Her group uncovered that pediatric high - grade astrocytomas (HGA) are molecularly and genetically distinct from adult tumors.They also identified a new molecular mechanism driving pediatric HGA, namely recurrent
somatic driver mutations in the tail of histone 3 variants (H3.3 and H3.1).
We were also the first to identify a new molecular mechanism driving pediatric GBM, namely recurrent
somatic driver mutations in histone molecules that lead to amino - acid substitutions at key residues (K27M, K36M, G34V / R).