Lung Cancer
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Lung cancer is one of the most common types of cancer. The lungs are a pair of cone-shaped organs situated inside the chest, they bring oxygen into the body and take out waste carbon dioxide. There is a strong link between smoking and lung cancer. There are two main categories of lung cancer; Small Cell Lung Cancer (SCLC) , and Non-Small Cell Lung Cancer (NSCLC).

Around 42,000 people are diagnosed with lung cancer each year. (Source: Cancer Research UK)

This page shows only UK resources. For a more extensive list of resources from around the world see CancerIndex: Lung Cancer

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Latest Research Publications

Information Patients and the Public (7 links)


Information for Health Professionals / Researchers (5 links)

Latest Research Publications

Showing publications with corresponding authors from the UK (Source: PubMed).

Taylor WS, Vaughan P, Trotter S, Rajesh PB
A rare association of pulmonary carcinoid, lymphoma, and sjögren syndrome.
Ann Thorac Surg. 2013; 95(3):1086-7 [PubMed]
Pulmonary carcinoid and pulmonary lymphoma are both rare cancers and are seldom seen together. Cases have been reported of their coexistence in the gastrointestinal tract, but our literature searches only found a single case of their coexistence in the lung. We discuss our case as well as the literature to try to find a connection and explanation for this occurrence.
Department of Thoracic Surgery, Heartlands Hospital, Birmingham


Goldstraw P
New staging system: how does it affect our practice?
J Clin Oncol. 2013; 31(8):984-91 [PubMed]
The anatomic extent of disease, as described by the TNM classification, remains the most powerful prognostic indicator for lung cancer. It is used daily by specialists in all branches of lung cancer care and research. Any new edition of the TNM classification is therefore an important event in the thoracic oncology community and one greeted with mixed feelings. The changes introduced in the seventh edition were the first for 13 years and arguably the most profound since the first data-driven revision more than 40 years earlier. Inevitably there will be concerns that any change in the T, N, or M descriptors and resultant stage groupings will have implications for previous treatment pathways. In this article, the changes to the classification are described, and their possible impacts on clinical care and research are discussed.
National Heart and Lung Institute, Imperial College, London


Lee WY, Kastelik J, Campbell A, et al.
A case report of dermatomyositis associated with small cell lung cancer.
Tumori. 2012; 98(6):158e-61e [PubMed]
Dermatomyositis associated with lung cancer is uncommon. Dermatomyositis associated with small cell lung cancer is very rare and carries a poor prognosis. We present a case of a patient with dermatomyositis associated with small cell carcinoma of the lung and review the literature.
Department of Respiratory Medicine, Castle Hill Hospital, Castle Road, Cottingham,United Kingdom. wha-yong.lee@hey.nhs.uk


Stead LF, Berri S, Wood HM, et al.
The transcriptional consequences of somatic amplifications, deletions, and rearrangements in a human lung squamous cell carcinoma.
Neoplasia. 2012; 14(11):1075-86 [PubMed] Free Access to Full Article
Lung cancer causes more deaths, worldwide, than any other cancer. Several histologic subtypes exist. Currently, there is a dearth of targeted therapies for treating one of the main subtypes: squamous cell carcinoma (SCC). As for many cancers, lung SCC karyotypes are often highly anomalous owing to large somatic structural variants, some of which are seen repeatedly in lung SCC, indicating a potential causal association for genes therein. We chose to characterize a lung SCC genome to unprecedented detail and integrate our findings with the concurrently characterized transcriptome. We aimed to ascertain how somatic structural changes affected gene expression within the cell in ways that could confer a pathogenic phenotype. We sequenced the genomes of a lung SCC cell line (LUDLU-1) and its matched lymphocyte cell line (AGLCL) to more than 50x coverage. We also sequenced the transcriptomes of LUDLU-1 and a normal bronchial epithelium cell line (LIMM-NBE1), resulting in more than 600 million aligned reads per sample, including both coding and non-coding RNA (ncRNA), in a strand-directional manner. We also captured small RNA (<30 bp). We discovered significant, but weak, correlations between copy number and expression for protein-coding genes, antisense transcripts, long intergenic ncRNA, and microRNA (miRNA). We found that miRNA undergo the largest change in overall expression pattern between the normal bronchial epithelium and the tumor cell line. We found evidence of transcription across the novel genomic sequence created from six somatic structural variants. For each part of our integrated analysis, we highlight candidate genes that have undergone the largest expression changes.
Leeds Institute of Molecular Medicine, University of Leeds, Leeds


