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Ann Thorac Surg 2006;81:1947
© 2006 The Society of Thoracic Surgeons
a Division of Thoracic and Visceral Organ Surgery, Gunma University Faculty of Medicine, 3-39-15 Showa-machi, Maebashi, Gunma, 371-8511 Japan
b Division of Thoracic Oncology, National Cancer Center Hospital East, 6-5-1 Kashiwanoha, Kashiwa, Chiba, 277-8577 Japan
(Email: kmshimiz{at}showa.gunma-u.ac.jp; ymorishit{at}med.gunma-u.ac.jp; jyoshida{at}east.ncc.go.jp; knagai{at}east.ncc.go.jp).
In their article on skip N2 metastases in nonsmall cell lung cancer (NSCLC) patients, Riquet and colleagues [1] suggest an explanation for the presence of skip metastasis. They suggest that skip metastasis is the result of desquamating tumor cells within the pleural space, which are reabsorbed by lymphatic vessels of the parietal or diaphragmatic pleura; such drainage involves mediastinal lymph node stations and theoretically induces (N1–) N2. This suggestion is based on the two previous findings of the authors. The presence of tumor cells in post-thoracotomy pleural lavage seemed to correlate with visceral pleural invasion (VPI) and particularly with a VPI subgroup, in which the tumor is exposed on the pleural surface and does not yet involve the parietal pleura [2]. Lymphatic drainage of the medial portion of the diaphragmatic pleura was made through the peri-tracheobronchial lymph node chains, explaining the greater frequency of mediastinal lymph node involvement observed in VPI cases [3, 4].
If this lymphatic drainage is truly the major tumor cell pathway of N2 metastasis in VPI patients, there should be more skip N2 cases than contiguous (N1+) N2 cases in VPI patients, because tumor cells would not travel through the hilar lymph nodes. However, their recent study did not demonstrate this possible role of VPI for (N1-) N2 metastasis (VPI+: [N1-] N2 25.9%, [N1+] N2 30.6%). This is consistent with our recent report on VPI in that there were significantly fewer skip N2 patients in the VPI group than in the non-VPI group (skip N2 patients: 17 of 73 VPI patients [23%] vs 36 of 90 non-VPI patients [40%]; p = 0.0235) [5]. Based on these findings, we suggest that the major VPI tumor cell pathway is through the subpleural lymphatics, hilar lymph nodes, and into the mediastinal lymph node. Such a pathway should result in less frequent skip N2 patients in the VPI patients, because VPI tumor cells would travel through the hilar lymph nodes rather than in non-VPI patients.
In our recent study, we assessed the relationship between VPI and other clinicopathologic characteristics, and we concluded that VPI is an independent indicator of NSCLC invasiveness and aggressiveness [5]. Riquet and colleagues attributed the poor prognosis of VPI NSCLC patients to desquamating tumor cells within the pleural space, which are reabsorbed by lymphatic vessels of the parietal or diaphragmatic pleura, drained to the mediastinal lymph node, and cause systematic dissemination. However, such a pathway is dubious. We postulate that the invasive and aggressive nature of VPI tumors is directly associated with their poor prognosis.
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  M. Riquet, P. Bagan, J. Assouad, C. Foucault, and C. Danel Reply. Ann. Thorac. Surg., May 1, 2006; 81(5): 1947 - 1948. [Full Text] [PDF]
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