MYCN-targeting vaccines and immunotherapeutics.
Amplification and concomitant overexpression of the MYCN oncogene is a frequent event in many malignancies including the childhood tumors, neuroblastoma and medulloblastoma. MYCN is only expressed in a defined time frame during early developmental processes, (1) which is beneficial for approaches combatting tumor-specific MYCN. However, MYCN is a transcription factors that was considered a poor drug target, until recent approaches suggested that down-regulation of MYCN could be possible by indirect targeting using Aurora kinase inhibitors or BET inhibitors. These concepts were proven using preclinical models (2-6) and are now entering clinical trials.
a Pediatric Oncology and Hematology , University Children's Hospital Essen, University of Duisburg-Essen , Essen , Germany.
Alexander
A
Schramm
b Pediatric Oncology and Hematology , University Medicine Greifswald , Greifswald , Germany.
Holger
H
Lode
D000818:Animals; D064127:Aurora Kinases / Q000037:antagonists & inhibitors; D019496:Cancer Vaccines / Q000627:therapeutic use*; D002986:Clinical Trials as Topic; D004353:Drug Evaluation, Preclinical; D006801:Humans; D008527:Medulloblastoma / Q000628:therapy*; D000071447:N-Myc Proto-Oncogene Protein / Q000037:antagonists & inhibitors*; D009419:Nerve Tissue Proteins / Q000037:antagonists & inhibitors; D009447:Neuroblastoma / Q000628:therapy*
D019496:Cancer Vaccines; C459801:MYCN protein, human; D000071447:N-Myc Proto-Oncogene Protein; D009419:Nerve Tissue Proteins; D064127:Aurora Kinases
DNA vaccination; MYCN; minigene; neuroblastoma