Yale University: Cancer origins from endogenous, exogenous and preventable mutational processes

A research team led by Yale University can now quantify the factors that cause DNA changes that play the most important role in tumor growth in most major tumor types

In a new paper published in the journal Molecular Biology and Evolution, they write that their new molecular analysis approach sheds light on a long-standing debate about how much control humans have over cancer development

Dr.

"We can now answer the question -- as far as we know -- 'What are the key mutations that turn these cells into cancer rather than normal tissue?'" he said

It is well known that some of the most prevalent cancers in the United States are highly preventable through human decisions

Scientists have previously shown that they can reliably predict how certain factors lead to specific mutations that alter a tissue's genome

"This gives us the final piece of the puzzle, linking what's happening in your genome to cancer," he explained

Some cancers are easier to control than others, they wrote in their report

For example, preventable factors account for a large proportion of bladder and skin tumor formation

Townsend suggested that local populations or occupations with high levels of cancer could also use the findings to uncover instances of exposure to carcinogens

"It can give people feedback on what the cause of their cancer is," he said

Not all genetic changes that cause tumors are incorporated into current methods, so more research is needed to fully understand complex genetic changes, such as duplicated genes or chromosomes

Still, the discovery could help public health officials quickly identify the source of cancers before they lead to more tumors, saving lives

"Public health interventions aimed at minimizing exposure to these preventable traits may reduce disease severity by preventing the accumulation of mutations that directly contribute to the cancer phenotype," the researchers wrote in the study

article title

Attribution of cancer origins to endogenous, exogenous, and preventable mutational processes