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@ARTICLE{Carceller:125607,
      author       = {F. Carceller and L. A. Fowkes and K. Khabra and L. Moreno
                      and F. Saran and A. Burford and A. Mackay and D. Jones$^*$
                      and V. Hovestadt$^*$ and L. V. Marshall and S. Vaidya and H.
                      Mandeville and N. Jerome and L. R. Bridges and R. Laxton and
                      S. Al-Sarraj and S. Pfister$^*$ and M. O. Leach and A. D. J.
                      Pearson and C. Jones and D.-M. Koh and S. Zacharoulis},
      title        = {{P}seudoprogression in children, adolescents and young
                      adults with non-brainstem high grade glioma and diffuse
                      intrinsic pontine glioma.},
      journal      = {Journal of neuro-oncology},
      volume       = {129},
      number       = {1},
      issn         = {1573-7373},
      address      = {Dordrecht [u.a.]},
      publisher    = {Springer Science + Business Media B.V},
      reportid     = {DKFZ-2017-01733},
      pages        = {109 - 121},
      year         = {2016},
      abstract     = {Pseudoprogression (PsP) is a treatment-related phenomenon
                      which hinders response interpretation. Its prevalence and
                      clinical impact have not been evaluated in
                      children/adolescents. We assessed the characteristics, risk
                      factors and prognosis of PsP in children/adolescents and
                      young-adults diagnosed with non-brainstem high grade gliomas
                      (HGG) and diffuse intrinsic pontine gliomas (DIPG). Patients
                      aged 1-21 years diagnosed with HGG or DIPG between 1995 and
                      2012 who had completed radiotherapy were eligible. PsP was
                      assessed according to study-specific criteria and correlated
                      with first-line treatment, molecular biomarkers and
                      survival. Ninety-one patients (47 HGG, 44 DIPG) were
                      evaluable. Median age: 10 years (range, 2-20). Eleven
                      episodes of PsP were observed in 10 patients (4 HGG, 6
                      DIPG). Rates of PsP: $8.5 \%$ (HGG); $13.6 \%$ (DIPG). Two
                      episodes of PsP were based on clinical findings alone; nine
                      episodes had concurrent radiological changes: increased size
                      of lesions (n = 5), new focal enhancement (n = 4).
                      Temozolomide, MGMT methylation or H3F3A mutations were not
                      found to be associated with increased occurrence of PsP. For
                      HGG, 1-year progression-free survival (PFS) was $41.9 \%$
                      no-PsP versus $100 \%$ PsP (p = 0.041); differences in
                      1-year overall survival (OS) were not significant. For DIPG,
                      differences in 1-year PFS and OS were not statistically
                      significant. Hazard ratio $(95 \%CI)$ of PsP for OS was
                      0.551 (0.168-1.803; p = 0.325) in HGG; and 0.308
                      (0.107-0.882; p = 0.028) in DIPG. PsP occurred in both
                      pediatric HGG and DIPG patients at a comparable rate to
                      adult HGG. PsP was associated with improved 1-yr PFS in HGG
                      patients. PsP had a protective effect upon OS in DIPG
                      patients.},
      cin          = {B062 / B060},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)B060-20160331},
      pnm          = {312 - Functional and structural genomics (POF3-312)},
      pid          = {G:(DE-HGF)POF3-312},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27180091},
      doi          = {10.1007/s11060-016-2151-8},
      url          = {https://inrepo02.dkfz.de/record/125607},
}