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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.
Non-stem cell origin for oligodendroglioma.