@techreport{FroehlichGniewoszHoffetal.2011,
  author    = {Fr{\"o}hlich, V. and Gniewosz, B. and Hoff, S. and Reinders, Heinz},
  title     = {Verhinderung von Br{\"u}chen in der Zeit des {\"U}bergangs Schule-Beruf. Abschlussbericht an die Stadt Stuttgart},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-66274},
  year      = {2011},
  abstract  = {Ein wichtiges bildungspolitisches Ziel ist die Redukation der Schulabbrecherzahlen gerade an unteren Bildungsg{\"a}ngen. Vor allem gewinnen in diesem Zusammenhang regionale Maßnahmen an Bedeutung, welche auf den Erhalt mindestens eines Hauptschulabschlusses abzielen. Der Band stellt die Ergebnisse der wissenschaftlichen Begleitung eines solchen regionalen Maßnahmenpakets vor, in dem es die Ausgangssituation f{\"u}r die Konzeption eines kommunalen Projektverbundes absteckt. Pr{\"a}sentiert werden Ergebnisse quantitativer Befragungen bei Jugendlichen sowie qualitative Experteninterviews mit in solchen Maßnahmen besch{\"a}ftigten P{\"a}dagogInnen.},
  subject      = {Schulabbruch},
  language  = {de}
}
@article{WaszakNorthcottBuchhalteretal.2018,
  author    = {Waszak, Sebastian M and Northcott, Paul A and Buchhalter, Ivo and Robinson, Giles W and Sutter, Christian and Groebner, Susanne and Grund, Kerstin B and Brugi{\`e}res, Laurence and Jones, David T W and Pajtler, Kristian W and Morrissy, A Sorana and Kool, Marcel and Sturm, Dominik and Chavez, Lukas and Ernst, Aurelie and Brabetz, Sebastian and Hain, Michael and Zichner, Thomas and Segura-Wang, Maia and Weischenfeldt, Joachim and Rausch, Tobias and Mardin, Balca R and Zhou, Xin and Baciu, Cristina and Lawerenz, Christian and Chan, Jennifer A and Varlet, Pascale and Guerrini-Rousseau, Lea and Fults, Daniel W and Grajkowska, Wiesława and Hauser, Peter and Jabado, Nada and Ra, Young-Shin and Zitterbart, Karel and Shringarpure, Suyash S and De La Vega, Francisco M and Bustamante, Carlos D and Ng, Ho-Keung and Perry, Arie and MacDonald, Tobey J and Driever, Pablo Hern{\´a}iz and Bendel, Anne E and Bowers, Daniel C and McCowage, Geoffrey and Chintagumpala, Murali M and Cohn, Richard and Hassall, Timothy and Fleischhack, Gudrun and Eggen, Tone and Wesenberg, Finn and Feychting, Maria and Lannering, Birgitta and Sch{\"u}z, Joachim and Johansen, Christoffer and Andersen, Tina V and R{\"o}{\"o}sli, Martin and Kuehni, Claudia E and Grotzer, Michael and Kjaerheim, Kristina and Monoranu, Camelia M and Archer, Tenley C and Duke, Elizabeth and Pomeroy, Scott L and Shelagh, Redmond and Frank, Stephan and Sumerauer, David and Scheurlen, Wolfram and Ryzhova, Marina V and Milde, Till and Kratz, Christian P and Samuel, David and Zhang, Jinghui and Solomon, David A and Marra, Marco and Eils, Roland and Bartram, Claus R and von Hoff, Katja and Rutkowksi, Stefan and Ramaswamy, Vijay and Gilbertson, Richard J and Korshunov, Andrey and Taylor, Michael D and Lichter, Peter and Malkin, David and Gajjar, Amar and Korbel, Jan O and Pfister, Stefan M},
  title     = {Spectrum and prevalence of genetic predisposition in medulloblastoma: a retrospective genetic study and prospective validation in a clinical trial cohort},
  series = {The Lancet Oncology},
  volume    = {19},
  journal   = {The Lancet Oncology},
  doi       = {10.1016/S1470-2045(18)30242-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-233425},
  pages     = {785-798},
  year      = {2018},
  abstract  = {Background Medulloblastoma is associated with rare hereditary cancer predisposition syndromes; however, consensus medulloblastoma predisposition genes have not been defined and screening guidelines for genetic counselling and testing for paediatric patients are not available. We aimed to assess and define these genes to provide evidence for future screening guidelines. Methods In this international, multicentre study, we analysed patients with medulloblastoma from retrospective cohorts (International Cancer Genome Consortium [ICGC] PedBrain, Medulloblastoma Advanced Genomics International Consortium [MAGIC], and the CEFALO series) and from prospective cohorts from four clinical studies (SJMB03, SJMB12, SJYC07, and I-HIT-MED). Whole-genome sequences and exome sequences from blood and tumour samples were analysed for rare damaging germline mutations in cancer predisposition genes. DNA methylation profiling was done to determine consensus molecular subgroups: WNT (MBWNT), SHH (MBSHH), group 3 (MBGroup3), and group 4 (MBGroup4). Medulloblastoma predisposition genes were predicted on the basis of rare variant burden tests against controls without a cancer diagnosis from the Exome Aggregation Consortium (ExAC). Previously defined somatic mutational signatures were used to further classify medulloblastoma genomes into two groups, a clock-like group (signatures 1 and 5) and a homologous recombination repair deficiency-like group (signatures 3 and 8), and chromothripsis was investigated using previously established criteria. Progression-free survival and overall survival were modelled for patients with a genetic predisposition to medulloblastoma. Findings We included a total of 1022 patients with medulloblastoma from the retrospective cohorts (n=673) and the four prospective studies (n=349), from whom blood samples (n=1022) and tumour samples (n=800) were analysed for germline mutations in 110 cancer predisposition genes. In our rare variant burden analysis, we compared these against 53 105 sequenced controls from ExAC and identified APC, BRCA2, PALB2, PTCH1, SUFU, and TP53 as consensus medulloblastoma predisposition genes according to our rare variant burden analysis and estimated that germline mutations accounted for 6\% of medulloblastoma diagnoses in the retrospective cohort. The prevalence of genetic predispositions differed between molecular subgroups in the retrospective cohort and was highest for patients in the MBSHH subgroup (20\% in the retrospective cohort). These estimates were replicated in the prospective clinical cohort (germline mutations accounted for 5\% of medulloblastoma diagnoses, with the highest prevalence [14\%] in the MBSHH subgroup). Patients with germline APC mutations developed MBWNT and accounted for most (five [71\%] of seven) cases of MBWNT that had no somatic CTNNB1 exon 3 mutations. Patients with germline mutations in SUFU and PTCH1 mostly developed infant MBSHH. Germline TP53 mutations presented only in childhood patients in the MBSHH subgroup and explained more than half (eight [57\%] of 14) of all chromothripsis events in this subgroup. Germline mutations in PALB2 and BRCA2 were observed across the MBSHH, MBGroup3, and MBGroup4 molecular subgroups and were associated with mutational signatures typical of homologous recombination repair deficiency. In patients with a genetic predisposition to medulloblastoma, 5-year progression-free survival was 52\% (95\% CI 40-69) and 5-year overall survival was 65\% (95\% CI 52-81); these survival estimates differed significantly across patients with germline mutations in different medulloblastoma predisposition genes. Interpretation Genetic counselling and testing should be used as a standard-of-care procedure in patients with MBWNT and MBSHH because these patients have the highest prevalence of damaging germline mutations in known cancer predisposition genes. We propose criteria for routine genetic screening for patients with medulloblastoma based on clinical and molecular tumour characteristics.},
  language  = {en}
}