As the eighth most common cancer worldwide and the sixth leading cause of cancer death, esophageal cancer is a global health burden, with approximately 482,000 new cases and 407,000 estimated deaths in 2008.1,2 In the West, the incidence of lower esophageal and/or esophagogastric junction adenocarcinoma (EAC) has increased substantially over the past 30 years, and that of squamous cell carcinoma has declined.3,4 In the United States, for patients with localized EAC who can withstand surgery, the most common recommendation is chemoradiation followed by surgery, or trimodality therapy (TMT).5,6 Despite advances in the treatment of localized EAC, the cure rate remains at 30% to 45% for patients with clinical stage II or III, and relapses are common.7-10 After TMT, most patients undergo surveillance for at least 5 years; however, the surveillance recommendations vary considerably and are often empiric in nature.6,10 Relapses seem to be related to the sensitivity of the primary EAC as determined by the residual cancer in the surgical specimen,11,12 particularly after chemoradiation.7,13,14 However, more detailed analysis with regard to surgical pathology stage (SPS), type of relapse, and timing of relapse has not been reported and may prove useful in developing an evidence-based customized surveillance strategy.
The authors recently reported the timing and frequency of locoregional-only relapses in patients with EAC after TMT, and discussed the low rate of local relapse in the cohort and the outcome of the salvage techniques that were implemented.15 This article provides a detailed analysis of the type and timing, timing of relapse, and their association with post-TMT SPS. Forming an association between SPS and frequency/timing of relapse could have considerable implications on the cost, frequency/duration, and anxiety associated with surveillance.
The authors wish to thank Drs. Garret Walsh, Zongxing Liao, Ara A. Vaporciyan, Reza J. Mehran, and William A. Ross for their invaluable clinical contribution.
This work was supported in part from philanthropic donations received from the Caporella, Dallas, Sultan, Park, Smith, Frazier, Oaks, Vanstekelenberg, and Cantu Families; by the Schechter Private Foundation, Rivercreek Foundation, Kevin Fund, Myer Fund, Dio Fund, and Milrod Fund; by a grant from the Multidisciplinary Research Program at The University of Texas MD Anderson Cancer Center; and by Grants No. CA129906 and CA172741 from the National Cancer Institute (J.A.A.). The authors have disclosed that they have no financial interests, arrangements, affiliations, or commercial interests with the manufacturers of any products discussed in this article or their competitors.
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