A number of Clemson University research projects are designed to advance critical understanding of how cancer cells function, but one project seeks to unlock some of the mysteries behind the most common type of cancer and lead to more effective treatments.

Jennifer Mason, assistant professor of genetics and biochemistry and a researcher in Clemsons Center for Human Genetics, has received more than $2.6 million in grant funding to investigate how cells repair DNA damage and what happens when those processes go wrong.

Such breakdowns can lead to mutations, according to Mason, a process at the heart of most cancers and increasingly tied to many diseases. Her research aims to answer many important questions about a particular DNA repair protein, known as FBH1, tied to the most common form of cancer, skin cancer, and its most deadly variant, melanoma.

Cancer is a disease of mutation, Mason says. The majority of cancers have an underlying defect that causes the cells to increase their mutation rate.

Masons work is being funded in part by a $792,000 research scholar grant from the American Cancer Society. Her research was inspired by a study that found missing or defective FBH1 in a majority of melanoma cases.

DNA damage is a natural process that happens in human cells, and one of the most common causes of such damage is ultraviolet light from exposure to sunlight. UV light is a major cause for melanoma, according to the American Cancer Society, and states with a high UV index, like South Carolina, tend to have higher incidences of melanoma in their populations.

Among the aims of Masons research is to find out why missing or defective FBH1 is resistant to DNA-destroying compounds, a property at the heart of most chemotherapies. Cracking that puzzle could lead to more effective cancer treatments.

Thats the hope of where someday this research will lead, she says.

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Clemson research could advance key understanding of cell mutation, pave way to new cancer treatments - Greenville Journal