{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Froldi F"],"funding":["Cancer Research UK","Francis Crick Institute","Medical Research Council","The Francis Crick Institute","National Health and Medical Research Council","Wellcome Trust"],"pagination":["e99895"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6443203"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["38(7)"],"pubmed_abstract":["Rewired metabolism of glutamine in cancer has been well documented, but less is known about other amino acids such as histidine. Here, we use <i>Drosophila</i> cancer models to show that decreasing the concentration of histidine in the diet strongly inhibits the growth of mutant clones induced by loss of Nerfin-1 or gain of Notch activity. In contrast, changes in dietary histidine have much less effect on the growth of wildtype neural stem cells and <i>Prospero</i> neural tumours. The reliance of tumours on dietary histidine and also on histidine decarboxylase (Hdc) depends upon their growth requirement for Myc. We demonstrate that Myc overexpression in <i>nerfin-1</i> tumours is sufficient to switch their mode of growth from histidine/Hdc sensitive to resistant. This study suggests that p"],"journal":["The EMBO journal"],"pubmed_title":["Histidine is selectively required for the growth of Myc-dependent dedifferentiation tumours in the &lt;i&gt;Drosophila&lt;/i&gt; CNS."],"pmcid":["PMC6443203"],"funding_grant_id":["MC_U117584237","10029","104566/Z/14/Z","MC_U117533887","10088","FC001088","APP1044704"],"pubmed_authors":["Gould AP","Froldi F","Pachnis P","Cheng LY","Szuperak M","Fernando T","Costas O"],"additional_accession":[]},"is_claimable":false,"name":"Histidine is selectively required for the growth of Myc-dependent dedifferentiation tumours in the &lt;i&gt;Drosophila&lt;/i&gt; CNS.","description":"Rewired metabolism of glutamine in cancer has been well documented, but less is known about other amino acids such as histidine. Here, we use <i>Drosophila</i> cancer models to show that decreasing the concentration of histidine in the diet strongly inhibits the growth of mutant clones induced by loss of Nerfin-1 or gain of Notch activity. In contrast, changes in dietary histidine have much less effect on the growth of wildtype neural stem cells and <i>Prospero</i> neural tumours. The reliance of tumours on dietary histidine and also on histidine decarboxylase (Hdc) depends upon their growth requirement for Myc. We demonstrate that Myc overexpression in <i>nerfin-1</i> tumours is sufficient to switch their mode of growth from histidine/Hdc sensitive to resistant. This study suggests that p","dates":{"release":"2019-01-01T00:00:00Z","publication":"2019 Apr","modification":"2026-07-17T01:31:31.53Z","creation":"2019-06-06T21:04:46Z"},"accession":"S-EPMC6443203","cross_references":{"pubmed":["30804004"],"doi":["10.15252/embj.201899895"]}}