study-examines-overlap-in-causes-of-cancer,-neurodevelopmental-disorders

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Exploring Shared Causes of Cancer and Neurodevelopmental Disorders: A New Perspective
Turner

Certain proteins in human cells associated with cancer also contribute to neurodevelopmental disorders, suggesting the potential to repurpose specific cancer treatments to address neurodevelopmental conditions. However, a recent study conducted by researchers at WashU Medicine and published in Cell Genomics indicates that these proteins may function differently in these two disease categories, complicating the assessment of whether a certain cancer treatment would be beneficial or detrimental for a neurodevelopmental disorder.

The team, spearheaded by senior author Tychele Turner, an assistant professor in genetics, utilized the Google DeepMind tool AlphaFold along with their own recently developed computational methods to simulate the disease-related alterations to proteins in nearly 40,000 families with neurodevelopmental disorders and over 10,000 sequenced tumors from five different cancer types.

In the majority of instances, the researchers discovered that alterations in any specific protein do not coincide in both disease classifications, highlighting the necessity of examining the detailed functions of proteins in a condition before attempting any interventions. For instance, if a protein’s activity is increased in cancer but decreased in a neurodevelopmental disorder, a treatment that diminishes the protein’s activity to combat cancer could negatively impact the neurodevelopmental condition by further lowering the activity of a protein that is already insufficiently active. This research is vital for guiding initiatives to repurpose treatments across these different disease categories.

Turner collaborated with the university’s Research Infrastructure Services to implement AlphaFold on campus as a tool accessible to all researchers.

The article Study examines overlap in causes of cancer, neurodevelopmental disorders appeared first on The Source.

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