Lymphedema is a complication of cancer treatment occurring in approximately 50% of patients who undergo lymph node resection. Despite its prevalence, the etiology of this disorder remains unknown. In this study, we determined the effect of soft tissue fibrosis on lymphatic function and the role of transforming growth factor (TGF)-1 in the regulation of this response. We determined TGF- expression patterns in matched biopsy specimens collected from lymphedematous and normal limbs of patients with secondary lymphedema. To determine the role of TGF- in regulating tissue fibrosis, we used a mouse model of lymphedema and inhibited TGF- function either systemically with a monoclonal antibody or locally by using a Lymphedema is a dreaded complication of cancer management that results from the disruption of lymphatic channels. It is estimated that 3 to 5 million Americans have chronic lymphedema and suffer from chronic swelling, recurrent infections, pain, impaired function, and decreased quality of life.1-4 Remarkably, despite the prevalence and morbidity of lymphedema, there is currently no known cure and treatment remains primarily symptomatic in nature with the goal of preventing disease progression. Patients are required to wear tight, uncomfortable garments for the rest of their lives and risk worsening of the condition with repeated infections. 5The development of effective treatment options for lymphedema has been hampered by the fact that the etiology of this disorder remains poorly understood. Thus, although it is clear that the initiating event in postsurgical lymphedema is injury to the lymphatic channels, it is unknown why some patients develop this complication while others who are identically treated do not. In addition, it remains unknown why lymphedema develops in some patients after seemingly trivial lymphatic injury. None of the authors have any commercial associations or financial relationships that would create a conflict of interest with the work presented in this article.Address reprint requests to Babak J.
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