It is impossible to predict exactly who will develop a cancer and who will not. We know that several "risk factors" may increase the chance of getting cancer and that risk increases with age. However, even with that in mind we seem to be able to explain only a certain number of cancers. Recently, Tomasetti and Vogelstein published a provocative article in Science stating that a large percentage of cancers may be due to "bad luck" (stochastic mutation events during DNA replication) and only a few to carcinogens, pathogens, or inherited genes and that this should impact public health policies. However, their intriguing analysis has numerous limitations, some of which have already been commented upon, including the likely biased subset of cancers and that finding a correlation does not signify a cause-effect mechanism. Here, we point out that there may also be an alternative explanation for the data, the cancer stem cell hypothesis, which postulates that cancers are derived from tissue stem cells and not from somatic differentiated cells. We also highlight the importance of the tissue microenvironment in the growth of transformed cells and outline a table of concurrent factors for several cancers. The message communicated to the public should not be one of helplessness in avoiding cancers, particularly given the now extensive knowledge of known risk factors and several agents/behaviors that can lower risk for specific cancers. While some tumors will still be due to chance, prevention should still be a primary goal for public health policies.

Strategies to Prevent "bad Luck" in Cancer

Noonan, Douglas
2015-01-01

Abstract

It is impossible to predict exactly who will develop a cancer and who will not. We know that several "risk factors" may increase the chance of getting cancer and that risk increases with age. However, even with that in mind we seem to be able to explain only a certain number of cancers. Recently, Tomasetti and Vogelstein published a provocative article in Science stating that a large percentage of cancers may be due to "bad luck" (stochastic mutation events during DNA replication) and only a few to carcinogens, pathogens, or inherited genes and that this should impact public health policies. However, their intriguing analysis has numerous limitations, some of which have already been commented upon, including the likely biased subset of cancers and that finding a correlation does not signify a cause-effect mechanism. Here, we point out that there may also be an alternative explanation for the data, the cancer stem cell hypothesis, which postulates that cancers are derived from tissue stem cells and not from somatic differentiated cells. We also highlight the importance of the tissue microenvironment in the growth of transformed cells and outline a table of concurrent factors for several cancers. The message communicated to the public should not be one of helplessness in avoiding cancers, particularly given the now extensive knowledge of known risk factors and several agents/behaviors that can lower risk for specific cancers. While some tumors will still be due to chance, prevention should still be a primary goal for public health policies.
2015
http://jnci.oxfordjournals.org/
Anticarcinogenic Agents; Chemoprevention; Humans; Neoplasms; Risk; Risk Factors; Selection Bias; Tumor Microenvironment; DNA Replication; Early Detection of Cancer; Mass Screening; Mutation; Neoplastic Stem Cells; Risk Reduction Behavior; Cancer Research; Oncology
Albini, Adriana; Cavuto, Silvio; Apolone, Giovanni; Noonan, Douglas
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11383/2049708
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