Select Page

Research Could Lead to Treatments for Muscle Wasting in Cancer Patients

by | Feb 4, 2019 | Improving Human Health and Community Vibrancy, Research News

Researchers have found that evidence of cachexia, or muscle loss in cancer patients that can be life-threatening, emerges early in tumor development, a discovery that broadens understanding of the complicated effects of cancer on the body and advances their study of the condition to find ways to treat or prevent it.

Cachexia is estimated to cause between 20 and 40 percent of cancer-related deaths, according to the researchers. They studied the development of cachexia in mice, and found that certain conditions associated with muscle wasting occur as early as one week after tumor implantation, weeks before muscle wasting begins. They published their results in the Journal of Cachexia, Sarcopenia and Muscle.

Nic Greene, assistant professor of exercise science in the College of Education and Health Professions at the University of Arkansas, worked with a team of graduate students including Jacob Brown, Megan Rosa-Caldwell and David Lee, as well as Tyrone Washington, associate professor of health, human performance and recreation, and collaborators including Jim Carson from the University of Tennessee Health Center and Michael Wiggs from the University of Texas at Tyler.

In order to learn more about cachexia, the researchers looked at mitochondrial quality in muscle cells.

“Skeletal muscle mass is regulated by a balance between making protein and degrading protein,” Greene. “If you degrade more than you make, you are going to waste. We believe healthy mitochondria are key to prevent the wasting process.”

Mitochondria are often referred to as the “powerhouse of the cell,” because they produce adenosine triphosphate, or ATP, which provides energy for all living cells. These organelles also produce a waste product called reactive oxygen species, or ROS, commonly known as “free radicals.” Impaired mitochondria must work harder to produce ATP, which leads to increased production of free radicals that can degrade the cell health.

The researchers observed both impaired mitochondrial quality and alterations in the cellular functions that are necessary to maintain muscle mass in the mice as early as one week after tumor implantation. These changes were observed several weeks before any signs of muscle wasting appeared. These results are the first step in developing future therapies to address the problem of muscle wasting.

“Cancer cachexia is often not treated before stage IV of cancer is reached,” the researchers write. “These data suggest targeting of muscle mitochondrial quality may be vital for the treatment and prevention of cancer cachexia either pharmacologically or through exercise.”

About The Author

Camilla Shumaker is the director of science and research communications. She graduated Summa Cum Laude with a bachelor's degree in English from the University of Arkansas in 2001. She also holds a Master of Fine Arts in Creative Writing from the U of A. From 2010 through 2017, she was the director of communications in the U of A College of Engineering. Camilla can be reached at camillas@uark.edu or (479) 575-7422.

Looking for an expert?

The University of Arkansas Campus Experts website is a searchable database of experts who can talk to the media on current events.

Trending Topics:
Mars
State and local economy
Environmental economics
Immigration politics

Deep Revolution in the Arkansas Ozarks: Phillips Discusses ‘Hipbillies’

The University Relations Science and Research Team

Camilla Shumaker
director of science and research communications
479-575-7422, camillas@uark.edu

Matt McGowan
science and research writer
479-575-4246, dmcgowa@uark.edu

Robert Whitby
science and research writer
479-387-0720, whitby@uark.edu

DeLani Bartlette
feature writer
479-575-5709, drbartl@uark.edu

More on University of Arkansas Research

Visit The Office of Research and Innovation for more information on research policies, support and analytics.

a graph showing research expenditure rising from under $120 million to over $170 million over ten years

Connect with Us