This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Goblirsch, M. J. Articles by Clohisy, D. R. Search for Related Content PubMed PubMed Citation Articles by Goblirsch, M. J. Articles by Clohisy, D. R.

Biology of Bone Cancer Pain

Authors' Affiliation: The University of Minnesota, Minneapolis, Minnesota

Requests for reprints: Denis R. Clohisy, Department of Orthopaedic Surgery, 420 Delaware Street Southeast, MMC 806, Minneapolis, MN 55455. Phone: 612-626-9934; Fax: 612-624-0944; E-mail: clohi001{at}umn.edu.

Bone cancer pain is a devastating manifestation of metastatic cancer. Unfortunately, current therapies can be ineffective, and when they are effective, the duration of the patient's survival typically exceeds the duration of pain relief. New, mechanistically based therapies are desperately needed. Study of experimental animal models has provided insight into the mechanisms that drive bone cancer pain and provides an opportunity for developing targeted therapies. Mechanisms that drive bone cancer pain include tumor-directed osteoclast-mediated osteolysis, tumor cells themselves, tumor-induced nerve injury, stimulation of transient receptor potential vanilloid type 1 ion channel, endothelin A, and host cell production of nerve growth factor. Current and future therapies include external beam radiation, osteoclast-targeted inhibiting agents, anti-inflammatory drugs, transient receptor potential vanilloid type 1 antagonists, and antibody therapies that target nerve growth factor or tumor angiogenesis. It is likely that a combination of these therapies will be superior to any one therapy alone.