000125607 001__ 125607
000125607 005__ 20240228143319.0
000125607 0247_ $$2doi$$a10.1007/s11060-016-2151-8
000125607 0247_ $$2pmid$$apmid:27180091
000125607 0247_ $$2ISSN$$a0167-594X
000125607 0247_ $$2ISSN$$a0167-594x
000125607 0247_ $$2ISSN$$a1573-7373
000125607 037__ $$aDKFZ-2017-01733
000125607 041__ $$aeng
000125607 082__ $$a610
000125607 1001_ $$aCarceller, Fernando$$b0
000125607 245__ $$aPseudoprogression in children, adolescents and young adults with non-brainstem high grade glioma and diffuse intrinsic pontine glioma.
000125607 260__ $$aDordrecht [u.a.]$$bSpringer Science + Business Media B.V$$c2016
000125607 3367_ $$2DRIVER$$aarticle
000125607 3367_ $$2DataCite$$aOutput Types/Journal article
000125607 3367_ $$0PUB:(DE-HGF)16$$2PUB:(DE-HGF)$$aJournal Article$$bjournal$$mjournal$$s1521723036_2109
000125607 3367_ $$2BibTeX$$aARTICLE
000125607 3367_ $$2ORCID$$aJOURNAL_ARTICLE
000125607 3367_ $$00$$2EndNote$$aJournal Article
000125607 520__ $$aPseudoprogression (PsP) is a treatment-related phenomenon which hinders response interpretation. Its prevalence and clinical impact have not been evaluated in children/adolescents. We assessed the characteristics, risk factors and prognosis of PsP in children/adolescents and young-adults diagnosed with non-brainstem high grade gliomas (HGG) and diffuse intrinsic pontine gliomas (DIPG). Patients aged 1-21 years diagnosed with HGG or DIPG between 1995 and 2012 who had completed radiotherapy were eligible. PsP was assessed according to study-specific criteria and correlated with first-line treatment, molecular biomarkers and survival. Ninety-one patients (47 HGG, 44 DIPG) were evaluable. Median age: 10 years (range, 2-20). Eleven episodes of PsP were observed in 10 patients (4 HGG, 6 DIPG). Rates of PsP: 8.5 % (HGG); 13.6 % (DIPG). Two episodes of PsP were based on clinical findings alone; nine episodes had concurrent radiological changes: increased size of lesions (n = 5), new focal enhancement (n = 4). Temozolomide, MGMT methylation or H3F3A mutations were not found to be associated with increased occurrence of PsP. For HGG, 1-year progression-free survival (PFS) was 41.9 % no-PsP versus 100 % PsP (p = 0.041); differences in 1-year overall survival (OS) were not significant. For DIPG, differences in 1-year PFS and OS were not statistically significant. Hazard ratio (95 %CI) of PsP for OS was 0.551 (0.168-1.803; p = 0.325) in HGG; and 0.308 (0.107-0.882; p = 0.028) in DIPG. PsP occurred in both pediatric HGG and DIPG patients at a comparable rate to adult HGG. PsP was associated with improved 1-yr PFS in HGG patients. PsP had a protective effect upon OS in DIPG patients.
