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000300613 1001_ $$0P:(DE-He78)a23e88cc676489fe05be8c178ceaf58e$$aSelt, Florian$$b0$$eFirst author$$udkfz
000300613 245__ $$aAssociation of phosphorylation status of ERK and genetic MAPK alterations in pediatric tumors.
000300613 260__ $$a[London]$$bSpringer Nature$$c2025
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000300613 520__ $$aThe mitogen-activated protein kinase (MAPK) pathway is one of the most frequently altered pathways in pediatric cancer. Activating genomic MAPK-alterations and phosphorylation of the MAPK downstream target ERK (pERK) were analyzed in the PTT2.0 registry to identify potential targets for MAPK-directed treatment in relapsed pediatric CNS tumors, sarcomas and other solid tumors. The present study investigates the association of ERK phosphorylation and genomic MAPK pathway alterations (mutations, fusions, amplifications) in the PTT2.0 dataset. PTT2.0 registry cases with available genomic and immunohistochemistry data (n = 235) were included. Samples with and without detected activating genomic MAPK alterations were compared regarding ERK phosphorylation, quantified by immunohistochemistry H-score. The association of pERK intensity and the presence of MAPK alteration was analyzed using a univariable binary logistic regression model.The mean pERK H-score was significantly higher in samples with activating genomic MAPK alterations. pERK H-score positively correlated with the presence of MAPK alterations. However, the pERK H-score predicted MAPK alterations only with a sensitivity of 58.3% and a specificity of 83.8%. The highest mean pERK H-scores were observed in low-grade gliomas, enriched for MAPK alterations, and in ependymoma, where MAPK alterations were absent. Although there is an association between pERK level and activating genetic MAPK alterations, the predictive power of pERK H-score for genetic MAPK alterations is low in pediatric tumors. Tumors/groups with absent genetic MAPK alterations but high pERK indicate a dissociation of the two parameters, as well as a possible MAPK pathway activation in the absence of genetic MAPK alterations.
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000300613 650_7 $$2Other$$aMAPK alterations
000300613 650_7 $$2Other$$aMolecular diagnostics
000300613 650_7 $$2Other$$aRelapsed pediatric tumors
000300613 650_7 $$2Other$$aTargeted therapy
000300613 650_7 $$2Other$$apERK
000300613 650_7 $$2Other$$apERK H-score
000300613 650_7 $$0EC 2.7.11.24$$2NLM Chemicals$$aExtracellular Signal-Regulated MAP Kinases
000300613 650_2 $$2MeSH$$aHumans
000300613 650_2 $$2MeSH$$aChild
000300613 650_2 $$2MeSH$$aPhosphorylation
000300613 650_2 $$2MeSH$$aFemale
000300613 650_2 $$2MeSH$$aMale
000300613 650_2 $$2MeSH$$aChild, Preschool
000300613 650_2 $$2MeSH$$aMAP Kinase Signaling System: genetics
000300613 650_2 $$2MeSH$$aAdolescent
000300613 650_2 $$2MeSH$$aExtracellular Signal-Regulated MAP Kinases: metabolism
000300613 650_2 $$2MeSH$$aExtracellular Signal-Regulated MAP Kinases: genetics
000300613 650_2 $$2MeSH$$aNeoplasms: genetics
000300613 650_2 $$2MeSH$$aNeoplasms: metabolism
000300613 650_2 $$2MeSH$$aNeoplasms: pathology
000300613 650_2 $$2MeSH$$aInfant
000300613 7001_ $$0P:(DE-He78)a5e60710c7515b3e1de74ced6928a9dd$$aSigaud, Romain$$b1$$udkfz
000300613 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b2$$udkfz
000300613 7001_ $$0P:(DE-He78)51bf9ae9cb5771b30c483e5597ef606c$$aCapper, David$$b3$$udkfz
000300613 7001_ $$0P:(DE-HGF)0$$aReuss, David$$b4
000300613 7001_ $$0P:(DE-He78)a8a10626a848d31e70cfd96a133cc144$$avon Deimling, Andreas$$b5$$udkfz
000300613 7001_ $$0P:(DE-He78)a7c1bbac024fa232d9c6b78443328d9d$$aPajtler, Kristian W$$b6$$udkfz
000300613 7001_ $$0P:(DE-He78)a6b5fcabf661bef95109dbee87dc5271$$avan Tilburg, Cornelis M$$b7$$udkfz
000300613 7001_ $$0P:(DE-He78)91375c34e903da7087095c309b80ea00$$aNesper-Brock, Martina$$b8$$udkfz
000300613 7001_ $$0P:(DE-He78)551bb92841f634070997aa168d818492$$aJones, David T W$$b9$$udkfz
000300613 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan M$$b10$$udkfz
000300613 7001_ $$0P:(DE-He78)a1f4b408b9155beb2a8f7cba4d04fe88$$aSahm, Felix$$b11$$udkfz
000300613 7001_ $$0P:(DE-He78)143af26de9d57bf624771616318aaf7c$$aWitt, Olaf$$b12$$udkfz
000300613 7001_ $$0P:(DE-He78)0be2f86573954f87e97f8a4dbb05cb0f$$aMilde, Till$$b13$$udkfz
000300613 7001_ $$0P:(DE-He78)3de637452ba900e2bdd359b8f41953bf$$aEcker, Jonas$$b14$$eLast author$$udkfz
000300613 773__ $$0PERI:(DE-600)2615211-3$$a10.1038/s41598-025-98514-x$$gVol. 15, no. 1, p. 13498$$n1$$p13498$$tScientific reports$$v15$$x2045-2322$$y2025
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