Bonaroti, Alisha R.

Summary: Adipose-derived stem cell therapy offers plastic surgeons a novel treatment alternative for conditions with few therapeutic options. Adipose-derived stem cells are a promising treatment because of their broad differentiation potential, capacity for self-renewal, and ease of isolation. Over the past decade, plastic surgeons have attempted to harness adipose-derived stem cells’ unique cellular characteristics to improve the survival of traditional fat grafting procedures, a process known as cell-assisted lipotransfer. However, the full implications of cell-assisted lipotransfer in clinical practice remain incompletely understood, stressing the urgent need to assess the scientific evidence supporting adipose-derived stem cell–based interventions. Furthermore, with the strict regulatory climate surrounding tissue explantation therapies, reviewing the safety and efficacy of these treatments will clarify their regulatory viability moving forward. In this report, the authors provide a comprehensive, up-to-date appraisal of best evidence-based practices supporting adipose-derived stem cell–derived therapies, highlighting the known mechanisms behind current clinical applications in tissue engineering and regenerative medicine specific to plastic and reconstructive surgery. The authors outline best practices for the harvest and isolation of adipose-derived stem cells and discuss why procedure standardization will elucidate the scientific bases for their broad use. Finally, the authors discuss challenges posed by U.S. Food and Drug Administration oversight of these cell-based therapies and examine the role of adipose-derived stem cell–based applications in the future of plastic surgery.

Summary: Breast implant–associated anaplastic large cell lymphoma (BIA-ALCL) is an emerging and highly treatable cancer of the immune system that can form around textured-surface breast implants. Although the underlying cause has yet to be elucidated, an emerging theme—linking pathogenesis to a chronic inflammatory state—continues to dominate the current literature. Specifically, the combination of increasing mutation burden and chronic inflammation leads to aberrant T-cell clonal expansion. However, the impetus remains largely unknown. Proposed mechanisms include a lipopolysaccharide endotoxin response, oncogenic transformation related to viral infection, associated trauma to the breast pocket, particulate matter digestion by capsular macrophages, chronic allergic inflammation, and genetic susceptibility. The Janus kinase–signal transducer and activator of transcription 3 (JAK-STAT3) pathway is a major signaling pathway that regulates a variety of intracellular growth and survival processes. Constitutive activation of JAK-STAT3 has been implicated in several malignancies, including lymphomas, and has recently been identified as a potential key mediator in BIA-ALCL. The purpose of this article is to review the cellular and molecular mechanisms of BIA-ALCL with a focus on the role of oncogenic JAK-STAT3 signaling in BIA-ALCL tumorigenesis and progression. Selected experimental work from the authors’ group on aberrant JAK-STAT3 signaling in BIA-ALCL is also included. The authors discuss how an inflammatory microenvironment may facilitate malignant transformation through the JAK-STAT3 pathway—highlighting its potential mechanistic role. The authors’ hope is that further investigation of this signaling pathway will reveal avenues for using JAK-STAT3 signaling as a prognostic indicator and novel therapeutic target in the case of advanced disease.