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@ARTICLE{RuizFernandezdeCordoba:178678,
      author       = {B. Ruiz-Fernandez de Cordoba and H. Moreno and K. Valencia
                      and N. Perurena and P. Ruedas and T. Walle$^*$ and A.
                      Pezonaga-Torres and J. Hinojosa and E. Guruceaga and A.
                      Pineda-Lucena and M. Abengozar-Muela and D. Cochonneau and
                      C. Zandueta and S. Martinez-Canarias and A. Teijeira and D.
                      Ajona and S. Ortiz-Espinosa and X. Morales and C. Ortiz de
                      Solorzano and M. Santisteban and L. I. Ramos-Garcia and L.
                      Guembe and V. Strnad and D. Heymann and S. Hervas-Stubbs and
                      R. Pio and M. E. Rodriguez-Ruiz and C. E. de Andrea and S.
                      Vicent and I. Melero and F. Lecanda and R. Martinez-Monge},
      title        = {{T}umor {ENPP}1({CD}203a)/{H}aptoglobin {A}xis {E}xploits
                      {M}yeloid-{D}erived {S}uppressor {C}ells to {P}romote
                      {P}ost-{R}adiotherapy {L}ocal {R}ecurrence in {B}reast
                      {C}ancer.},
      journal      = {Cancer discovery},
      volume       = {12},
      number       = {5},
      issn         = {2159-8274},
      address      = {Philadelphia, Pa.},
      reportid     = {DKFZ-2022-00194},
      pages        = {1356-1377},
      year         = {2022},
      note         = {2022 May 2;12(5):1356-1377},
      abstract     = {Locoregional failure (LRF) in breast cancer patients
                      post-surgery and post-irradiation (IR) is linked to a dismal
                      prognosis. In a refined new model, we identified Enpp1
                      (Ectonucleotide pyrophosphatase /phosphodiesterase 1/CD203a)
                      to be closely associated with LRF. Enpp1high circulating
                      tumor cells (CTC) contribute to relapse by a self-seeding
                      mechanism. This process requires the infiltration of
                      PMN-MDSC and neutrophil extracellular traps (NET) formation.
                      Genetic and pharmacological Enpp1 inhibition or NET blockade
                      extend relapse-free survival. Furthermore, in combination
                      with fractionated irradiation (FD), Enpp1 abrogation
                      obliterates LRF. Mechanistically, Enpp1-generated
                      adenosinergic metabolites enhance Haptoglobin (Hp)
                      expression. This inflammatory mediator elicits myeloid
                      invasiveness and promotes NET formation. Accordingly, a
                      significant increase in ENPP1 and NET formation is detected
                      in relapsed human breast cancer tumors. Moreover, high ENPP1
                      or HP levels are associated with poor prognosis. These
                      findings unveil the ENPP1/HP axis as an unanticipated
                      mechanism exploited by tumor cells linking inflammation to
                      immune remodeling favoring local relapse.},
      cin          = {E055},
      ddc          = {610},
      cid          = {I:(DE-He78)E055-20160331},
      pnm          = {315 - Bildgebung und Radioonkologie (POF4-315)},
      pid          = {G:(DE-HGF)POF4-315},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35086922},
      doi          = {10.1158/2159-8290.CD-21-0932},
      url          = {https://inrepo02.dkfz.de/record/178678},
}