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Newtown, NSW, Australia
Dr. Barnes is Associate Professor, University of Sydney, and Respiratory Physician, Royal Prince Alfred Hospital.
Correspondence to: David J. Barnes, FCCP, Royal Prince Alfred Hospital Medical Center, 100 Carillon Ave, Newtown 2042, NSW, Australia; e-mail: davidb{at}med.usyd.edu.au
The current staging system for non-small cell lung cancer (NSCLC) has served us well for a number of years.1 It has helped us in the evidence-based planning of treatment, the discussion of prognosis with our patients, and also the conduct and interpretation of clinical trials. The advent of positron emission tomography (PET) scanning has clearly improved the accuracy of this staging, with the outcome being both the upstaging and downstaging of our patients. It will be interesting to see whether upstaging via PET scanning (with subsequent exclusion of some patients from futile surgery) will result in better 5-year survival rates for patients undergoing surgery.
Perhaps the most complex and unsatisfactory aspect of our TNM staging system is in the assessment of nodal (N) disease. Clinical staging of N disease can involve the use of a number of investigation modalities including CT scan, PET scan, mediastinoscopy, and, more recently, endobronchial ultrasound with transbronchial needle aspiration. Pathologic staging of N disease, on the other hand, includes intraoperative lymph node sampling and formal node clearance. At present, mediastinal node (N2) disease is lumped together in stage IIIA. However there is a huge variation in the extent of N2 disease, ranging from incidental nodal metastases found in the final pathology of surgical specimens (but not clinically evident) right through to bulky multistation, unresectable lymphadenopathy. Clearly, these variations in stage IIIA (N2) disease have far-reaching implications with respect to both therapy and prognosis. Lumping all stage IIIA (N2) disease into one stage is clearly inappropriate, and we need formal recognition of a subclassification of stage IIIA (N2) disease that takes into account these variations. There have been previous calls for such a change in the classification of N2 disease.2
So, in this setting of complex N disease assessment, along comes this elegant study by Lee and colleagues3 published in the current issue of CHEST (see page 993). These authors have prospectively analyzed both the risk factors for extranodal extension in NSCLC patients and its adverse impact on prognosis. The presence of extranodal extension (ie, the presence of cancer cells beyond the capsule of the involved nodes) is associated with female gender, adenocarcinoma, advanced disease stage, vascular invasion, and the overexpression of p53. To me, there are three main implications of this study with respect to the importance of extranodal extension, as follows:
So, where to now? In my view, this study by Lee and colleagues3 further emphasizes the need for the clarification of N disease in our NSCLC staging system. This system needs to take into account both the vagaries of N2 disease and the presence or absence of extranodal extension. While we do not want to unnecessarily overcomplicate matters too much, we do need a staging system that more accurately reflects the modern-life complexities in lung cancer management. Lee and colleagues3 are to be applauded for further muddying the waters (!) of nodal disease assessment.
Footnotes
The author has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.
References
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