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000167455 0247_ $$2ISSN$$a1523-5866
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000167455 041__ $$aeng
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000167455 1001_ $$aBaroni, Lorena$$b0
000167455 245__ $$aUltra high-risk PFA ependymoma is characterized by loss of chromosome 6q.
000167455 260__ $$aOxford$$bOxford Univ. Press$$c2021
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000167455 500__ $$a2021 Aug 2;23(8):1360-1370
000167455 520__ $$aWithin PF-EPN-A, 1q gain is a marker of poor prognosis, however, it is unclear if within PF-EPN-A additional cytogenetic events exist which can refine risk stratification.Five independent non-overlapping cohorts of PF-EPN-A were analyzed applying genome wide methylation arrays for chromosomal and clinical variables predictive of survival.Across all cohorts, 663 PF-EPN-A were identified. The most common broad copy number event was 1q gain (18.9%), followed by 6q loss (8.6%), 9p gain (6.5%), and 22q loss (6.8%). Within 1q gain tumors, there was significant enrichment for 6q loss (17.7%), 10q loss (16.9%) and 16q loss (15.3%). The 5-year progression free survival (PFS) was strikingly worse in those patients with 6q loss, with a 5-year PFS of 50% (95%CI 45-55%) for balanced tumors, compared with 32% (95%CI 24-44%) for 1q gain only, 7.3% (95%CI 2.0-27%) for 6q loss only and 0 for both 1q gain and 6q loss (p=1.65x10 -13 ). After accounting for treatment, 6q loss remained the most significant independent predictor of survival in PF-EPN-A but is not in PF-EPN-B. Distant relapses were more common in 1q gain irrespective of 6q loss. RNA-sequencing comparing 6q loss to 6q balanced PF-EPN-A suggests that 6q loss forms a biologically distinct group.We have identified an ultra high-risk PF-EPN-A ependymoma subgroup, which can be reliably ascertained using cytogenetic markers in routine clinical use. A change in treatment paradigm is urgently needed for this particular subset of PF-EPN-A where novel therapies should be prioritized for upfront therapy.
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000167455 650_7 $$2Other$$a1q gain
000167455 650_7 $$2Other$$a6qloss
000167455 650_7 $$2Other$$aPFA
000167455 650_7 $$2Other$$aPFB
000167455 650_7 $$2Other$$aependymoma
000167455 650_7 $$2Other$$aposterior fossa
000167455 650_7 $$2Other$$asubgrouping
000167455 7001_ $$aSundaresan, Lakshmikirupa$$b1
000167455 7001_ $$aHeled, Ayala$$b2
000167455 7001_ $$aColtin, Hallie$$b3
000167455 7001_ $$0P:(DE-He78)a7c1bbac024fa232d9c6b78443328d9d$$aPajtler, Kristian W$$b4$$udkfz
000167455 7001_ $$aLin, Tong$$b5
000167455 7001_ $$aMerchant, Thomas E$$b6
000167455 7001_ $$aMcLendon, Roger$$b7
000167455 7001_ $$aFaria, Claudia$$b8
000167455 7001_ $$aBuntine, Molly$$b9
000167455 7001_ $$aWhite, Christine L$$b10
000167455 7001_ $$0P:(DE-He78)f746aa965c4e1af518b016de3aaff5d9$$aPfister, Stefan M$$b11$$udkfz
000167455 7001_ $$aGilbert, Mark R$$b12
000167455 7001_ $$aArmstrong, Terri S$$b13
000167455 7001_ $$aBouffet, Eric$$b14
000167455 7001_ $$aKumar, Sachin$$b15
000167455 7001_ $$aTaylor, Michael D$$b16
000167455 7001_ $$aAldape, Kenneth D$$b17
000167455 7001_ $$aEllison, David W$$b18
000167455 7001_ $$aGottardo, Nicholas G$$b19
000167455 7001_ $$0P:(DE-He78)4c28e2aade5f44d8eca9dd8e97638ec8$$aKool, Marcel$$b20$$udkfz
000167455 7001_ $$0P:(DE-He78)8d9c904a6cea14d4c99c78ba46e41f93$$aKorshunov, Andrey$$b21$$udkfz
000167455 7001_ $$aHansford, Jordan R$$b22
000167455 7001_ $$aRamaswamy, Vijay$$b23
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