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Trans-NIH Angiogenesis Workshop; May 20-21, 2013
  • Abstracts

    Energy Balance and Cancer Angiogenesis

    Stephen D. Hursting, PhD, MPH  [ View bio ]
    (Department of Nutritional Sciences, The University of Texas at Austin, and Department of Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center)

    The prevalence of obesity, an established risk and progression factor for many cancers, has risen steadily during the past several decades in the United States and in many other countries. Unfortunately, the mechanisms underlying the obesity and cancer connection are not well understood, and new targets and strategies for offsetting the impact of obesity on cancer are urgently needed. The evidence on key biological mechanisms underlying the obesity-cancer link will be discussed, with examples from the literature and our own work. Emphasis will be placed on the obesity-induced alterations in growth factors, such as vascular endothelial growth factor (VEGF), leptin, and insulin-like growth factor-1 and their signals, particularly the mammalian target of rapamycin (mTOR) and VEGF pathways. Also discussed will be the cross-talk between growth factors and the obesity-induced proinflammatory environment, including the interactions between epithelial tissues (in which most cancers arise) and macrophages, adipocytes, and endothelial cells. Examples will include genetic or pharmacologic inhibition of promising targets for blocking the effects of obesity on tumor development and progression in murine models of breast, skin and pancreatic cancer. Understanding the impact and underlying mechanisms of obesity on growth signaling, chronic inflammation, and angiogenesis will identify promising mechanistic targets and strategies for disrupting the obesity-cancer link.

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Workshop Organizer: NIH

NCI:Nancy Emenaker, PhD, RD
Suzanne Forry-Schaudies, PhD
NHLBI:Yunling Gao, MD, PhD
NIDDK: Teresa Jones, MD

NIH - National Institutes of Health: Turning Discovery Into Health

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