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Individualised treatment in non-small cell lung cancer: precise tissue diagnosis for all?
  1. Richard Booton1,
  2. Fiona Blackhall2,
  3. Keith Kerr3
  1. 1Respiratory Research Group, Faculty of Medical and Human Sciences, The University of Manchester, Manchester Academic Health Science Centre & NIHR Translational Research Facility in Respiratory Medicine, University Hospital of South Manchester, UK
  2. 2Department of Medical Oncology, The Christie Hospital NHS Foundation Trust
  3. 3Department of Pathology, The University of Aberdeen
  1. Correspondence to Dr Richard Booton, The University of Manchester, North West Lung Centre, University Hospital of South Manchester, Southmoor Road, Manchester M23 9LT, UK; richard.booton{at}

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A number of key advances in the therapeutic management of lung cancer have signposted the need for substantial changes in the diagnostic pathway and techniques for patients with suspected lung cancer. Cell-type-specific agents are available to treat lung cancer and, together with new molecular markers, they can improve outcomes through individualised treatment regimens. For example, a prospective phase III trial of platinum-based chemotherapy in advanced non-small cell lung cancer (NSCLC) demonstrated that the combination of cisplatin/pemetrexed improved outcomes for patients with non-squamous tumours, but that cisplatin/gemcitabine was better in patients with squamous histology.1 Bevacizumab, a monoclonal antibody to vascular endothelial growth factor, plus chemotherapy is a standard of care in advanced NSCLC but is contraindicated in squamous cell subtypes due to the association with life-threatening haemoptysis.2 Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKI) are indicated in first and second-line treatment of advanced NSCLC but are more effective in female, non-smokers with adenocarcinoma, an effect most likely mediated by the presence of sensitising EGFR gene mutations.3 4 Most recently, the National Institute for Health and Clinical Excellence (NICE) has approved the use of gefitinib (an EGFR TKI) in advanced NSCLC for patients demonstrating EGFR mutation positivity.5 In addition, EGFR gene copy number by fluorescence in-situ hybridisation may also help to predict favourable outcomes with EGFR TKI or cetuximab-containing therapy.6 EGFR mutation positivity may ‘trump’ the clinical phenotype as a predictor of response and improved survival following EGFR TKI, even in patients with a low performance score (PS 3, 4). A recent report describing first-line treatment with gefitinib in EGFR mutation-positive patients (50% with metastatic brain disease) demonstrated a response rate of 90% and a startling improvement in PS from 3, 4 to 0, 1 of 68% and 1-year survival of 63%.7 Taken together …

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  • Funding RB has received honoraria and research support from Eli Lily, Chiesi and Astra Zeneca. FB has received honoraria and research support from Eli Lily, Astra-Zeneca, Roche, Pfizer and Boehringer. KK has received financial support to attend international meetings or honoraria for advisory boards/lectures from Eli Lilly, AstraZeneca, Roche, Merck, Glaxo Smith Kline, Boeringher Ingelheim and Bayer Pharmaceuticals.

  • Competing interests None.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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