Cook GJ, Yip C, Siddique M, et al.
Are pretreatment 18F-FDG PET tumor textural features in non-small cell lung cancer associated with response and survival after chemoradiotherapy?
J Nucl Med. 2013; 54(1):19-26 [PubMed]
UNLABELLED: There is evidence in some solid tumors that textural features of tumoral uptake in (18)F-FDG PET images are associated with response to chemoradiotherapy and survival. We have investigated whether a similar relationship exists in non-small cell lung cancer (NSCLC).
METHODS: Fifty-three patients (mean age, 65.8 y; 31 men, 22 women) with NSCLC treated with chemoradiotherapy underwent pretreatment (18)F-FDG PET/CT scans. Response was assessed by CT Response Evaluation Criteria in Solid Tumors (RECIST) at 12 wk. Overall survival (OS), progression-free survival (PFS), and local PFS (LPFS) were recorded. Primary tumor texture was measured by the parameters coarseness, contrast, busyness, and complexity. The following parameters were also derived from the PET data: primary tumor standardized uptake values (SUVs) (mean SUV, maximum SUV, and peak SUV), metabolic tumor volume, and total lesion glycolysis.
RESULTS: Compared with nonresponders, RECIST responders showed lower coarseness (mean, 0.012 vs. 0.027; P = 0.004) and higher contrast (mean, 0.11 vs. 0.044; P = 0.002) and busyness (mean, 0.76 vs. 0.37; P = 0.027). Neither complexity nor any of the SUV parameters predicted RECIST response. By Kaplan-Meier analysis, OS, PFS, and LPFS were lower in patients with high primary tumor coarseness (median, 21.1 mo vs. not reached, P = 0.003; 12.6 vs. 25.8 mo, P = 0.002; and 12.9 vs. 20.5 mo, P = 0.016, respectively). Tumor coarseness was an independent predictor of OS on multivariable analysis. Contrast and busyness did not show significant associations with OS (P = 0.075 and 0.059, respectively), but PFS and LPFS were longer in patients with high levels of each (for contrast: median of 20.5 vs. 12.6 mo, P = 0.015, and median not reached vs. 24 mo, P = 0.02; and for busyness: median of 20.5 vs. 12.6 mo, P = 0.01, and median not reached vs. 24 mo, P = 0.006). Neither complexity nor any of the SUV parameters showed significant associations with the survival parameters.
CONCLUSION: In NSCLC, baseline (18)F-FDG PET scan uptake showing abnormal texture as measured by coarseness, contrast, and busyness is associated with nonresponse to chemoradiotherapy by RECIST and with poorer prognosis. Measurement of tumor metabolic heterogeneity with these parameters may provide indices that can be used to stratify patients in clinical trials for lung cancer chemoradiotherapy.
Division of Imaging Sciences and Biomedical Engineering, Kings College London, London


