Inhibition of Dll4 signalling inhibits tumour growth by deregulating angiogenesis

John Ridgway, Gu Zhang, Yan Wu, Scott Stawicki, Wei-Ching Liang, Yvan Chanthery, Joe Kowalski, Ryan J. Watts, Christopher Callahan, Ian Kasman, Mallika Singh, May Chien, Christine Tan, Jo-Anne S. Hongo, Fred de Sauvage, Greg Plowman and Minhong Yan ()
Additional contact information
John Ridgway: Tumor Biology & Angiogenesis
Gu Zhang: Tumor Biology & Angiogenesis
Yan Wu: Antibody Engineering
Scott Stawicki: Antibody Engineering
Wei-Ching Liang: Antibody Engineering
Yvan Chanthery: Tumor Biology & Angiogenesis
Joe Kowalski: Tumor Biology & Angiogenesis
Ryan J. Watts: Tumor Biology & Angiogenesis
Christopher Callahan: Pathology
Ian Kasman: Pathology
Mallika Singh: Molecular Biology, Genentech, Inc.
May Chien: Molecular Biology, Genentech, Inc.
Christine Tan: Antibody Engineering
Jo-Anne S. Hongo: Antibody Engineering
Fred de Sauvage: Molecular Biology, Genentech, Inc.
Greg Plowman: Tumor Biology & Angiogenesis
Minhong Yan: Tumor Biology & Angiogenesis

Nature, 2006, vol. 444, issue 7122, 1083-1087

Abstract: Blood line VEGF, or vascular endothelial growth factor, is the best-characterized inducer of tumour angiogenesis, and the blockade of VEGF has become an important tool in cancer therapy. But VEGF blockade is not effective against all tumours, so the search for alternative approaches continues. Two groups this week report that one such alternative could be blockade of Dll4, Delta-like ligand 4. This transmembrane molecule is part of the Notch signalling pathway. It was known to be essential for normal development of blood vessels in the embryo: the new work shows that it is also required for tumour angiogenesis. It may be a viable — and potentially well tolerated — alternative in patients with solid tumours that are resistant to anti-VEGF therapy.

Date: 2006
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DOI: 10.1038/nature05313

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