fig1
Figure 1. Molecular and genetic features of RMS. Primary genetic alterations and fusion oncoproteins associated with the RMS subtypes. RMS: Rhabdomyosarcomas; WHO: World Health Organization; FN-RMS: fusion-negative RMS; LOI: loss of imprinting; LOH: loss of heterozygosity; RAS: rat sarcoma; NRAS: neuroblastoma RAS viral oncogene homolog; KRAS: Kirsten rat sarcoma viral oncogene homolog; HRAS: Harvey rat sarcoma viral oncogene homolog; NF1: neurofibromin 1; PIK3CA: phosphatidylinositol-4,5-bisphosphate 3 kinase catalytic subunit alpha; FP-RMS: fusion-positive RMS; PAX: paired box gene; PAX3/7: paired box 3/7; FOXO1/4: forkhead box O1/4; NCOA1/2: nuclear receptor co-activator 1/2; INO80D: INO80 complex subunit D; VGLL2/3: vestigial-like family member 2/3; CITED: Cbp/P300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 1; SRF: serum response factor; TEAD1: TEA domain family member 1; MEIS1: myeloid ecotropic viral integration site 1 homolog; MYOD1: myogenic differentiation 1; EWSR1: EWS RNA binding protein 1; FUS: fused in sarcoma; TFCP2: transcription factor CP2; CAV1: caveolin 1; MET: mesenchymal-epithelial transition factor; HMGA2: high-mobility group AT-hook 2; NEGR1: neuronal growth regulator 1.
