delete extraneous refs

+@article{deschGenotypingCirculatingTumor2020,

+ title = {Genotyping Circulating Tumor {{DNA}} of Pediatric {{Hodgkin}} Lymphoma},

+ author = {Desch, Ann-Kathrin and Hartung, Kristin and Botzen, Ante and Brobeil, Alexander and Rummel, Mathias and Kurch, Lars and Georgi, Thomas and Jox, Theresa and Bielack, Stefan and Burdach, Stefan and Classen, Carl Friedrich and Claviez, Alexander and Debatin, Klaus-Michael and Ebinger, Martin and Eggert, Angelika and Faber, Jörg and Flotho, Christian and Frühwald, Michael and Graf, Norbert and Jorch, Norbert and Kontny, Udo and Kramm, Christof and Kulozik, Andreas and Kühr, Joachim and Sykora, Karl-Walter and Metzler, Markus and Müller, Hermann L. and Nathrath, Michaela and Nüßlein, Thomas and Paulussen, Michael and Pekrun, Arnulf and Reinhardt, Dirk and Reinhard, Harald and Rössig, Claudia and Sauerbrey, Axel and Schlegel, Paul-Gerhardt and Schneider, Dominik T. and Scheurlen, Wolfram and Schweigerer, Lothar and Simon, Thorsten and Suttorp, Meinolf and Vorwerk, Peter and Schmitz, Roland and Kluge, Regine and Mauz-Körholz, Christine and Körholz, Dieter and Gattenlöhner, Stefan and Bräuninger, Andreas},

+ date = {2020-01},

+ journaltitle = {Leukemia},

+ shortjournal = {Leukemia},

+ volume = {34},

+ number = {1},

+ eprint = {31431735},

+ eprinttype = {pmid},

+ pages = {151--166},

+ issn = {1476-5551},

+ doi = {10.1038/s41375-019-0541-6},

+ abstract = {We used hybrid capture-targeted next-generation sequencing of circulating cell-free DNA (ccfDNA) of pediatric Hodgkin lymphoma (PHL) patients to determine pathogenic mechanisms and assess the clinical utility of this method. Hodgkin-Reed/Sternberg (HRS) cell-derived single nucleotide variants, insertions/deletions, translocations and VH-DH-JH rearrangements were detected in pretherapy ccfDNA of 72 of 96 patients. Number of variants per patient ranged from 1 to 21 with allele frequencies from 0.6 to 42\%. Nine translocation breakpoints were detected. Genes involved in JAK/STAT, NFkB and PI3K signaling and antigen presentation were most frequently affected. SOCS1 variants, mainly deletions, were found in most circulating tumor (ct) DNAs, and seven of the nine translocation breakpoints involved SOCS1. Analysis of VH-DH-JH rearrangements revealed an origin of PHL HRS cells from partially selected germinal center B cells. Amounts of pretherapy ctDNA were correlated with metabolic tumor volumes. Furthermore, in all ccfDNA samples of 43 patients with early response assessment quantitative qPET\,{$<$}\,3, indicative of a favorable clinical course, ctDNA was not detectable. In contrast, in five of six patients with qPET\,{$>$}\,3, indicative of an unfavorable clinical course, ctDNA remained detectable. ccfDNA analysis of PHL is thus a suitable approach to determine pathogenic mechanisms and monitor therapy response.},

+ langid = {english},

+ keywords = {Adolescent,Child,Child Preschool,Circulating Tumor DNA,Female,Genotype,Hodgkin Disease,Humans,Male},

+ file = {/Users/rmorin/Zotero/storage/ZAV2XQXF/Desch et al. - 2020 - Genotyping circulating tumor DNA of pediatric Hodg.pdf}

+}

+