These data demonstrated that homozygous deletion of CDKN2A, found in 68.5% of 3635PXA patient tumor cells, was well maintained and increased to 100% in the PDOX model and cultured xenograft cells; interestingly, monolayer cells were enriched with disomy 9 cells while neurospheres favored the growth of trisomy and quadrisomy 9 tumor cells. The gene discussed is CDKN2A; the disease is neoplasm.