title: Infantile Hemangioma Originates From A Dysregulated But Not Fully Transformed Multipotent Stem Cell.
abstract: Infantile hemangioma (IH) is the most common tumor of infancy. Its cellular origin and biological signals for uncontrolled growth are poorly understood, and specific pharmacological treatment is unavailable. To understand the process of hemangioma-genesis we characterized the progenitor hemangioma-derived stem cell (HemSC) and its lineage and non-lineage derivatives. For this purpose we performed a high-throughput (HT) phenotypic and gene expression analysis of HemSCs, and analyzed HemSC-derived tumorspheres. We found that IH is characterized by high expression of genes involved in vasculogenesis, angiogenesis, tumorigenesis and associated signaling pathways. These results show that IH derives from a dysregulated stem cell that remains in an immature, arrested stage of development. The potential biomarkers we identified can afford the development of diagnostic tools and precision-medicine therapies to "rewire" or redirect cellular transitions at an early stage, such as signaling pathways or immune response modifiers.
authors: Department of Medicine, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.|VasculoTox Inc., New York, NY 10001, USA.
authors: Shaghayegh
authors: S
authors: Harbi
authors: Department of Neurosurgery, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
authors: Rong
authors: R
authors: Wang
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Michael
authors: M
authors: Gregory
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Nicole
authors: N
authors: Hanson
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.|Pfizer Inc., Pearl River, NY 10965, USA.
authors: Keith
authors: K
authors: Kobylarz
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Kamilah
authors: K
authors: Ryan
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Yan
authors: Y
authors: Deng
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Peter
authors: P
authors: Lopez
authors: Department of Pathology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Luis
authors: L
authors: Chiriboga
authors: Department of Medicine, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.|Department of Cell Biology, New York University School of Medicine, 550 First Avenue New York, NY 10016, USA.
authors: Paolo
authors: P
authors: Mignatti
mesh_terms: D014408:Biomarkers, Tumor / Q000235:genetics / Q000378:metabolism; D002454:Cell Differentiation / Q000235:genetics; D049109:Cell Proliferation; D002471:Cell Transformation, Neoplastic; D000071063:Endoglin / Q000235:genetics / Q000378:metabolism; D015972:Gene Expression Regulation, Neoplastic; D006391:Hemangioma / Q000209:etiology / Q000473:pathology*; D061307:Human Umbilical Vein Endothelial Cells; D006801:Humans; D007223:Infant; D039902:Multipotent Stem Cells / Q000378:metabolism / Q000473:pathology*; D014411:Neoplastic Stem Cells / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000235:genetics; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014407:Tumor Cells, Cultured
chemical_list: D014408:Biomarkers, Tumor; C064206:ENG protein, human; D000071063:Endoglin; D016212:Transforming Growth Factor beta