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Douglas Hanahan

Researcher at University of California, San Francisco

Publications -  104
Citations -  57294

Douglas Hanahan is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Carcinogenesis & Angiogenesis. The author has an hindex of 64, co-authored 104 publications receiving 54159 citations. Previous affiliations of Douglas Hanahan include Cold Spring Harbor Laboratory & École Polytechnique Fédérale de Lausanne.

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The hallmarks of cancer.

TL;DR: This work has been supported by the Department of the Army and the National Institutes of Health, and the author acknowledges the support and encouragement of the National Cancer Institute.
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Modes of resistance to anti-angiogenic therapy.

TL;DR: Emerging data support a proposition that two modes of unconventional resistance underlieAngiogenesis inhibitors targeting the vascular endothelial growth factor signalling pathways are affording demonstrable therapeutic efficacy in mouse models of cancer and in an increasing number of human cancers.
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Antiangiogenic Therapy Elicits Malignant Progression of Tumors to Increased Local Invasion and Distant Metastasis

TL;DR: It is reported that angiogenesis inhibitors targeting the VEGF pathway demonstrate antitumor effects in mouse models of pancreatic neuroendocrine carcinoma and glioblastoma but concomitantly elicit tumor adaptation and progression to stages of greater malignancy, with heightened invasiveness and in some cases increased lymphatic and distant metastasis.
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MMP-9/Gelatinase B Is a Key Regulator of Growth Plate Angiogenesis and Apoptosis of Hypertrophic Chondrocytes

TL;DR: Transplantation of wild-type bone marrow cells rescues vascularization and ossification in gelatinase B-null growth plates, indicating that these processes are mediated by gelatinaseB-expressing cells of bone marrow origin, designated chondroclasts.
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Drug resistance by evasion of antiangiogenic targeting of VEGF signaling in late-stage pancreatic islet tumors

TL;DR: Function-blocking antibodies to VEGF receptors R1 and R2 were used to probe their roles in controlling angiogenesis in a mouse model of pancreatic islet carcinogenesis, finding phenotypic resistance to V EGFR2 blockade emerged.