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@ARTICLE{Tran:290573,
      author       = {D. H. Tran and D. Kim and R. Kesavan and H. Brown and T.
                      Dey and M. H. Soflaee and H. S. Vu and A. Tasdogan$^*$ and
                      J. Guo and D. Bezwada and H. Al Saad and F. Cai and A.
                      Solmonson and H. Rion and R. Chabatya and S. Merchant and N.
                      J. Manales and V. T. Tcheuyap and M. Mulkey and T. P.
                      Mathews and J. Brugarolas and S. J. Morrison and H. Zhu and
                      R. J. DeBerardinis and G. Hoxhaj},
      title        = {{D}e novo and salvage purine synthesis pathways across
                      tissues and tumors.},
      journal      = {Cell},
      volume       = {187},
      number       = {14},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2024-01170},
      pages        = {3602-3618.e20},
      year         = {2024},
      note         = {2024 Jul 11;187(14):3602-3618.e20},
      abstract     = {Purine nucleotides are vital for RNA and DNA synthesis,
                      signaling, metabolism, and energy homeostasis. To synthesize
                      purines, cells use two principal routes: the de novo and
                      salvage pathways. Traditionally, it is believed that
                      proliferating cells predominantly rely on de novo synthesis,
                      whereas differentiated tissues favor the salvage pathway.
                      Unexpectedly, we find that adenine and inosine are the most
                      effective circulating precursors for supplying purine
                      nucleotides to tissues and tumors, while hypoxanthine is
                      rapidly catabolized and poorly salvaged in vivo.
                      Quantitative metabolic analysis demonstrates comparative
                      contribution from de novo synthesis and salvage pathways in
                      maintaining purine nucleotide pools in tumors. Notably,
                      feeding mice nucleotides accelerates tumor growth, while
                      inhibiting purine salvage slows down tumor progression,
                      revealing a crucial role of the salvage pathway in tumor
                      metabolism. These findings provide fundamental insights into
                      how normal tissues and tumors maintain purine nucleotides
                      and highlight the significance of purine salvage in cancer.},
      keywords     = {cancer metabolism (Other) / de novo purine synthesis
                      (Other) / in vivo isotope tracing (Other) / nucleotide diet
                      (Other) / nucleotide metabolism (Other) / purine bases
                      (Other) / purine degradation (Other) / purine salvage
                      (Other) / tissue (Other) / tumor growth (Other)},
      cin          = {ED01},
      ddc          = {610},
      cid          = {I:(DE-He78)ED01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:38823389},
      doi          = {10.1016/j.cell.2024.05.011},
      url          = {https://inrepo02.dkfz.de/record/290573},
}