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Your search keyword '"Cao, Renhai"' showing total 20 results
Start Over Author "Cao, Renhai" Journal proceedings of the national academy of sciences of the united states of america
20 results on '"Cao, Renhai"'

9. Pericyte–fibroblast transition promotes tumor growth and metastasis

Author

Hosaka, Kayoko, Yang, Yunlong, Seki, Takahiro, Fischer, Carina, Dubey, Olivier, Fredlund, Erik, Hartman, Johan, Religa, Piotr, Morikawa, Hiromasa, Ishii, Yoko, Sasahara, Masakiyo, Larsson, Ola, Cossu, Giulio, Cao, Renhai, Lim, Sharon, and Cao, Yihai

Published
2016

19. Anti-VEGF agents confer survival advantages to tumor-bearing mice by improving cancer-associated systemic syndrome.

Author

Yuan Xue, Religa, Piotr, Cao, Renhai, Jon Hansen, Anker, Franco Lucchini, Jones, Bernt, Wu, Van, Zhenping Zhu, Pytowski, Bronislaw, Yuxiang Liang, Zhong, Weide, Vezzoni, Paolo, Rozell, Björn, and Yihai Cao

Subjects
VASCULAR endothelial growth factors, TUMORS, CANCER, ENDOCRINE system, SYNDROMES, MICE
Abstract

The underlying mechanism by which anti-VEGF agents prolong cancer patient survival is poorly understood. We show that in a mouse tumor model, VEGF systemically impairs functions of multiple organs including those in the hematopoietic and endocrine systems, leading to early death. Anti-VEGF antibody, bevacizumab, and anti-VEGF receptor 2 (VEGFR-2), but not anti-VEGFR-1, reversed VEGF-induced cancer- associated systemic syndrome (CASS) and prevented death in tumor- bearing mice. Surprisingly, VEGFR2 blockage improved survival by rescuing mice from CASS without significantly compromising tumor growth, suggesting that "off-tumor" VEGF targets are more sensitive than the tumor vasculature to anti-VEGF drugs. Similarly, VEGF-induced CASS occurred in a spontaneous breast cancer mouse model overexpressing neu. Clinically, VEGF expression and CASS severity positively correlated in various human cancers. These findings define novel therapeutic targets of anti-VEGF agents and provide mechanistic insights into the action of this new class of clinically available anti-VEGF cancer drugs [ABSTRACT FROM AUTHOR]

Published
2008
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20. Nitric oxide permits hypoxia-induced lymphatic perfusion by controlling arterial-lymphatic conduits in zebrafish and glass catfish.

Author

Dahl Ejby Jensen L, Cao R, Hedlund EM, Söll I, Lundberg JO, Hauptmann G, Steffensen JF, and Cao Y

Subjects
Aging, Animals, Perfusion, Arteries metabolism, Catfishes metabolism, Hypoxia metabolism, Lymphatic Vessels metabolism, Nitric Oxide metabolism, Zebrafish metabolism
Abstract

The blood and lymphatic vasculatures are structurally and functionally coupled in controlling tissue perfusion, extracellular interstitial fluids, and immune surveillance. Little is known, however, about the molecular mechanisms that underlie the regulation of bloodlymphatic vessel connections and lymphatic perfusion. Here we show in the adult zebrafish and glass catfish (Kryptopterus bicirrhis) that blood-lymphatic conduits directly connect arterial vessels to the lymphatic system. Under hypoxic conditions, arterial-lymphatic conduits (ALCs) became highly dilated and linearized by NO-induced vascular relaxation, which led to blood perfusion into the lymphatic system. NO blockage almost completely abrogated hypoxia-induced ALC relaxation and lymphatic perfusion. These findings uncover mechanisms underlying hypoxia-induced oxygen compensation by perfusion of existing lymphatics in fish. Our results might also imply that the hypoxia-induced NO pathway contributes to development of progression of pathologies, including promotion of lymphatic metastasis by modulating arterial-lymphatic conduits, in the mammalian system.

Published
2009
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