Hundreds of potential targets for new cancer drugs that could starve tumours have been identified by scientists who analysed gene expression data from 22 types of malignancies.
The study revealed a number of cancer-associated changes in the metabolism of cells. To support their uncontrolled growth, cancer cells need to reprogram and "supercharge" a cell's normal metabolism, the researchers explained.
Pinpointing these metabolic changes could prove important in efforts to develop drugs that interfere with cancer metabolism, according to the study, which was published online in the journal Nature Biotechnology.
Only few genes involved in major metabolic processes
"The importance of this new study is its scope," lead investigator Dennis Vitkup, an associate professor of biomedical informatics at Columbia University Medical Center, said in a center news release. "So far, people have focused mainly on a few genes involved in major metabolic processes. Our study provides a comprehensive, global view of diverse metabolic alterations at the level of gene expression."
One of the major findings was that cancer-induced changes in metabolism are significantly different in various types of tumors.
"Our study clearly demonstrates that there are no single and universal changes in cancer metabolism," study co-author Dr Matthew Vander Heiden, an assistant professor at MIT, said in the news release. "That means that to understand transformation in cancer metabolism, researchers will need to consider how different tumor types adapt their metabolism to meet their specific needs."
Targeting metabolism may be a way to strike cancer at its roots, according to Vitkup.
"You can knock out one, but the cells will usually find another pathway to turn on proliferation. Targeting metabolism may be more powerful, because if you starve a cell of energy or materials, it has nowhere to go," he explained.
The U.S. National Cancer Institute has more about cancer.
(Copyright © 2013 HealthDay. All rights
Copyright © 2016 HealthDay. All rights reserved.