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Molecular Classification of Ependymal Tumors across All CNS Compartments, Histopathological Grades, and Age Groups.
Combined MYC and P53 defects emerge at medulloblastoma relapse and define rapidly progressive, therapeutically targetable disease.
Drugging MYCN through an allosteric transition in Aurora kinase A.
When deletions gain functions: commandeering epigenetic mechanisms.
MLL3 is a haploinsufficient 7q tumor suppressor in acute myeloid leukemia.
EGFR phosphorylates tumor-derived EGFRvIII driving STAT3/5 and progression in glioblastoma.
A rare population of CD24(+)ITGB4(+)Notch(hi) cells drives tumor propagation in NSCLC and requires Notch3 for self-renewal.
Distinct neural stem cell populations give rise to disparate brain tumors in response to N-MYC.
Asymmetry-defective oligodendrocyte progenitors are glioma precursors.
Delineation of two clinically and molecularly distinct subgroups of posterior fossa ependymoma.