Sheel AR, McShane J, Poullis MP
Survival of patients with or without symptoms undergoing potentially curative resections for primary lung cancer.
Ann Thorac Surg. 2013; 95(1):276-84 [PubMed]
BACKGROUND: Numerous historical screening programs to detect lung cancer have been undertaken. With technologic advances, complimentary diagnostic tests have been developed; however, only the National Lung Cancer Trial has demonstrated increased survival. Following the success of this study, screening programs are being trialled in several countries. Screening should, in theory, reduce lung cancer deaths by identifying asymptomatic patients with earlier tumors. This study asked whether lung cancer patients who are asymptomatic at presentation have a better survival than those who present with symptoms.
METHODS: This was a retrospective analysis of a validated prospective thoracic surgery database from a tertiary center in the Northwest of England. Included were 1,546 consecutive patients (826 men, 720 women) who received operative intervention for non-small cell lung cancer. The main outcome measures included 5-year survival and univariate and multivariate Cox regression analysis.
RESULTS: Cancer stage, age, and operation type were confirmed as being of prognostic importance, validating previous studies. Survival between asymptomatic or symptomatic patients did not differ significantly (p = 0.489), regardless of stage. The hazard ratios (with 95% confidence intervals) for variables associated with poorer outcome identified by Cox's regression analysis were male sex, 1.34 (1.15 to 1.56); advancing age, 1.03 (1.02 to 1.04); advancing stage, 3.30 (2.69 to 4.04); and pneumonectomy, 1.24 (1.01 to 1.52). Symptoms were not a significant variable affecting survival on multivariate analysis.
CONCLUSIONS: This retrospective study from the Northwest of England showed that in our subset of lung cancer patients undergoing resection, asymptomatic patients with non-small cell lung cancer do not have improved survival, implying it is a systemic disease in many at diagnosis. Care should be taken when generalizing the results of the National Lung Screening Trial to all populations until further validation has been performed.
Department of Cardiothoracic Surgery, Liverpool Heart and Chest Hospital, Liverpool


Fitzsimmons D, Wheelwright S, Johnson CD
Quality of life in pulmonary surgery: choosing, using, and developing assessment tools.
Thorac Surg Clin. 2012; 22(4):457-70 [PubMed]
There is mounting recognition that, to aid surgical decision making, treatment efficacy needs to be measured in a variety of ways, with health-related quality of life now widely regarded as an important outcome in pulmonary surgical populations. The aim of this review is to provide a comprehensive overview of the key issues to consider if an investigator wishes to incorporate health-related quality of life assessment into trials and studies of pulmonary surgery, drawing on recent studies of lung cancer surgery as an example.
Swansea Centre for Health Economics, College of Human and Health Sciences, Swansea University, Singleton Park, Swansea


Higgins G, Roper KM, Watson IJ, et al.
Variant Ciz1 is a circulating biomarker for early-stage lung cancer.
Proc Natl Acad Sci U S A. 2012; 109(45):E3128-35 [PubMed] Free Access to Full Article
There is an unmet need for circulating biomarkers that can detect early-stage lung cancer. Here we show that a variant form of the nuclear matrix-associated DNA replication factor Ciz1 is present in 34/35 lung tumors but not in adjacent tissue, giving rise to stable protein quantifiable by Western blot in less than a microliter of plasma from lung cancer patients. In two independent sets, with 170 and 160 samples, respectively, variant Ciz1 correctly identified patients who had stage 1 lung cancer with clinically useful accuracy. For set 1, mean variant Ciz1 level in individuals without diagnosed tumors established a threshold that correctly classified 98% of small cell lung cancers (SCLC) and non-SCLC patients [receiver operator characteristic area under the curve (AUC) 0.958]. Within set 2, comparison of patients with stage 1 non-SCLC with asymptomatic age-matched smokers or individuals with benign lung nodules correctly classified 95% of patients (AUCs 0.913 and 0.905), with overall specificity of 76% and 71%, respectively. Moreover, using the mean of controls in set 1, we achieved 95% sensitivity among patients with stage 1 non-SCLC patients in set 2 with 74% specificity, demonstrating the robustness of the classification. RNAi-mediated selective depletion of variant Ciz1 is sufficient to restrain the growth of tumor cells that express it, identifying variant Ciz1 as a functionally relevant driver of cell proliferation in vitro and in vivo. The data show that variant Ciz1 is a strong candidate for a cancer-specific single marker capable of identifying early-stage lung cancer within at-risk groups without resort to invasive procedures.
Cizzle Biotech, University of York, Yorkshire YO10 5DD
Research funded by:


