A
Amato J. Giaccia
Researcher at Stanford University
Publications - 430
Citations - 54116
Amato J. Giaccia is an academic researcher from Stanford University. The author has contributed to research in topics: Hypoxia (medical) & Cancer. The author has an hindex of 108, co-authored 419 publications receiving 49876 citations. Previous affiliations of Amato J. Giaccia include Vanderbilt University & University of California, San Francisco.
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Radiobiology for the radiologist
Eric J. Hall,Amato J. Giaccia +1 more
TL;DR: Radiobiology for the radiologist, Radiobiology in general, Radiology for radiologists as mentioned in this paper, Radiology in the field of radiology, radiology for radiology.
Journal ArticleDOI
Matrix Crosslinking Forces Tumor Progression by Enhancing Integrin Signaling
Kandice R. Levental,Hongmei Yu,Laura Kass,Johnathon N. Lakins,Mikala Egeblad,Janine T. Erler,Sheri F. T. Fong,Katalin Csiszar,Amato J. Giaccia,Wolfgang Weninger,Mitsuo Yamauchi,David L. Gasser,Valerie M. Weaver +12 more
TL;DR: Reduction of lysyl oxidase-mediated collagen crosslinking prevented MMTV-Neu-induced fibrosis, decreased focal adhesions and PI3K activity, impeded malignancy, and lowered tumor incidence, and data show how collagenCrosslinking can modulate tissue fibrosis and stiffness to force focal adhesion, growth factor signaling and breast malignancies.
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Hypoxia-mediated selection of cells with diminished apoptotic potential in solid tumours
Thomas G. Graeber,Cynthia Osmanian,Tyler Jacks,David E. Housman,Cameron J. Koch,Scott W. Lowe,Scott W. Lowe,Amato J. Giaccia +7 more
TL;DR: It is proposed that hypoxia provides a physiological selective pressure in tumours for the expansion of variants that have lost their apoptotic potential, and in particular for cells acquiring p53mutations.
Journal Article
The unique physiology of solid tumors: opportunities (and problems) for cancer therapy
Janice M. Brown,Amato J. Giaccia +1 more
TL;DR: Four areas that are under active investigation of hypoxia-selective cytotoxins take advantage of the unique low oxygen tension in the majority of human solid tumors, and attempts to use gene therapy activated either by the low oxygen environment or by necrotic regions of tumors are discussed.
Journal ArticleDOI
The complexity of p53 modulation: emerging patterns from divergent signals
TL;DR: The activity of p53 can increase in normal tissues when undergoing pathophysiological changes that result in oxidative or redox stress, such as ischemia and reperfusion injury of the brain, heart, and other tissues.