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Ananth Kadambi

Researcher at Harvard University

Publications -  8
Citations -  2371

Ananth Kadambi is an academic researcher from Harvard University. The author has contributed to research in topics: Angiogenesis & Vascular endothelial growth factor. The author has an hindex of 7, co-authored 7 publications receiving 2262 citations.

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Predominant role of endothelial nitric oxide synthase in vascular endothelial growth factor-induced angiogenesis and vascular permeability

TL;DR: It is suggested that eNOS plays a predominant role in VEGF-induced angiogenesis and vascular permeability in vivo, and selective modulation of eN OS activity is a promising strategy for altering angiogenic and vascular porousness in vivo.
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Lymphatic metastasis in the absence of functional intratumor lymphatics.

TL;DR: Functional lymphatics associated with mouse tumors expressing normal or elevated levels of vascular endothelial growth factor–C (VEGF-C) are examined to suggest that the functional lymphatics in the tumor margin alone are sufficient for lymphatic metastasis and should be targeted therapeutically.
Journal Article

Vascular Accumulation of a Novel Photosensitizer, MV6401, Causes Selective Thrombosis in Tumor Vessels after Photodynamic Therapy

TL;DR: Mechanistic insights into antitumor vascular effects of PDT are provided and novel strategies for tumor treatment with PDT are suggested and suggested.
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A mathematical model of the contribution of endothelial progenitor cells to angiogenesis in tumors: implications for antiangiogenic therapy

TL;DR: Model simulations of various antiangiogenic strategies show that those therapies that effectively target both endothelial and endothelial progenitor cells, either by restoring the balance between angiogenic stimulators and inhibitors or by targeting both types of cells directly, are most effective at delaying tumor growth.
Journal Article

Vascular endothelial growth factor (VEGF)-C differentially affects tumor vascular function and leukocyte recruitment: role of VEGF-receptor 2 and host VEGF-A.

TL;DR: In vivo growth and vascular function in tumors derived from two VEGF-C-overexpressing and mock-transfected cell lines are quantified and suggest that VEGFR-2 signaling is critical for tumor angiogenesis and vascular permeability and that V EGFR-3 signaling does not compensate for VEG FR-2 blockade.