SOLNA, Sweden — We hear it often in the medical world: a drug for one condition can also help people with a completely different disease. For researchers, testing and repurposing safe medications can sometimes lead to wonderful breakthroughs. A new study from Sweden is doing just that and may have discovered a novel treatment for childhood cancer. A team from Karolinska Institutet says a common antidepressant may stop the tumor growth in patients with childhood sarcoma.
“Although this study was done in mice and we do not yet know how translatable the results are to humans, it gives us hope for repurposing common drugs for young cancer patients desperately requiring better treatment options,” says study first author Caitrín Crudden in a university release.
The study looked at similarities between two major groups of receptors on the surface of the cells. G protein-coupled receptors (GPCRs) are the usual targets of more than half of the drugs manufactured to treat allergies, asthma, depression, anxiety, and high blood pressure. To this point, they have not been widely tested against cancer.
Receptor tyrosine kinases (RTKs) on the other hand, are a common target of breast and colon cancer drugs. Scientists say these receptors seem to have a connection to a variety of cell abnormalities found in cancer patients.
Fighting the key to childhood cancer
The study finds one of the key RTK receptors in several forms of cancers, including childhood sarcoma, is the insulin-like growth factor receptor (IGF1R). Although previous experiments to treat cancer through this receptor failed, the Swedish team discovered IGF1R shares signaling modules with GPCRs.
Targeting GPCRs, researchers used Paroxetine to treat childhood (Ewing) sarcoma cells and mice with the disease. This anti-depressant impairs a serotonin reuptake receptor which is a part of the GPCR family. The results reveal the drug significantly lowers the number of IGF1R receptors on the surface of malignant cells. This helped to suppress the growth of tumors.
“We have developed a novel strategy to control the activity of these tumor-driving receptors by striking the GPCRs,” says principle investigator Leonard Girnita. “To our knowledge this represents a new paradigm for the entire class of cancer-relevant RTKs and could be used as a starting point for the rational design of specific therapeutics in virtually any pathological conditions. This is especially important considering the huge number of GPCR-targeting medicines already in clinical use and with low toxicity.”
Moving forward, the team plans to create strategies that selectively target several RTKs and take their findings into clinical trials.
The study appears in the journal Cancer Research.