. The author has an hindex of 33, co-authored 140 publications receiving 3668 citations. Previous affiliations of Seyedhossein Aharinejad include University of Vienna & University of Massachusetts Medical School.

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Colony-Stimulating Factor-1 Blockade by Antisense Oligonucleotides and Small Interfering RNAs Suppresses Growth of Human Mammary Tumor Xenografts in Mice

TL;DR: It is demonstrated that CSF-1 and CSF -1 receptor are potential therapeutic targets for the treatment of mammary cancer and mouse survival significantly increased after CSf-1 blockade.
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Colony-stimulating factor-1 antibody reverses chemoresistance in human MCF-7 breast cancer xenografts.

TL;DR: In combination with CMF, anti-CSF-1 Fab reversed chemoresistance of MCF-7 xenografts, suppressing tumor development by 56%, down-regulating expression of theChemoresistance genes breast cancer-related protein, multidrug resistance gene 1, and glucosylceramide synthase, and prolonging survival significantly.
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Arteriogenesis depends on circulating monocytes and macrophage accumulation and is severely depressed in op/op mice

TL;DR: Evidence is provided for the preeminent role of monocytes/macrophages during arteriogenesis in a genuine model of monocyte deficiency, i.e., without pharmacological intervention, in osteopetrotic (op/op) mice.
Journal Article

Colony-stimulating factor-1 antisense treatment suppresses growth of human tumor xenografts in mice.

TL;DR: The results suggest that human embryonic and colon cancer cells up-regulate host CSF-1 and MMP-2 expression, which could be a novel strategy in treatment of solid tumors.
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Selective Downregulation of VEGF-A 165 , VEGF-R 1 , and Decreased Capillary Density in Patients With Dilative but Not Ischemic Cardiomyopathy

TL;DR: Whether downregulation of certain VEGF isoforms in DCM is a cause or consequence of this disorder remains unclear, although upregulated V EGF levels in ICM are most likely the result of ischemia.