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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

Anders Valind's public data