Cancer prevention: Molecular and epidemiologic consensus

doi:10.1126/science.aau3830

. 2018 Sep 28;361(6409):1317-1318.

doi: 10.1126/science.aau3830.

Cancer prevention: Molecular and epidemiologic consensus

Mingyang Song^{1

2}, Bert Vogelstein³, Edward L Giovannucci^{1

4}, Walter C Willett^{5

4}, Cristian Tomasetti^{6

7}

Affiliations

¹ Departments of Epidemiology and Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
² Clinical and Translational Epidemiology Unit and Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
³ Ludwig Center and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA. bertvog@gmail.com wwillett@hsph.harvard.edu.
⁴ Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA.
⁵ Departments of Epidemiology and Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA. bertvog@gmail.com wwillett@hsph.harvard.edu.
⁶ Division of Biostatistics and Bioinformatics, Department of Oncology, Sidney Kimmel Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
⁷ Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.

PMID: 30262488
PMCID: PMC6260589
DOI: 10.1126/science.aau3830

Cancer prevention: Molecular and epidemiologic consensus

Mingyang Song et al. Science. 2018.

. 2018 Sep 28;361(6409):1317-1318.

doi: 10.1126/science.aau3830.

Authors

Mingyang Song^{1

2}, Bert Vogelstein³, Edward L Giovannucci^{1

4}, Walter C Willett^{5

4}, Cristian Tomasetti^{6

7}

Affiliations

¹ Departments of Epidemiology and Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA.
² Clinical and Translational Epidemiology Unit and Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.
³ Ludwig Center and Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, MD, USA. bertvog@gmail.com wwillett@hsph.harvard.edu.
⁴ Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA, USA.
⁵ Departments of Epidemiology and Nutrition, Harvard T. H. Chan School of Public Health, Boston, MA, USA. bertvog@gmail.com wwillett@hsph.harvard.edu.
⁶ Division of Biostatistics and Bioinformatics, Department of Oncology, Sidney Kimmel Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
⁷ Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA.

PMID: 30262488
PMCID: PMC6260589
DOI: 10.1126/science.aau3830

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Figures

**Fig 1.. Connecting epidemiologic and genetic perspectives on cancer.**
Solid tumors of adults evolve through a stepwise accumulation of three or more genetic alterations, but these are not the only determinants of cancer incidence. Hereditary factors can predispose individuals to cancer, generally via an initiating mutation to all stem cells. Random, replicative errors every time a cell divides can contribute to cancers at the indicated phases of tumorigenesis. Environmental factors can play a role during all phases.

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References

1. Mortality GBD, C. Causes of Death, Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 388, 1459–1544 (2016). - PMC - PubMed
1. Ma J, Ward EM, Siegel RL, Jemal A, Temporal Trends in Mortality in the United States, 1969–2013. JAMA 314, 1731–1739 (2015). - PubMed
1. Eckhouse S, Lewison G, Sullivan R, Trends in the global funding and activity of cancer research. Mol Oncol 2, 20–32 (2008). - PMC - PubMed
1. Diaz LA Jr. et al., The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers. Nature 486, 537–540 (2012). - PMC - PubMed
1. Tomasetti C, Vogelstein B, Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78–81 (2015). - PMC - PubMed

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[1] Mortality GBD, C. Causes of Death, Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 388, 1459–1544 (2016). - PMC - PubMed

[2] Mortality GBD, C. Causes of Death, Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet 388, 1459–1544 (2016). - PMC - PubMed

[3] Ma J, Ward EM, Siegel RL, Jemal A, Temporal Trends in Mortality in the United States, 1969–2013. JAMA 314, 1731–1739 (2015). - PubMed

[4] Ma J, Ward EM, Siegel RL, Jemal A, Temporal Trends in Mortality in the United States, 1969–2013. JAMA 314, 1731–1739 (2015). - PubMed

[5] Eckhouse S, Lewison G, Sullivan R, Trends in the global funding and activity of cancer research. Mol Oncol 2, 20–32 (2008). - PMC - PubMed

[6] Eckhouse S, Lewison G, Sullivan R, Trends in the global funding and activity of cancer research. Mol Oncol 2, 20–32 (2008). - PMC - PubMed

[7] Diaz LA Jr. et al., The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers. Nature 486, 537–540 (2012). - PMC - PubMed

[8] Diaz LA Jr. et al., The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers. Nature 486, 537–540 (2012). - PMC - PubMed

[9] Tomasetti C, Vogelstein B, Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78–81 (2015). - PMC - PubMed

[10] Tomasetti C, Vogelstein B, Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science 347, 78–81 (2015). - PMC - PubMed

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Cancer prevention: Molecular and epidemiologic consensus

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Cancer prevention: Molecular and epidemiologic consensus

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