Metabolic rewiring is a hallmark of cancer and it is becoming increasingly clear that metabolic adaptations in tumours are not only driven by proliferative demands, but are highly context-dependent. In this study, we explore how the genetic profile of tumours determines how these respond to perturbations in amino acid metabolism. Using a combination of dietary manipulations and genetics, we show that histidine deprivation or knockdown of histidine metabolic enzymes inhibits the growth of neural tumours induced by nerfin-1 loss of function. nerfin-1 encodes for a zinc-finger transcription factor required to maintain neurons in a differentiated state. Upon its loss, post-mitotic neurons dedifferentiate and acquire a stem cell fate in a step-wise process that relies on Myc-dependent cellular growth. Manipulations of histidine metabolism inhibit nerfin-1 tumour growth by reducing Myc expression and nucleolar volume, and decreasing the overall rate of dedifferentiation. Interestingly, neural tumours caused by Notch hyperactivation, which are the result of a Myc-dependent reversion of intermediate neural progenitors to stem cells also show a similar sensitivity to histidine metabolism inhibition. In contrast, none of these perturbations have major effects upon the growth of normal neural stem cells, epithelial tumours or prospero mutant neural tumours. This study shows that the sensitivity of tumours to dietary manipulations depends on the tumour genetic profile but also on its origin and mode of growth. Moreover, the metabolic vulnerabilities we identified have the potential to inform the search of metabolic interventions that specifically inhibit tumours without affecting normal cells.