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

Compliments of Greenville Journal

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 Clemson’s 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.”

Mason’s 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 Mason’s 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.

“That’s the hope of where someday this research will lead,” she says.

Cell mutation fast facts

  • Human cells replicate frequently as a normal part of biological functions, and almost as frequently such cells suffer damage as a part of natural processes like exposure to UV light.
  • Normally, such damage is repaired through a number of mechanisms, including through the action of the FBH1 protein featured in the new Clemson University research.
  • When such damage is not repaired, it can lead to cell mutation, which in turn can lead to cancer and other diseases.

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Tamia Sumpter

Tamia is a driven senior undergraduate Bioengineering student currently enrolled at Clemson University. With a strong foundation in her field, she has honed her skills through hands-on experience in research and development at Eli Lilly & Company. During her time in the ADME department, Tamia contributed significantly by working on siRNAs and their applications in finding In Vitro-In Vivo Correlation (IVIVC). Looking ahead, Tamia has set her sights on a promising career in law. She aspires to specialize in Intellectual Property Law, with a particular focus on serving as in-house counsel for leading medical device or pharmaceutical companies. Her enthusiasm for this role is palpable as she prepares to embark on her legal journey! She is also a proud member of the Omicron Phi chapter of Delta Sigma Theta Sorority, Inc., PEER Mentor for Clemson PEER/WiSE, and currently serves as the President of Clemson Bioengineering Organization (CBO). With her unique blend of scientific knowledge and legal interests, Tamia is poised to make a meaningful impact in the healthcare and life sciences industries.