title: Photodynamic therapy suppresses tumor growth in an in vivo model of human hemangioma.
abstract: The authors investigated the efficacy of photodynamic therapy against infantile hemangioma using a hemangioma animal model. Eighty-three hemangioma specimens from five children were implanted into nude mice. The gross and volume changes of the implants were evaluated for up to 13 weeks. The histological change of the implant was evaluated at 5 weeks after transplantation. Photodynamic therapy was performed between 6 and 10 weeks after transplantation. The photosensitizer uptake of the implant was evaluated at 24 h after photosensitizer administration. The implant response was evaluated at 0, 12, and 24 h after light delivery. The change in ATF3 levels, a transcription factor induced under severe hypoxic conditions, was investigated immediately after treatment. The implant volume increased slowly during the first 4 weeks and then involuted. At 5 weeks after transplantation, plump endothelial cells formed tightly packed sinusoidal channels, and the endothelial cells were positive for CD31 and GLUT1 expression. At 24 h after photosensitizer administration, confocal analysis showed that the photosensitizer was present within CD31-positive cells. The implant volume was significantly decreased in the treated implants compared with the untreated implants (p < 0.0001). At 24 h after light delivery, most cells had collapsed. ATF3 expression increased gradually and then reached a maximum level at 4 h after treatment. Photodynamic therapy was effective in the treatment of infantile hemangioma. Apoptosis, a major mechanism of hemangioma destruction in the early phase, might be caused by ischemic injury as well as direct effects of photodynamic therapy.
authors.affiliation: Department of Plastic and Reconstructive Surgery, Institute of Health Sciences, Gyeongsang National University Hospital, Gyeongsang National University School of Medicine, Jinju, Republic of Korea.
authors.forename: Jaehoon
authors.initials: J
authors.lastname: Choi
authors.forename: Woo Jung
authors.initials: WJ
authors.lastname: Kim
authors.forename: Sang Woo
authors.initials: SW
authors.lastname: Park
authors.forename: Lianji
authors.initials: L
authors.lastname: Xu
authors.forename: Sang-Hyon
authors.initials: SH
authors.lastname: Kim
authors.forename: Hye Sook
authors.initials: HS
authors.lastname: Min
authors.forename: Geun-Yong
authors.initials: GY
authors.lastname: Kwon
authors.forename: Chung-Hyun
authors.initials: CH
authors.lastname: Cho
authors.forename: Sukwha
authors.initials: S
authors.lastname: Kim
authors.forename: Tae Hyun
authors.initials: TH
authors.lastname: Choi
mesh_terms: D051700:Activating Transcription Factor 3 / Q000096:biosynthesis; D000818:Animals; D017209:Apoptosis; D002648:Child; D017323:Dihematoporphyrin Ether / Q000627:therapeutic use; D005260:Female; D051272:Glucose Transporter Type 1 / Q000096:biosynthesis; D006391:Hemangioma / Q000628:therapy*; D006801:Humans; D008297:Male; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D010778:Photochemotherapy; D017319:Photosensitizing Agents / Q000627:therapeutic use; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D014183:Transplantation, Heterologous
chemical_list: C490449:ATF3 protein, human; D051700:Activating Transcription Factor 3; D051272:Glucose Transporter Type 1; D017319:Photosensitizing Agents; D019408:Platelet Endothelial Cell Adhesion Molecule-1; C495677:SLC2A1 protein, human; D017323:Dihematoporphyrin Ether