title: Growth Attenuation of Cutaneous Angiosarcoma With Propranolol-Mediated β-Blockade.
abstract: OBJECTIVE
  Patients with stage T2 multilesion angiosarcomas of the scalp and face that are larger than 10 cm demonstrate a 2-year survival rate of 0%. To our knowledge, major therapeutic advances against this disease have not been reported for decades. Preclinical data indicate that blocking β-adrenergic signaling with propranolol hydrochloride disrupts angiosarcoma cell survival and xenograft angiosarcoma progression.
  
  
  METHODS
  A patient presented with a β-adrenergic-positive multifocal stage T2 cutaneous angiosarcoma (≥20 cm) involving 80% of the scalp, left forehead, and left cheek, with no evidence of metastasis. The patient was immediately administered propranolol hydrochloride, 40 mg twice a day, as his workup progressed and treatment options were elucidated. Evaluation of the proliferative index of the tumor before and after only 1 week of propranolol monotherapy revealed a reduction in the proliferative index of the tumor by approximately 34%. A combination of propranolol hydrochloride, 40 mg 3 times a day, paclitaxel poliglumex, 2 mg/m2 infused weekly, and radiotherapy during the subsequent 8 months resulted in extensive tumor regression with no detectable metastases.
  
  
  CONCLUSIONS
  Our data suggest that β-blockade alone substantially reduced angiosarcoma proliferation and, in combination with standard therapy, is effective for reducing the size of the tumor and preventing metastases. If successful, β-blockade could be the first major advancement in the treatment of angiosarcoma in decades.
authors.affiliation: Mohs Micrographic Surgery and Cutaneous Oncology, San Leandro, California.
authors.forename: William
authors.initials: W
authors.lastname: Chow
authors.affiliation: Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso.
authors.forename: Clarissa N
authors.initials: CN
authors.lastname: Amaya
authors.affiliation: Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso.
authors.forename: Steven
authors.initials: S
authors.lastname: Rains
authors.affiliation: Mohs Micrographic Surgery and Cutaneous Oncology, San Leandro, California.
authors.forename: Michael
authors.initials: M
authors.lastname: Chow
authors.affiliation: Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St Paul4Masonic Cancer Center, University of Minnesota, Minneapolis.
authors.forename: Erin B
authors.initials: EB
authors.lastname: Dickerson
authors.affiliation: Department of Biomedical Sciences, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso.
authors.forename: Brad A
authors.initials: BA
authors.lastname: Bryan
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000008:administration & dosage; D000972:Antineoplastic Agents, Phytogenic / Q000008:administration & dosage; D003131:Combined Modality Therapy; D005145:Face / Q000473:pathology; D006394:Hemangiosarcoma / Q000473:pathology / Q000628:therapy*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017239:Paclitaxel / Q000008:administration & dosage*; D011433:Propranolol / Q000008:administration & dosage*; D012535:Scalp / Q000473:pathology; D012878:Skin Neoplasms / Q000473:pathology / Q000628:therapy*; D016896:Treatment Outcome
chemical_list: D000319:Adrenergic beta-Antagonists; D000972:Antineoplastic Agents, Phytogenic; D011433:Propranolol; D017239:Paclitaxel