Advertisement

European Journal of Epidemiology

, Volume 34, Issue 5, pp 447–449 | Cite as

“Bad luck” hypothesis and cancer prevention: translating the debate to more actions

  • Mingyang SongEmail author
COMMENTARY
  • 460 Downloads

Etiologic research constitutes an essential part of both biology and epidemiology. For cancer, our biological understanding about its root cause has been significantly advanced by genetic research in the past few decades. It is now widely accepted that cancer is the result of accumulation of gene mutations that successively increase cell proliferation [1]. On the other hand, population-based epidemiologic studies have focused on extrinsic and hereditary causes of cancer and identified a variety of modifiable risk factors. These data have been translated into effective prevention strategies (e.g., tobacco control) that have largely contributed to the decline in cancer mortality in the recent decades (e.g., 27% decrease between 1991 and 2016 in the United States) [2].

While each of the two major branches of cancer research—molecular biology and epidemiology—has made substantial contributions to cancer etiology, they have developed largely independently and the threads that connect them...

Notes

Funding support

This work was supported by the National Institutes of Health (K99CA215314 and R00CA215314) and the American Cancer Society (MRSG-17-220-01 – NEC).

Compliance with ethical standards

Conflict of interest

The author has no conflict of interest to disclose.

References

  1. 1.
    Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA Jr, Kinzler KW. Cancer genome landscapes. Science. 2013;339(6127):1546–58.  https://doi.org/10.1126/science.1235122.CrossRefPubMedPubMedCentralGoogle Scholar
  2. 2.
    Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin. 2019.  https://doi.org/10.3322/caac.21551.CrossRefPubMedGoogle Scholar
  3. 3.
    Song M, Vogelstein B, Giovannucci EL, Willett WC, Tomasetti C. Cancer prevention: molecular and epidemiologic consensus. Science. 2018;361(6409):1317–8.  https://doi.org/10.1126/science.aau3830.CrossRefPubMedGoogle Scholar
  4. 4.
    Tomasetti C, Vogelstein B. Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions. Science. 2015;347(6217):78–81.  https://doi.org/10.1126/science.1260825.CrossRefPubMedPubMedCentralGoogle Scholar
  5. 5.
    Song M, Giovannucci EL. Cancer risk: many factors contribute. Science. 2015;347(6223):728–9.  https://doi.org/10.1126/science.aaa6094.CrossRefPubMedGoogle Scholar
  6. 6.
    Tomasetti C, Li L, Vogelstein B. Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention. Science. 2017;355(6331):1330–4.  https://doi.org/10.1126/science.aaf9011.CrossRefPubMedPubMedCentralGoogle Scholar
  7. 7.
    Song M, Giovannucci E. Preventable incidence and mortality of carcinoma associated with lifestyle factors among white adults in the United States. JAMA Oncol. 2016;2(9):1154–61.  https://doi.org/10.1001/jamaoncol.2016.0843.CrossRefPubMedPubMedCentralGoogle Scholar
  8. 8.
    Alexandrov LB, Nik-Zainal S, Wedge DC, et al. Signatures of mutational processes in human cancer. Nature. 2013;500(7463):415–21.  https://doi.org/10.1038/nature12477.CrossRefPubMedPubMedCentralGoogle Scholar
  9. 9.
    Alexandrov LB, Ju YS, Haase K, et al. Mutational signatures associated with tobacco smoking in human cancer. Science. 2016;354(6312):618–22.  https://doi.org/10.1126/science.aag0299.CrossRefPubMedPubMedCentralGoogle Scholar
  10. 10.
    Letouze E, Shinde J, Renault V, et al. Mutational signatures reveal the dynamic interplay of risk factors and cellular processes during liver tumorigenesis. Nat Commun. 2017;8(1):1315.  https://doi.org/10.1038/s41467-017-01358-x.CrossRefPubMedPubMedCentralGoogle Scholar
  11. 11.
    Govindan R, Ding L, Griffith M, et al. Genomic landscape of non-small cell lung cancer in smokers and never-smokers. Cell. 2012;150(6):1121–34.  https://doi.org/10.1016/j.cell.2012.08.024.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer Nature B.V. 2019

Authors and Affiliations

  1. 1.Departments of Epidemiology and NutritionHarvard T.H. Chan School of Public HealthBostonUSA
  2. 2.Clinical and Translational Epidemiology UnitMassachusetts General Hospital and Harvard Medical SchoolBostonUSA
  3. 3.Division of GastroenterologyMassachusetts General HospitalBostonUSA

Personalised recommendations