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@ARTICLE{Dewi:124343,
      author       = {D. L. Dewi and S. R. Mohapatra and S. Blanco Cabañes and
                      I. Adam and L. F. Somarribas Patterson and B. Berdel and M.
                      Kahloon and L. Thürmann and S. Loth and K. Heilmann$^*$ and
                      D. Weichenhan$^*$ and O. Mücke$^*$ and I. Heiland and P.
                      Wimberger$^*$ and J. D. Kuhlmann$^*$ and K.-H. Kellner and
                      S. Schott and C. Plass$^*$ and M. Platten$^*$ and C.
                      Gerhäuser$^*$ and S. Trump and C. Opitz$^*$},
      title        = {{S}uppression of indoleamine-2,3-dioxygenase 1 expression
                      by promoter hypermethylation in {ER}-positive breast
                      cancer.},
      journal      = {OncoImmunology},
      volume       = {6},
      number       = {2},
      issn         = {2162-402X},
      address      = {Austin, Tex.},
      publisher    = {Landes Bioscience},
      reportid     = {DKFZ-2017-01222},
      pages        = {e1274477 -},
      year         = {2017},
      abstract     = {Kynurenine formation by tryptophan-catabolic
                      indoleamine-2,3-dioxygenase 1 (IDO1) plays a key role in
                      tumor immune evasion and inhibition of IDO1 is efficacious
                      in preclinical models of breast cancer. As the response of
                      breast cancer to immune checkpoint inhibitors may be
                      limited, a better understanding of the expression of
                      additional targetable immunomodulatory pathways is of
                      importance. We therefore investigated the regulation of IDO1
                      expression in different breast cancer subtypes. We
                      identified estrogen receptor α (ER) as a negative regulator
                      of IDO1 expression. Serum kynurenine levels as well as
                      tumoral IDO1 expression were lower in patients with
                      ER-positive than ER-negative tumors and an inverse
                      relationship between IDO1 and estrogen receptor mRNA was
                      observed across 14 breast cancer data sets. Analysis of
                      whole genome bisulfite sequencing, 450k, MassARRAY and
                      pyrosequencing data revealed that the IDO1 promoter is
                      hypermethylated in ER-positive compared with ER-negative
                      breast cancer. Reduced induction of IDO1 was also observed
                      in human ER-positive breast cancer cell lines. IDO1
                      induction was enhanced upon DNA demethylation in ER-positive
                      but not in ER-negative cells and methylation of an IDO1
                      promoter construct reduced IDO1 expression, suggesting that
                      enhanced methylation of the IDO1 promoter suppresses IDO1 in
                      ER-positive breast cancer. The association of ER
                      overexpression with epigenetic downregulation of IDO1
                      appears to be a particular feature of breast cancer as IDO1
                      was not suppressed by IDO1 promoter hypermethylation in the
                      presence of high ER expression in cervical or endometrial
                      cancer.},
      cin          = {C010 / G160 / G161 / L301 / L101},
      ddc          = {610},
      cid          = {I:(DE-He78)C010-20160331 / I:(DE-He78)G160-20160331 /
                      I:(DE-He78)G161-20160331 / I:(DE-He78)L301-20160331 /
                      I:(DE-He78)L101-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28344890},
      pmc          = {pmc:PMC5353999},
      doi          = {10.1080/2162402X.2016.1274477},
      url          = {https://inrepo02.dkfz.de/record/124343},
}