Cancer researchers found a way to hinder cells' ability to create fat molecules. They then pitted this treatment against cancer's fatty acid synthesis — which is crucial to tumor development — and were able to effectively stunt tumor growth, according to a new study published in Nature Medicine.
Previous work establishing ties between cancer and metabolic processes led researchers to hypothesize that interrupting cancer's lipid production could hinder tumor expansion. Cancer cells are more reliant on lipid synthesis than normal cells.
In multiple laboratory tests including animal models and transplanted human lung cancer cells, researchers targeted an enzyme critical to lipid synthesis called Acetyl-CoA carboxylase with an inhibitor called ND-646. The results were promising. Tumor mass for animals treated with ND-646 shrank by approximately two-thirds when compared to untreated animals. Treating human lung cancer cells with ND-646 in tandem with a common cancer treatment called carboplatin suppressed cancer growth in 87 percent of the treated tumors. Treatment with carboplatin alone yields a tumor suppression rate of 50 percent.
"This is the first time anyone has shown that this enzyme, ACC, is required for the growth of tumors and this represents compelling data validating the concept of being able to target fat synthesis as a novel anticancer approach," said Reuben Shaw, PhD, one of the study's authors and a professor at the Salk Institute for Biological Studies in La Jolla, Calif. "The implications are that we have a very promising drug for clinical trials for subtypes of lung cancer as well as liver and other types of cancer. This represents a new weapon in the arsenal to fight cancer."
More articles on healthcare quality:
Joint Commission, NQF seek Eisenberg Patient Safety and Quality Award nominations
American Academy of Pediatrics: Stop prescribing codeine to babies
Depression during pregnancy linked to gestational diabetes