000125607 536__ $$0G:(DE-HGF)POF3-312$$a312 - Functional and structural genomics (POF3-312)$$cPOF3-312$$fPOF III$$x0
000125607 588__ $$aDataset connected to CrossRef, PubMed,
000125607 7001_ $$aFowkes, Lucy A$$b1
000125607 7001_ $$aKhabra, Komel$$b2
000125607 7001_ $$aMoreno, Lucas$$b3
000125607 7001_ $$aSaran, Frank$$b4
000125607 7001_ $$aBurford, Anna$$b5
000125607 7001_ $$aMackay, Alan$$b6
000125607 7001_ $$0P:(DE-He78)551bb92841f634070997aa168d818492$$aJones, David$$b7$$udkfz
000125607 7001_ $$0P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc$$aHovestadt, Volker$$b8$$udkfz
000125607 7001_ $$aMarshall, Lynley V$$b9
000125607 7001_ $$aVaidya, Sucheta$$b10
000125607 7001_ $$aMandeville, Henry$$b11
000125607 7001_ $$aJerome, Neil$$b12
000125607 7001_ $$aBridges, Leslie R$$b13
000125607 7001_ $$aLaxton, Ross$$b14
000125607 7001_ $$aAl-Sarraj, Safa$$b15
000125607 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan$$b16$$udkfz
000125607 7001_ $$aLeach, Martin O$$b17
000125607 7001_ $$aPearson, Andrew D J$$b18
000125607 7001_ $$aJones, Chris$$b19
000125607 7001_ $$aKoh, Dow-Mu$$b20
000125607 7001_ $$aZacharoulis, Stergios$$b21
000125607 773__ $$0PERI:(DE-600)2007293-4$$a10.1007/s11060-016-2151-8$$gVol. 129, no. 1, p. 109 - 121$$n1$$p109 - 121$$tJournal of neuro-oncology$$v129$$x1573-7373$$y2016
000125607 909CO $$ooai:inrepo02.dkfz.de:125607$$pVDB
000125607 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)551bb92841f634070997aa168d818492$$aDeutsches Krebsforschungszentrum$$b7$$kDKFZ
000125607 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)744146d3b5a3df1e0ac555e5bf1ee5cc$$aDeutsches Krebsforschungszentrum$$b8$$kDKFZ
000125607 9101_ $$0I:(DE-588b)2036810-0$$6P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aDeutsches Krebsforschungszentrum$$b16$$kDKFZ
000125607 9131_ $$0G:(DE-HGF)POF3-312$$1G:(DE-HGF)POF3-310$$2G:(DE-HGF)POF3-300$$3G:(DE-HGF)POF3$$4G:(DE-HGF)POF$$aDE-HGF$$bGesundheit$$lKrebsforschung$$vFunctional and structural genomics$$x0
000125607 9141_ $$y2016
000125607 915__ $$0StatID:(DE-HGF)0420$$2StatID$$aNationallizenz
000125607 915__ $$0StatID:(DE-HGF)0100$$2StatID$$aJCR$$bJ NEURO-ONCOL : 2015
000125607 915__ $$0StatID:(DE-HGF)0200$$2StatID$$aDBCoverage$$bSCOPUS
000125607 915__ $$0StatID:(DE-HGF)0300$$2StatID$$aDBCoverage$$bMedline
000125607 915__ $$0StatID:(DE-HGF)0310$$2StatID$$aDBCoverage$$bNCBI Molecular Biology Database
000125607 915__ $$0StatID:(DE-HGF)0199$$2StatID$$aDBCoverage$$bThomson Reuters Master Journal List
000125607 915__ $$0StatID:(DE-HGF)0110$$2StatID$$aWoS$$bScience Citation Index
000125607 915__ $$0StatID:(DE-HGF)0150$$2StatID$$aDBCoverage$$bWeb of Science Core Collection
000125607 915__ $$0StatID:(DE-HGF)0111$$2StatID$$aWoS$$bScience Citation Index Expanded
000125607 915__ $$0StatID:(DE-HGF)1110$$2StatID$$aDBCoverage$$bCurrent Contents - Clinical Medicine
000125607 915__ $$0StatID:(DE-HGF)9900$$2StatID$$aIF < 5
000125607 9201_ $$0I:(DE-He78)B062-20160331$$kB062$$lPädiatrische Neuroonkologie$$x0
000125607 9201_ $$0I:(DE-He78)B060-20160331$$kB060$$lMolekulare Genetik$$x1
000125607 980__ $$ajournal
000125607 980__ $$aVDB
000125607 980__ $$aI:(DE-He78)B062-20160331
000125607 980__ $$aI:(DE-He78)B060-20160331
000125607 980__ $$aUNRESTRICTED