Molecular mechanisms of the preventable causes of cancer in the United States
- Erica A. Golemis1,
- Paul Scheet2,
- Tim N. Beck1,3,
- Eward M. Scolnick4,
- David J. Hunter5,
- Ernest Hawk6 and
- Nancy Hopkins7
- 1Program in Molecular Therapeutics, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA;
- 2Department of Epidemiology, University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA;
- 3Molecular and Cell Biology and Genetics Program, Drexel University College of Medicine, Philadelphia, Pennsylvania 19129, USA;
- 4Eli and Edythe L. Broad Institute of the Massachusetts Institute of Technology and Harvard University, Cambridge, Massachusetts 02142, USA;
- 5Nuffield Department of Population Health, University of Oxford, Medical Sciences Division, Oxford OX3 7LF, United Kingdom;
- 6Division of Cancer Prevention and Population Sciences, University of Texas M.D. Anderson Cancer Center, Houston Texas 77030, USA;
- 7Koch Institute for Integrative Cancer Research, Biology Department, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA
- Corresponding authors: nhopkins{at}mit.edu, ehawk{at}mdanderson.org
Abstract
Annually, there are 1.6 million new cases of cancer and nearly 600,000 cancer deaths in the United States alone. The public health burden associated with these numbers has motivated enormous research efforts into understanding the root causes of cancer. These efforts have led to the recognition that between 40% and 45% of cancers are associated with preventable risk factors and, importantly, have identified specific molecular mechanisms by which these exposures modify human physiology to induce or promote cancer. The increasingly refined knowledge of these mechanisms, which we summarize here, emphasizes the need for greater efforts toward primary cancer prevention through mitigation of modifiable risk factors. It also suggests exploitable avenues for improved secondary prevention (which includes the development of therapeutics designed for cancer interception and enhanced techniques for noninvasive screening and early detection) based on detailed knowledge of early neoplastic pathobiology. Such efforts would complement the current emphasis on the development of therapeutic approaches to treat established cancers and are likely to result in far greater gains in reducing morbidity and mortality.
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Footnotes
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Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.314849.118.
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Freely available online through the Genes & Development Open Access option.
This article, published in Genes & Development, is available under a Creative Commons License (Attribution 4.0 International), as described at http://creativecommons.org/licenses/by/4.0/.