Childhood cancers arise during development. When a particular genetic mutation occurs at a specific stage of development, the normal growth control mechanisms are bypassed. In DNB, we build on our expertise in developmental biology to elucidate the cellular etiology of childhood solid tumors. Why are some developing tissues more vulnerable to malignant transformation than others? How are childhood cancers different from adult cancers? Are the normal developmental pathways still active in tumor cells? Can we exploit those pathways to develop novel therapies? What can we learn about normal development by studying childhood cancer? We share all of our discoveries, expertise and resources with scientists around the world to advance cures for childhood solid tumors.
Matricellular protein WISP2 is an endogenous inhibitor of collagen linearization and cancer metastasis
In primary tumors, the linearization of collagen fibers promotes cancer cell invasion and metastasis and is indicative of poor prognosis. This study from the Labelle lab uncovers WISP2 as the first inhibitor of collagen linearization ever identified and reveals that collagen architecture can be normalized and metastasis inhibited by therapeutically restoring a high WISP2:WISP1 ratio.
Patient-derived models recapitulate heterogeneity of molecular signatures and drug response in pediatric high-grade glioma
In vitro and in vivo disease models reflecting the intimate connection between developmental context and pathogenesis of pediatric HGG are essential to advance understanding and identify therapeutic vulnerabilities. Dr. Suzanne Baker and colleagues created unique new models and an online interactive data portal for exploration of associated detailed molecular characterization and HTS chemical sensitivity data, providing a rich resource for pediatric brain tumor research.
