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Journal of Clinical Oncology, Vol 25, No 7 (March 1), 2007: pp. 906-907 © 2007 American Society of Clinical Oncology. DOI: 10.1200/JCO.2006.09.6933
New Proposal for Postsurgery Pathologic Staging of Esophageal or Gastroesophageal Junction Adenocarcinoma: Why Bother?Department of Gastrointestinal Medical Oncology, The University of Texas M.D. Anderson Cancer Center, Houston, TX To the Editor: Lagarde et al1 should be commended for an extensive and painstaking review of the prognostic factors of esophageal or gastroesosphageal adenocarcinoma. Their article serves as a useful reference for those interested in this disease process. They point out that the current classification of these tumors is outdated. For a long time, various groups have expressed considerable dissatisfaction with the current staging system. A variety of modifications have been proposed, but no group has provided a solution that is acceptable to all others. The authors have very clearly pointed out that surgery as primary therapy (most frequently diagnosed cancer is stage II or III) results in a dismal outcome (< 25% 5-year survival rate) and the results of randomized trials of preoperative chemoradiotherapy trials have been equivocal. The goal of preoperative chemoradiotherapy is not just to improve local control, but all such trials strived to improve overall survival (the primary end point) of the patients. Contrary to the authors’ assertion that response to preoperative chemoradiotherapy has a minor prognostic impact on prognosis, the pathologic stage after preoperative chemoradiotherapy remains the most important independent prognostic factor in a multivariate analysis of patients undergoing preoperative chemoradiotherapy2 and similar findings have been reported by other major institutions.3,4 The authors do not point out that clinical stage (cT or cN) does not predict patient outcome whether surgery is used as primary therapy or not and certainly not in the setting of preoperative chemoradiotherapy.2-4 The authors go on to propose that a sophisticated postoperative staging system for localized esophageal and gastroesophageal junction adenocarcinoma should be developed. Such a new system may be of some academic interest, however, its value should be questioned, particularly when we consider the future approaches to improve the outcome of such patients. Should we continue to offer surgery as the primary therapy for clinical stage II or III esophageal or gastroesophageal junction cancer? No, not based on the utterly disappointing results. The 5-year survival rate of patients with postsurgery pathologic stage IIA after surgery as primary therapy is less than 35% and those with any stage higher than IIA results in a less than 20% 5-year survival rate.5 What is to be accomplished by a new staging system with such poor results? The future improvements in the outcome are hardly likely from subjecting more and more patients with stage II or III cancer to surgery first and developing a new postsurgery pathologic classification, as proposed. That would be just too simplistic and without considerations to failure of the current approaches in patients with localized carcinoma of the esophagus and esophageal junction. Moreover, the use of preoperative therapy (particularly chemoradiotherapy) has increased in North America and in Europe.6,7 This trend is not likely to subside and further reduces the value of a postoperative classification after surgery as primary therapy. Clearly, obvious solutions are lacking, but the future is in confronting the bigger picture of the diversity in clinical biology of these tumors (that is to say that not all patients within a given clinical or postsurgical stage are the same after receiving the same therapy [surgery in this case]) and the true drivers of this clinical biologic diversity are the molecular biology of the cancer and patient genetics. We are just scratching the surface of our understanding that the considerable heterogeneity in molecular biology and patient genetics is the true determinant of patient outcome and gross pretreatment or postsurgical parameters have much less impact.8-12 Currently, we do not know what to do with such information, and much work needs to be done. I am hoping we would be diverting more resources to develop strategies in identifying biomarkers for individualization of therapy (molecular staging as a dominant component to clinical/pathologic parameters) and in the development of new therapeutic targets. Hopefully, that will lead to improved patient outcome and reduced complications. AUTHOR’S DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author indicated no potential conflicts of interest. REFERENCES
1. Lagarde SM, ten Kate FJW, Reitsma JB, et al: Prognostic factors in adenocarcinoma of the esophagus and gastroesophageal junction. J Clin Oncol 24:4347-4355, 2006 2. Chirieac LR, Swisher SG, Ajani JA, et al: Posttherapy pathologic stage predicts survival in patients with esophageal carcinoma receiving preoperative chemoradiation. Cancer 103:1347-1355, 2005[CrossRef][Medline] 3. Rizk NP, Bains MS, Ilson DH, et al: The AJCC staging system does not predict survival in patients receiving multimodality therapy for esophageal cancer. J Clin Oncol 23:16S, 2005 (abstr 4005) 4. Gibson M, Burtness B, Heath E, et al: Effect of neoadjuvant chemoradiotherapy on pathologic stage and survival in patients with locally advanced esophageal cancer. J Clin Oncol 22:14S, 2004 (abstr 4032) 5. Rice TW, Blackstone EH, Rybicki LA, et al: Refining esophageal cancer staging. J Thorac Cardiovasc Surg 125:1103-1113, 2003 6. Suntharalingam M, Moughan J, Coia LR, et al: Outcome results of the 1996-1999 patterns of care survey on the national practice for patients receiving radiation therapy for carcinoma of the esophagus. J Clin Oncol 23:2325-2331, 2005 7. Stein H-J, Siewert JR: Improved prognosis of resected esophageal cancer. World J Surg 28:520-525, 2004[Medline] 8. Wu X, Gu J, Wu TT, et al: Genetic variations in radiation and chemotherapy drug action pathways predict clinical outcomes in esophageal cancer. J Clin Oncol 24:3789-3798, 2006 9. Izzo JG, Malhotra U, Wu TT, et al: Association of activated transcription factor nuclear factor kappa B with chemoradiation resistance and poor outcome in esophageal carcinoma. J Clin Oncol 24:748-754, 2006 10. Hamilton JP, Sato P, Greenwald BD, et al: Promoter methylation and response to chemotherapy and radiation in esophageal cancer. Clin Gastroenterol Hepatol 4:701-708, 2006[CrossRef][Medline] 11. Luthra R, Wu TT, Luthra MG, et al: Gene expression profiling of localized esophageal carcinoma: Association with pathologic response to preoperative chemoradiation. J Clin Oncol 24:259-267, 2005[Medline] 12. Izzo JG, Correa AM, Wu TT, et al: Nuclear factor-kappa B status, chemoradiation resistance, and metastatic progression in esophageal carcinoma. Mol Cancer Ther 5:1-8, 2006
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Copyright © 2007 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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