Deacon K, Onion D, Kumari R, et al.
Elevated SP-1 transcription factor expression and activity drives basal and hypoxia-induced vascular endothelial growth factor (VEGF) expression in non-small cell lung cancer.
J Biol Chem. 2012; 287(47):39967-81 [PubMed] Free Access to Full Article
VEGF plays a central role in angiogenesis in cancer. Non-small cell lung cancer (NSCLC) tumors have increased microvascular density, localized hypoxia, and high VEGF expression levels; however, there is a lack of understanding of how oncogenic and tumor microenvironment changes such as hypoxia lead to greater VEGF expression in lung and other cancers. We show that NSCLC cells secreted higher levels of VEGF than normal airway epithelial cells. Actinomycin D inhibited all NSCLC VEGF secretion, and VEGF minimal promoter-luciferase reporter constructs were constitutively active until the last 85 base pairs before the transcription start site containing three SP-1 transcription factor-binding sites; mutation of these VEGF promoter SP-1-binding sites eliminated VEGF promoter activity. Furthermore, dominant negative SP-1, mithramycin A, and SP-1 shRNA decreased VEGF promoter activity, whereas overexpression of SP-1 increased VEGF promoter activity. Chromatin immunoprecipitation assays demonstrated SP-1, p300, and PCA/F histone acetyltransferase binding and histone H4 hyperacetylation at the VEGF promoter in NSCLC cells. Cultured NSCLC cells expressed higher levels of SP-1 protein than normal airway epithelial cells, and double-fluorescence immunohistochemistry showed a strong correlation between SP-1 and VEGF in human NSCLC tumors. In addition, hypoxia-driven VEGF expression in NSCLC cells was SP-1-dependent, with hypoxia increasing SP-1 activity and binding to the VEGF promoter. These studies are the first to demonstrate that overexpression of SP-1 plays a central role in hypoxia-induced VEGF secretion.
Centre for Respiratory Research, University of Nottingham, Nottingham, NG5 1PB


Shawgi M, James J, Prescott M, McWilliam L
Unilateral adrenal metastasis from non–small-cell lung cancer demonstrating very high FDG uptake with a standardized uptake value in excess of sixty.
Clin Nucl Med. 2012; 37(8):812-4 [PubMed]
We report the case of a 52-year-old man who presented with a 2-week history of dyspnea and wheeze. CT scan of the chest showed a large soft-tissue lesion in the right main bronchus extending into the trachea. Pathologic examination of endoscopic tracheal biopsies showed features consistent with a non–small-cell lung carcinoma. 18F-FDG PET/CT showed very high uptake of FDG in the bronchial tumor (high standardized uptake values: 25.1) and unexpected very intense uptake in the left adrenal gland (high standardized uptake values: 62.5). Laparoscopic adrenalectomy was performed, and subsequent histopathological examination confirmed metastatic non–small-cell carcinoma in the adrenal gland. Although adrenal malignancies are generally metabolically active, such high uptake of FDG within a metastatic lesion has not been reported previously.
Nuclear Medicine Centre, Central Manchester University Hospitals, Manchester


Nikolaidis G, Raji OY, Markopoulou S, et al.
DNA methylation biomarkers offer improved diagnostic efficiency in lung cancer.
Cancer Res. 2012; 72(22):5692-701 [PubMed] Free Access to Full Article
The exceptional high mortality of lung cancer can be instigated to a high degree by late diagnosis. Despite the plethora of studies on potential molecular biomarkers for lung cancer diagnosis, very few have reached clinical implementation. In this study, we developed a panel of DNA methylation biomarkers and validated their diagnostic efficiency in bronchial washings from a large retrospective cohort. Candidate targets from previous high-throughput approaches were examined by pyrosequencing in an independent set of 48 lung tumor/normal paired. Ten promoters were selected and quantitative methylation-specific PCR (qMSP) assays were developed and used to screen 655 bronchial washings from the Liverpool Lung Project (LLP) subjects divided into training (194 cases and 214 controls) and validation (139 cases and 109 controls) sets. Three statistical models were used to select the optimal panel of markers and to evaluate the performance of the discriminatory algorithms. The final logit regression model incorporated hypermethylation at p16, TERT, WT1, and RASSF1. The performance of this 4-gene methylation signature in the validation set showed 82% sensitivity and 91% specificity. In comparison, cytology alone in this set provided 43% sensitivity at 100% specificity. The diagnostic efficiency of the panel did not show any biases with age, gender, smoking, and the presence of a nonlung neoplasm. However, sensitivity was predictably higher in central (squamous and small cell) than peripheral (adenocarcinomas) tumors, as well as in stage 2 or greater tumors. These findings clearly show the impact of DNA methylation-based assays in the diagnosis of cytologically occult lung neoplasms. A prospective trial is currently imminent in the LLP study to provide data on the enhancement of diagnostic accuracy in a clinical setting, including by additional markers.
Department of Molecular & Clinical Cancer Medicine, University of Liverpool, Liverpool
Research funded by:


