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      Nutrition, inflammation and cancer

      Author(s): , ,
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      Journal: Nature Immunology
      Publisher: Springer Nature

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          Evolution of the cancer stem cell model.

          Antonija Kreso, John E. Dick (2014)
          Genetic analyses have shaped much of our understanding of cancer. However, it is becoming increasingly clear that cancer cells display features of normal tissue organization, where cancer stem cells (CSCs) can drive tumor growth. Although often considered as mutually exclusive models to describe tumor heterogeneity, we propose that the genetic and CSC models of cancer can be harmonized by considering the role of genetic diversity and nongenetic influences in contributing to tumor heterogeneity. We offer an approach to integrating CSCs and cancer genetic data that will guide the field in interpreting past observations and designing future studies. Copyright © 2014 Elsevier Inc. All rights reserved.
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            Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions.

            Cristian Tomasetti, Bert Vogelstein (2015)
            Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue's homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to "bad luck," that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes. Copyright © 2015, American Association for the Advancement of Science.
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              Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention

              Cristian Tomasetti, Lu Li, Bert Vogelstein (2017)
              Cancers are caused by mutations that may be inherited, induced by environmental factors, or result from DNA replication errors (R). We studied the relationship between the number of normal stem cell divisions and the risk of 17 cancer types in 69 countries throughout the world. The data revealed a strong correlation (median = 0.80) between cancer incidence and normal stem cell divisions in all countries, regardless of their environment. The major role of R mutations in cancer etiology was supported by an independent approach, based solely on cancer genome sequencing and epidemiological data, which suggested that R mutations are responsible for two-thirds of the mutations in human cancers. All of these results are consistent with epidemiological estimates of the fraction of cancers that can be prevented by changes in the environment. Moreover, they accentuate the importance of early detection and intervention to reduce deaths from the many cancers arising from unavoidable R mutations.
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                Author and article information

                Journal
                Title: Nature Immunology
                Abbreviated Title: Nat Immunol
                Publisher: Springer Nature
                ISSN (Print): 1529-2908
                ISSN (Electronic): 1529-2916
                Publication date Created: July 19 2017
                Publication date (Print): July 19 2017
                Volume: 18
                Issue: 8
                Pages: 843-850
                Article
                DOI: 10.1038/ni.3754
                PubMed ID: 28722707
                SO-VID: 02f017fe-b0b0-4ebb-91fc-4cc9a785ee38
                Copyright © © 2017
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