Glioblastoma (GBM) is the most common and aggressive form of brain cancer. Response to standard-of-care treatment is poor, with a two-year survival rate of only 15 percent. Research is beginning to provide a better understanding of the processes underlying cell-to-cell differences within GBM tumors – a crucial finding because these differences contribute to therapy resistance.
The ultimate goal is to identify what pathways can be targeted to block glioma progression.
To this end, a multi-institutional team led by Professor Roel Verhaak, Ph.D., of The Jackson Laboratory (JAX) and Ana C. deCarvalho, Ph.D., Assistant Professor from Henry Ford Health System’s Hermelin Brain Tumor Center in Detroit, MI, tracked genomic alterations detected in patient samples during tumor cell evolution in culture, in patient-derived xenograft (PDX) mouse models from the cultures, as well as before and after treatment in patients. In a recent paper in Nature Genetics, the team reports that tumor progression was often driven by cancer-promoting genes, known as oncogenes, on extrachromosomal pieces of DNA.
Detailed analyses of the tumor cells from patient to culture to mouse revealed that, for the most part, the cells retained the same genomic lesions. This is good news overall, as it indicates that PDX
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