Raji OY, Duffy SW, Agbaje OF, et al.
Predictive accuracy of the Liverpool Lung Project risk model for stratifying patients for computed tomography screening for lung cancer: a case-control and cohort validation study.
Ann Intern Med. 2012; 157(4):242-50 [PubMed]
BACKGROUND: External validation of existing lung cancer risk prediction models is limited. Using such models in clinical practice to guide the referral of patients for computed tomography (CT) screening for lung cancer depends on external validation and evidence of predicted clinical benefit.
OBJECTIVE: To evaluate the discrimination of the Liverpool Lung Project (LLP) risk model and demonstrate its predicted benefit for stratifying patients for CT screening by using data from 3 independent studies from Europe and North America.
DESIGN: Case-control and prospective cohort study.
SETTING: Europe and North America.
PATIENTS: Participants in the European Early Lung Cancer (EUELC) and Harvard case-control studies and the LLP population-based prospective cohort (LLPC) study.
MEASUREMENTS: 5-year absolute risks for lung cancer predicted by the LLP model.
RESULTS: The LLP risk model had good discrimination in both the Harvard (area under the receiver-operating characteristic curve [AUC], 0.76 [95% CI, 0.75 to 0.78]) and the LLPC (AUC, 0.82 [CI, 0.80 to 0.85]) studies and modest discrimination in the EUELC (AUC, 0.67 [CI, 0.64 to 0.69]) study. The decision utility analysis, which incorporates the harms and benefit of using a risk model to make clinical decisions, indicates that the LLP risk model performed better than smoking duration or family history alone in stratifying high-risk patients for lung cancer CT screening.
LIMITATIONS: The model cannot assess whether including other risk factors, such as lung function or genetic markers, would improve accuracy. Lack of information on asbestos exposure in the LLPC limited the ability to validate the complete LLP risk model.
CONCLUSION: Validation of the LLP risk model in 3 independent external data sets demonstrated good discrimination and evidence of predicted benefits for stratifying patients for lung cancer CT screening. Further studies are needed to prospectively evaluate model performance and evaluate the optimal population risk thresholds for initiating lung cancer screening.
Roy Castle Lung Cancer Research Programme, The University of Liverpool Cancer Research Centre, Institute of Translational Medicine, The University of Liverpool, Liverpool L3 9TA
Research funded by:


Lüchtenborg M, Jakobsen E, Krasnik M, et al.
The effect of comorbidity on stage-specific survival in resected non-small cell lung cancer patients.
Eur J Cancer. 2012; 48(18):3386-95 [PubMed]
AIM: To quantify the effect of comorbidity on stage-specific survival in resected non-small cell lung cancer (NSCLC) patients.
METHODS: From the Danish Lung Cancer Registry, 20,461 patients diagnosed with lung cancer between 1st January 2005 and 31st December 2010 were identified. Among 3152 NSCLC patients who underwent surgical resection, mortality hazard ratios were calculated during three consecutive time periods following surgery (0-1 month, 1 month-1 year and >1 year) according to Charlson comorbidity score (CCS 0, 1, 2, 3+), Eastern Cooperative Oncology Group (ECOG) performance status, lung function, age, sex, pathological T (pT) and N (pN) stage using Cox proportional hazard modelling. The Kaplan Meier method was used to describe stage-specific survival according to the CCS.
RESULTS: Severe comorbidity (CCS 3+) was independently associated with significantly higher death rates throughout the three periods of follow-up [Hazard ratio (HR) 2.06 (1.13-3.75) for CCS 3+ in 0-1 month, 1.57 (1.17-2.12) 3+ during1 month-1 year and 1.84 (1.42-2.37) after 1 year]. Stage-specific 5-year survival in patients with severe comorbidity was significantly lower than in patients without comorbid disease [e.g. 38% (95% confidence interval (CI) 23-53%) for pT1 and CCS 3+ versus 69% (62-75%) for pT1 and CCS 0].
CONCLUSION: Severe comorbidity affects survival of NSCLC patients who undergo surgical resection by as much as a single stage increment and this effect persists throughout follow-up. Further research may be necessary to help identify which patients are most likely to benefit from surgery.
King's College London, School of Medicine, Thames Cancer Registry, 42 Weston Street, London


