Surgical resection for residual N2 disease after induction chemotherapy

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Abstract

Background. Induction therapy is a common treatment modality for patients with stage IIIA non-small cell lung cancer (NSCLC). Although mediastinal nodal downstaging after induction therapy is generally considered a favorable prognostic feature, the benefit of resection in the presence of residual N 2 disease is controversial. In this study we analyzed our experience with resection after induction chemotherapy in patients with residual N 2 disease to more precisely define the role of surgical resection in this group of patients. Methods. In this retrospective analysis, we reviewed the records of 78 patients with N2 disease who received induction therapy with preoperative intent between 1990 and 2003. All patients had potentially resectable disease. Survival analysis was performed using the Kaplan-Meier method. A Cox proportional hazards regression model was used to evaluate multiple prognostic factors. Results. There were 78 patients (39 men) with a median age of 64 years. Sixty had nonsquamous histology. Resection was performed in 52 patients (47 R0). Hospital mortality was 1.9%. A complete pathologic response occurred in 2 of 52 (3.8%) patients and 19 of 52 (36%) patients had no residual N2 disease. Overall 5-year survival for resected patients was 23%. Overall 5-year survival was 30% for N 0-N1 patients and 19% for those with residual N 2 disease. Multivariable analysis identified clinical response to therapy (p = 0.0007) and histology (p = 0.01), but not residual N2 disease (p = 0.65), as important prognostic variables. Conclusions. Surgical resection may be a viable option for patients with residual N2 disease after induction chemotherapy, provided an R0 resection can be performed. © 2005 by The Society of Thoracic Surgeons.

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Port, J. L., Korst, R. J., Lee, P. C., Levin, M. A., Becker, D. E., Keresztes, R., & Altorki, N. K. (2005). Surgical resection for residual N2 disease after induction chemotherapy. Annals of Thoracic Surgery, 79(5), 1686–1690. https://doi.org/10.1016/j.athoracsur.2004.10.057

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