Vascular normalization in Rgs5-deficient tumours promotes immune destruction
Juliana Hamzah,
Manfred Jugold,
Fabian Kiessling,
Paul Rigby,
Mitali Manzur,
Hugo H. Marti,
Tamer Rabie,
Sylvia Kaden,
Hermann-Josef Gröne,
Günter J. Hämmerling,
Bernd Arnold and
Ruth Ganss ()
Additional contact information
Juliana Hamzah: Western Australian Institute for Medical Research, UWA Centre for Medical Research, Perth, Western Australia 6000, Australia
Manfred Jugold: Juniorgroup Molecular Imaging
Fabian Kiessling: Juniorgroup Molecular Imaging
Paul Rigby: Centre for Microscopy, Characterisation and Analysis, The University of Western Australia, Perth, Western Australia 6000, Australia
Mitali Manzur: Western Australian Institute for Medical Research, UWA Centre for Medical Research, Perth, Western Australia 6000, Australia
Hugo H. Marti: Institute of Physiology and Pathophysiology, University of Heidelberg
Tamer Rabie: Institute of Physiology and Pathophysiology, University of Heidelberg
Sylvia Kaden: and
Hermann-Josef Gröne: and
Günter J. Hämmerling: German Cancer Research Center, 69120 Heidelberg, Germany
Bernd Arnold: German Cancer Research Center, 69120 Heidelberg, Germany
Ruth Ganss: Western Australian Institute for Medical Research, UWA Centre for Medical Research, Perth, Western Australia 6000, Australia
Nature, 2008, vol. 453, issue 7193, 410-414
Abstract:
Anticancer immunotherapy: It's in the blood RGS5, a signalling protein that regulates the activity of G proteins, is shown to be an important regulator of the tumour vasculature. Deletion of Rgs5 leads to normalization of blood vessels of tumours, making them less leaky and improving their coverage with pericytes. As a consequence, more immune cells that can target the tumour cells actually reach the tumour, which enhances the survival of tumour-bearing mice. Thus RGS5 signalling might be a target for anticancer therapy, in particular in combination with approaches that enhance an antitumour immune response.
Date: 2008
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:453:y:2008:i:7193:d:10.1038_nature06868
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DOI: 10.1038/nature06868
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