Title: Dietary Glucose May Drive Tumor Growth in Animal Models
An animal study conducted by researchers at Georgetown Lombardi Comprehensive Cancer Center raises questions about the consequences of glucose on increased activity of an oncogene that drives tumor growth.
“… If we can show that this is a generalized phenomenon, it could have important implications for care, and may help explain the observation that human diet does affect cancer treatment and growth,” says Dr. Maria Laura Avantaggiati, lead investigator of the study.
— An animal study conducted by researchers at Georgetown Lombardi Comprehensive Cancer Center raises questions about the consequences of glucose on increased activity of an oncogene that drives tumor growth.
Glucose is the plant-based sugar that fuels cell life. Oncogenes are genes that have the potential to cause cancer.
In the study recently published in the journal Cell Cycle, the scientists report, for the first time, that high levels of glucose in the diet of animals with cancer is linked to increased expression of a mutant gene.
More Research Needed
The mutant gene acts as a tumor suppressor, but many scientists believe that mutant p53 acts as an oncogene.
Dr. Maria Laura Avantaggiati stresses that the findings do not mean that cutting back on sugar would have an impact on patients with cancer.
“We have not studied the effect of glucose on cancer growth in humans, so we cannot make that link at this point,” she says. “Furthermore, there are many different types of [gene] mutations and we have studied only some of them.”
Diet and Cancer
“But if we can show that this is a generalized phenomenon,” she adds, “it could have important implications for care, and may help explain the observation that human diet does affect cancer treatment and growth.”
Avantaggiati, the study’s senior investigator, is an associate professor of oncology at Lombardi, part of Georgetown University Medical Center (GUMC).
The five-year study, funded by the National Institutes of Health (NIH) and the National Cancer Institute (NCI), was conducted in collaboration with Avantaggiati’s GUMC colleagues and co-authors Dr. Chris Albanese, associate professor molecular oncology, and Dr. Olga Rodriguez, assistant professor molecular oncology.
The study was funded by NIH grants R01 CA102746 and R01 CA129003 and NCI grants (P30CA051008).