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Colon Cancer Prevention

Dietary Modulation of Cellular and Molecular Mechanisms

  • American Institute for Cancer Research

Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 470)

Table of contents

  1. Front Matter
    Pages i-viii
  2. Leonard Augenlicht, Anna Velcich, John Mariadason, Michael Bordonaro, Barbara Heerdt
    Pages 15-22
  3. Paul Polakis, Matt Hart, Bonnee Rubinfeld
    Pages 23-32
  4. Connye N. Kuratko
    Pages 33-43
  5. G. D. Stoner, G. T. Budd, R. Ganapathi, B. De Young, L. A. Kresty, M. Nitert et al.
    Pages 45-53
  6. Henry J. Thompson, Weiqin Jiang, Zongjian Zhu
    Pages 77-84
  7. Randall W. Burt
    Pages 99-104
  8. Robert S. Chapkin, Joanne R. Lupton
    Pages 105-118
  9. Back Matter
    Pages 163-165

About this book

Introduction

The Eighth Annual Research Conference of the American Institute for Cancer Research, held in Washington, D.C., September 3-4, 1998, was on the subject "Colon Cancer Prevention: Dietary Modulation of Cellular and Molecular Mechanisms," with participants representing various disciplines interested in this area. One of the speak­ ers provided an appropriate quote from 17th century physician Thomas Adams: "Pre­ vention is better than healing because it saves the labor of being sick," which aptly describes the need for the prevention of cancer. An overview of normal and abnormal colonic development emphasized that although the typical human colon undergoes 1013 cell divisions by age 60, with the asso­ ciated possibilities for error, relatively few colon tumors develop. Since dietary modu­ lation leads to extremely small changes in colonic cells over a long period, animal models are useful to time, observe, and delineate the events associated with colon cancer. In the development colon cancer, the inactivation of the adenomatous polyposis coli (Apc) gene is one of the earliest known events. Normally Apc downregulates the cellular protein beta-catenin, but this is lost during cancer development. Beta-catenin may itself be an oncogene; it has a short half-life, but it is stabilized by binding to is more prevalent in the cell nucleus, the gene shuttles caherin. Although the Apc between the nucleus and the cytoplasm.

Keywords

apoptosis cancer prevention carcinogenesis cell genetics inflammation prevention

Editors and affiliations

  • American Institute for Cancer Research
    • 1
  1. 1.USA

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4615-4149-3
  • Copyright Information Kluwer Academic / Plenum Publishers, New York 1999
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4613-6861-8
  • Online ISBN 978-1-4615-4149-3
  • Series Print ISSN 0065-2598
  • Buy this book on publisher's site
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