Staging of esophageal carcinoma.

See related article on page 1091. I n this month’s issue of the Journal, Rice and colleagues1 report a thorough retrospective analysis of prospectively collected data titled “Role of Clinically Determined Depth of Tumor Invasion in the Treatment of Esophageal Carcinoma” The report has 3 major conclusions. First, the authors conclude that clinical staging with endoscopic ultrasonography (EUS) reliably reflects pathologic staging with an accuracy of 87%. This observation adds to the growing body of data indicating that EUS is the most reliable method available for the clinical staging of esophageal cancer. Second, they conclude that the tumor and nodal responses to induction therapy (chemoradiotherapy) are linked. This implies that a benefit seen in downstaging T (tumor) indicates a similar downstaging of N (nodal disease). They then ask the following pertinent question: Does downstaging T portend an improved survival? The answer is partially provided in their third conclusion that when nodal disease persists, the downstaging of the tumor does not improve survival. This implies that even though T and N stage are linked in both their occurrence and response to induction therapy, N is predominant and independent of T in predicting survival. With these points made, they attempt to identify, with clinical staging methodology, subgroups of patients who are likely to benefit from induction therapy. Overall, the report is a movement away from the current trend toward the belief that neoadjuvant therapy is the standard of care for all patients with esophageal cancer. Their movement is justified by the failure of prospective randomized clinical trials to show a convincing and consistent benefit of neoadjuvant therapy in carcinoma of the esophagus (Table 1).2-8 In an effort to identify subgroups of patients who would benefit from induction therapy, Rice and colleagues1 have made 3 major observations. First, they observed that patients with clinical stage T3 N0 disease appear to have a benefit from induction therapy (see Rice and colleagues’ Figure 2). Several concerns about their data need to be addressed before incorporating these observations into clinical practice. First, they have clearly shown that there is often a difference between the clinical assessment of tumor depth (clinical T stage) and the depth of tumor invasion on the histologic examination of the resected specimen (pathologic T stage). When this occurs, they have chosen to explain the difference as a result of the downstaging of the tumor by means of induction therapy when it is equally plausible that it might be due to, at least in some cases, inaccurate initial clinical staging; that is, patients with lesser disease might have had their disease overstaged, resulting in a perceived but not true downstaging of the tumor by means of induction therapy. Rice and colleagues’ Appendix Table 1 shows the overall accuracy of EUS in patients treated with surgical intervention alone. For T3 tumors, staging errors occurred in 18 of 112 patients, with 15 (13%) having been overstaged. In most cases the overstaged tumors were actually T1 in depth. Applying this information to the group of 28 patients depicted in Rice and colleagues’ Figure 2, one could expect that 4 patients with apparent T3 N0 disease actually had T1 to T2 N0 disease with a potential for better survival. This could explain the difference in survival shown in patients with clinical stage T3 N0 disease because the difference between the expected (untreated patients) and observed (treated patients) survival at 5 years was only 4 patients. The second concern is that expected survival of the clinically staged T3 N0 subgroup on From the University of Southern California, Department of Surgery, Keck School of Medicine.