Study Reveals Different Roles of Cancer-Related Proteins in Neurodevelopmental Disorders

Recent research has highlighted that certain proteins implicated in cancer also play critical roles in neurodevelopmental disorders. A comprehensive analysis led by Washington University in St. Louis utilized advanced computational tools, including DeepMind's AlphaFold, to model disease-causing changes in proteins across nearly 40,000 families with neurodevelopmental conditions and over 10,000 tumor samples from five distinct cancer types. The findings demonstrate that, in most cases, alterations in the same protein do not overlap between neurodevelopmental disorders and cancer, indicating that these proteins may function differently depending on the disease context.

This research underscores the complexity of repurposing cancer therapies for neurodevelopmental conditions. For instance, a protein that is overactive in cancer might be underactive in a neurodevelopmental disorder. Administering a drug to inhibit that protein could benefit cancer patients but potentially worsen neurodevelopmental symptoms by further decreasing its activity. As such, detailed understanding of protein function in specific diseases is essential before attempting targeted treatments.

The study's insights imply that therapeutic strategies should be carefully tailored, considering the unique roles proteins play in each disease. This nuanced approach is vital in advancing personalized medicine and could open pathways for new treatments that address the underlying mechanisms of neurodevelopmental disorders without unintended side effects.

The complete study, published in Cell Genomics, provides a significant step forward in understanding the molecular distinctions and overlaps between cancer and neurodevelopmental diseases, paving the way for safer and more effective therapeutic interventions. For more details, visit the original publication or the source: https://medicalxpress.com/news/2025-04-cancer-linked-proteins-functions-neurodevelopmental.html.