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@ARTICLE{Rusu:144386,
      author       = {P. Rusu$^*$ and C. Shao$^*$ and A. Neuerburg$^*$ and A. A.
                      Acikgöz$^*$ and Y. Wu$^*$ and P. Zou$^*$ and P. Phapale and
                      T. S. Shankar$^*$ and K. Döring and S. Dettling and H.
                      Körkel-Qu$^*$ and G. Bekki$^*$ and B. Costa$^*$ and T.
                      Guo$^*$ and O. Friesen$^*$ and M. Schlotter$^*$ and M.
                      Heikenwalder$^*$ and D. F. Tschaharganeh$^*$ and B.
                      Bukau$^*$ and G. Kramer and P. Angel$^*$ and C. Herold-Mende
                      and B. Radlwimmer$^*$ and H. Liu$^*$},
      title        = {{GPD}1 {S}pecifically {M}arks {D}ormant {G}lioma {S}tem
                      {C}ells with a {D}istinct {M}etabolic {P}rofile.},
      journal      = {Cell stem cell},
      volume       = {25},
      number       = {2},
      issn         = {1934-5909},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DKFZ-2019-01839},
      pages        = {241 - 257.e8},
      year         = {2019},
      note         = {DKFZ-ZMBH Alliance},
      abstract     = {Brain tumor stem cells (BTSCs) are a chemoresistant
                      population that can drive tumor growth and relapse, but the
                      lack of BTSC-specific markers prevents selective targeting
                      that spares resident stem cells. Through a
                      ribosome-profiling analysis of mouse neural stem cells
                      (NSCs) and BTSCs, we find glycerol-3-phosphate dehydrogenase
                      1 (GPD1) expression specifically in BTSCs and not in NSCs.
                      GPD1 expression is present in the dormant BTSC population,
                      which is enriched at tumor borders and drives tumor relapse
                      after chemotherapy. GPD1 inhibition prolongs survival in
                      mouse models of glioblastoma in part through altering
                      cellular metabolism and protein translation, compromising
                      BTSC maintenance. Metabolomic and lipidomic analyses confirm
                      that GPD1+ BTSCs have a profile distinct from that of NSCs,
                      which is dependent on GPD1 expression. Similar GPD1
                      expression patterns and prognostic associations are observed
                      in human gliomas. This study provides an attractive
                      therapeutic target for treating brain tumors and new
                      insights into mechanisms regulating BTSC dormancy.},
      cin          = {A240 / B060 / A100 / F180 / F190 / A250},
      ddc          = {570},
      cid          = {I:(DE-He78)A240-20160331 / I:(DE-He78)B060-20160331 /
                      I:(DE-He78)A100-20160331 / I:(DE-He78)F180-20160331 /
                      I:(DE-He78)F190-20160331 / I:(DE-He78)A250-20160331},
      pnm          = {311 - Signalling pathways, cell and tumor biology
                      (POF3-311)},
      pid          = {G:(DE-HGF)POF3-311},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:31303549},
      doi          = {10.1016/j.stem.2019.06.004},
      url          = {https://inrepo02.dkfz.de/record/144386},
}