Can you prevent a diagnosis, or is it just bad luck?

Poker player holding playing cards

The old saying "the devil is in the details" often fits when communicating about science.

That saying appears pertinent to a Johns Hopkins research study published in the journal Science.

Headlines across the nation blared phrases like "most cancers due to bad luck," or that two-thirds of cancers are due to random chance, suggesting that, for most people, there's nothing that can be done to prevent getting cancer.

The journal article's abstract says "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."

But criticism of the journal article, its conclusions and resulting news coverage poured in.


Simply put, there's a lot more that goes into somebody's cancer risk than random chance. The risk varies by the area of the body, type of cancer and a host of other factors.

"Some tissues are overtaken by cancer more readily than others, and mutations accumulating in stem cells explained two-thirds of that variability," Jennifer Couzin-Frankel clarified after the uproar began.

Mayo Clinic statistical geneticist Susan Slager, Ph.D., contacted by the Post-Bulletin to provide context, said, in simple terms, "there's variability of lifetime risk across the (types of) cancers … and there's variability across cell divisions." In other words, cells divide differently and at different rates in different parts of the body. Even the same type of cancer may grow at different rates in different people.

There is some relationship between cell division and risk of getting a cancer, Slager said.

"So (the study) doesn't say any particular person has a random factor of getting that cancer. It just says there's some relationship of, if that cancer that you happen to have has a high rate of cell division … the higher the risk of that cancer."

But, she emphasized, it's not two-thirds random variability for any cancer.

"They're just trying to show that the variability across the cancers can be explained by the cell divisions," Slager said. "But any particular one cancer, you can't say it's two-thirds is caused by cell division."

Couzin-Frankel noted that major cancer types, such as breast cancer, for example, were not included in the researchers' analysis. That, too, can muddy the waters of the study's conclusions.


And, Couzin-Frankel notes, just because two pieces of information correlate, it does not mean that one causes the other.

"The authors assumed that a correlation between the number of stem cell divisions and cancer risk meant one was causing the other, something their data couldn't prove," Washington University (St. Louis) cancer-prevention specialist Graham Colditz points out in Couzin-Frankel's article.

Mayo's Slager acknowledged how difficult it is to parse out the meaning of research results such as these.

She studies chronic lymphocytic leukemia (CLL).

"There are not a lot of environmental factors that are associated with risk of getting CLL," she said. "I know that, based on what we know today, it looks to be a genetic disease — an inherited genetic disease."

Some CLL cases are related to the body's functioning itself, rather than to genetics.

"This paper is telling me, 'Oh, it looks like the amount of cell division also has a factor in (risk of) getting this disease," Slager said.

Environment, cell division, somatic variance (non-inherited variance within the body) and inherited variance from parents are all involved in CLL.


"So what proportion? How much of it is cell division? How much is inherited variance and how much is environment? I don't know that," Slager said. "What I know today is that it's not very much environment and it's a lot of inherited genetics."

The Johns Hopkins study suggests cell division might play a role.

"But how much of it is cell division? I don't know," Slager said. "But it's not two-thirds."

In other words, community members should take the coverage of the Johns Hopkins study with a grain of salt. Cancer incidence is higher when a person has high rates of cell divisions.

But each individual cancer will have to be studied in order to see how important the cell-division role is, Slager said.

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