Anders Valind

Publications

• The immune cell atlas of human neuroblastoma
• A dynamic mutational landscape associated with an inter-regionally diverse immune response in malignant rhabdoid tumour
• Reply to Heng: Inborn aneuploidy and chromosomal instability
• BCOR internal tandem duplication and YWHAE-NUTM2B/E fusion are mutually exclusive events in clear cell sarcoma of the kidney.
• Somatic Genetic Variation in Children: from Mosaicism to Cancer
• DEVOLUTION—A method for phylogenetic reconstruction of aneuploid cancers based on multiregional genotyping data
• Branching copy number evolution and parallel immune profiles across the regional tumor space of resected pancreatic cancer
• Convergent evolution of 11p allelic loss in multifocal Wilms tumors arising in WT1 mutation carriers
• Whole chromosome gain does not in itself confer cancer-like chromosomal instability.
• Reply to Duesberg: Stability of peritriploid and triploid states in neoplastic and nonneoplastic cells
• Elevated tolerance to aneuploidy in cancer cells: estimating the fitness effects of chromosome number alterations by in silico modelling of somatic genome evolution.
• Activation of human telomerase reverse transcriptase through gene fusion in clear cell sarcoma of the kidney.
• Confined trisomy 8 mosaicism of meiotic origin: A rare cause of aneuploidy in childhood cancer.
• Intratumoral genome diversity parallels progression and predicts outcome in pediatric cancer.
• Four evolutionary trajectories underlie genetic intratumoral variation in childhood cancer
• Aberrant epigenetic regulation in clear cell sarcoma of the kidney featuring distinct DNA hypermethylation and EZH2 overexpression.
• The fetal thymus has a unique genomic copy number profile resulting from physiological T cell receptor gene rearrangement
• Neuroblastoma with flat genomic profile
• Extensive clonal branching shapes the evolutionary history of high-risk pediatric cancers
• Tracing the evolution of aneuploid cancers by multiregional sequencing with CRUST
• Re: Case reports and systematic review suggest that children may experience similar long‐term effects to adults after clinical COVID‐19
• Immune checkpoint inhibitors in Wilms' tumor and Neuroblastoma: What now?
• ZMIZ1-associated neurodevelopmental disorder and Hirschsprung disease
• Tracing the evolution of aneuploid cancers by multiregional sequencing with CRUST
• Macrophage infiltration promotes regrowth in MYCN-amplified neuroblastoma after chemotherapy
• Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S4 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S4 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S1 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Table S1 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Figure S1 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Figure S1 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Fig S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Fig S3 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Fig S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Fig S2 from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Data from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• Data from Resolving the Pathogenesis of Anaplastic Wilms Tumors through Spatial Mapping of Cancer Cell Evolution
• A Gradual Transition Toward Anaplasia in Wilms Tumor Through Tolerance to Genetic Damage
• Haemostasis during early treatment of childhood acute lymphoblastic leukaemia with the ALLTogether protocol
• Fig S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Fig S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Figure S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S4 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Fig S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Data from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S4 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S2 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Fig S3 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Table S1 from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Data from Resolving the pathogenesis of anaplastic Wilms tumors through spatial mapping of cancer cell evolution
• Early evolutionary branching across spatial domains predisposes to clonal replacement under chemotherapy in neuroblastoma