Objectives/Hypothesis
Although the multidisciplinary tumor board (MTB) is accepted as best practice for the management of head and neck squamous cell carcinoma (HNSCC), there is limited evidence showing its impact on survival. Our goal was to investigate the impact of an MTB following the hiring of a fellowship‐trained head and neck surgeon and implementation of an MTB at our institution. We hypothesized that these changes would demonstrate an improvement in survival.
Study Design
Retrospective chart review.
Methods
A review of HNSCC treated at our institution between October 2006 and May 2015 was performed. The cohort was divided into pre‐MTB (October 2006–February 2011) and post‐MTB (February 2011–May 2015) cohorts. Patient demographics, cancer stage, and treatment outcomes were reviewed. Univariate, multivariate, and survival analysis were performed.
Results
The study included 224 patients, 98 in the pre‐MTB cohort and 126 in the post‐MTB cohort. Of total patients, 139 (62%) were black and 91 (40%) were on Medicaid or uninsured. Average follow‐up time was 2.8 years, and most cases were advanced stage (68%). On Kaplan‐Meier evaluation, overall survival and disease‐specific survival were significantly improved in the post‐MTB cohort compared with the pre‐MTB cohort, with a 5‐year disease‐specific survival of 52% vs. 75% (P = .003). A matched cohort analysis showed that the post‐MTB cohort had significantly lower risk of death (hazard ratio: 0.48).
Conclusions
Our study demonstrates that treatment of HNSCC by a dedicated multidisciplinary team results in improved survival. Multidisciplinary care should be considered best practice in the care of HNSCC.
Level of Evidence
3b Laryngoscope, 130:946–950, 2020
Radiation-induced endothelial/vascular injury is a major complicating factor in radiotherapy and a leading cause of morbidity and mortality in nuclear or radiological catastrophes. Exposure of tissue to ionizing radiation (IR) leads to the release of oxygen radicals and proteases that result in loss of endothelial barrier function and leukocyte dysfunction leading to tissue injury and organ damage. Microvascular endothelial cells are particularly sensitive to IR and radiation-induced alterations in endothelial cell function are thought to be a critical factor in organ damage through endothelial cell activation, enhanced leukocyte-endothelial cell interactions, increased barrier permeability and initiation of apoptotic pathways. These radiation-induced inflammatory responses are important in early and late radiation pathologies in various organs. A better understanding of mechanisms of radiation-induced endothelium dysfunction is therefore vital, as radiobiological response of endothelium is of major importance for medical management and therapeutic development for radiation injuries. In this review, we summarize the current knowledge of cellular and molecular mechanisms of radiation-induced endothelium damage and their impact on early and late radiation injury. Furthermore, we review established and emerging in vivo and in vitro models that have been developed to study the mechanisms of radiation-induced endothelium damage and to design, develop and rapidly screen therapeutics for treatment of radiation-induced vascular damage. Currently there are no specific therapeutics available to protect against radiation-induced loss of endothelial barrier function, leukocyte dysfunction and resulting organ damage. Developing therapeutics to prevent endothelium dysfunction and normal tissue damage during radiotherapy can serve as the urgently needed medical countermeasures.
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