By Bill Thomas | May 15, 2024
Outside of brain cancer, neuroblastoma is the most common form of solid tumor pediatric cancer, accounting for an estimated 15% of all childhood cancer deaths. Often diagnosed in children under the age of five, the disease typically originates in a patient’s adrenal glands or in the nerve tissues of their neck, chest, abdomen, or pelvis.
Children with neuroblastoma are divided into three risk categories – low, intermediate, and high – with high-risk cases having a five-year survival rate of less than 50%. Those odds may soon improve, however, thanks to findings recently published in the scientific journal Oncogene.
According to the paper, researchers at the University of California, San Francisco have identified a universal, essential biomarker for neuroblastoma: oncoprotein AF1q. This breakthrough has the potential to revolutionize the way doctors treat neuroblastoma, allowing for the development of more effective, less toxic treatment options.
Though AF1q is already known to play a role in leukemia and solid tumor progression, UC San Francisco researchers suspected that the oncoprotein might be similarly important to tumors of neural origin. To test this hypothesis, the researchers compared AF1q gene expression across 37 different types of pediatric and adult malignancies. They also analyzed the effects of gene silencing and gene editing on different cancer cell lines.
The pediatric cancer researchers found that AF1q was expressed at the highest levels in neuroblastoma compared to all other tumor types, that neuroblastoma cells were more reliant on AF1q than any other cell line, and that when they silenced AF1q in the neuroblastoma cells, it appeared to initiate cell death and slow tumor development. Most promising of all, however, is AF1q’s seeming ability to maintain high cellular levels of N-myc, another oncoprotein linked to high-risk neuroblastoma.
“N-myc has long been considered an ‘undruggable’ target in neuroblastoma,” Dr. Julie Saba, the senior study author, said in a press release issued by UC San Francisco. “But now we see AF1q as a potential Achilles heel we can use to destabilize that target.”
Anyone interested in learning more about the UC San Francisco’s findings can read the full press release or the paper published in Oncogene. To stay up-to-date with all the latest news shaping the future of pediatric cancer treatment, don’t forget to follow the Pediatric Cancer Research Foundation Profectus blog!
