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Nodal downstaging predicts survival following induction chemotherapy for stage IIIA (N2) non‐small cell lung cancer in CALGB protocol #8935
Author(s) -
Jaklitsch Michael T.,
Herndon James E.,
DeCamp Malcolm M.,
Richards William G.,
Kumar Parvesh,
Krasna Mark J.,
Green Mark R.,
Sugarbaker David J.
Publication year - 2006
Publication title -
journal of surgical oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.201
H-Index - 111
eISSN - 1096-9098
pISSN - 0022-4790
DOI - 10.1002/jso.20644
Subject(s) - medicine , vinblastine , surgery , chemotherapy , radiation therapy , induction chemotherapy , stage (stratigraphy) , cisplatin , lung cancer , oncology , paleontology , biology
Background and Objectives CALGB 8935 was a phase II protocol for mediastinoscopically staged IIIA (N2) non‐small cell lung cancer. Induction cisplatin/vinblastine chemotherapy was followed by surgical resection, adjuvant cisplatin/vinblastine, and radiotherapy. We now evaluate the prognosis of pathologic nodes. Methods Failure‐free survival was calculated from a landmark 3 months after resection to account for heterogeneity in adjuvant therapy. Results Nine of 42 (21%) resected patients had no residual N2 disease. This subset of 9 had a median failure‐free interval of 47.8 months from landmark, whereas the 33 patients (79%) with persistent N2 disease had a median failure‐free survival of 8.2 months from landmark (P=0.01). Although 21/42 (50%) had an incomplete resection (positive highest resected node and/or margin), completeness of resection did not influence failure‐free survival. There were 3 distant and no local recurrences among the N2 negative group, and 12 local recurrences among patients with residual N2 disease (P=0.041). Conclusions These data suggest: (1) persistent N2 disease following induction chemotherapy is unfavorable; (2) patients downstaged to N2 negative may benefit from surgical resection; however, (3) 33% of N2 negative patients suffered disease relapse. J. Surg. Oncol. 2006;94:599–606. © 2006 Wiley‐Liss, Inc.