McHugh BJ, Murdoch A, Haslett C, Sethi T
Loss of the integrin-activating transmembrane protein Fam38A (Piezo1) promotes a switch to a reduced integrin-dependent mode of cell migration.
PLoS One. 2012; 7(7):e40346 [PubMed] Free Access to Full Article
Lung cancer is one of the most common fatal diseases in the developed world. The disease is rarely cured by currently available therapies, with an overall survival rate of ∼10%. Characterizing novel proteins that offer crucial insights into the processes of lung tumour invasion and metastasis may therefore provide much-needed prognostic markers, and influence therapeutic strategies. Aberrant function of the integrin family of heterodimeric cell surface receptors is a common theme in cancer--investigation into novel integrin activity regulators may offer crucial insights into the processes of tumour invasion and metastasis and may reveal insights into potential therapeutic targets. We previously described that depletion of the novel multi-transmembrane domain protein Fam38A, located at the endoplasmic reticulum (ER), inactivates endogenous beta1 integrin affinity, reducing cell adhesion. We now show that depletion of Fam38A, also now known as Piezo1, causes anchorage independence and a switch to a reduced integrin-dependent mode of cell migration/invasion, a novel phenotype for this integrin-regulating protein. Normal lung epithelial cells show increased rates of migration by 2D time-lapse microscopy and increased capacity to invade into matrigel, despite having decreased integrin affinity. We confirm greatly depleted Fam38A expression in small cell lung cancer (SCLC) lines where a form of reduced integrin-dependent migration, i.e. amoeboid migration, is a known phenotype. We propose that loss of Fam38A expression may cause increased cell migration and metastasis in lung tumours.
Medical Research Council Centre for Inflammation Research, University of Edinburgh, Edinburgh, Midlothian
Research funded by:
  • Chief Scientist Office


Donaldson K, Poland CA
Inhaled nanoparticles and lung cancer - what we can learn from conventional particle toxicology.
Swiss Med Wkly. 2012; 142:w13547 [PubMed]
Manufactured nanoparticles (MNP) represent a growth area in industry where their interesting and useful properties bestow advantage over conventional particles for many purposes. This review specifically addresses the potential for lung cancer in those who might be exposed to airborne MNP. There is no strong evidence that MNP are carcinogenic and MNP come in a wide spectrum of materials, sizes, shapes and compositions and it is likely that the hazard will vary across different MNP types dependent upon their intrinsic properties. Low toxicity low solubility (LTLS) MNP are unlikely to pose a substantial cancer risk as they are not very biologically active. Nanoparticles with a more reactive surface may undoubtedly generate inflammation more readily and inflammation could be sufficiently intense to lead to secondary carcinogenesis via the oxidants and mitogens produced during inflammation. There is some evidence in vitro that MNP can gain access to the nucleus and the genetic material if specifically designed to do so by surface modification and that nanoparticles such as carbon nanotubes (CNT) can cause genetic aberrations by a primary mechanism additional to the inflammation-mediated one; these potential mechanisms require further study. High aspect ratio nanoparticles (HARN) are MNP that are fibre-shaped and analogously to asbestos might pose a special cancer hazard to the lungs, pleural and peritoneal mesothelium. Recent research suggests that the existing fibre pathogenicity paradigm is adequate for describing the hazard of HARN and that making the HARN of a non-biopersistent material or restricting the length could, via benign-by-design principles, allow safe HARN to be produced.
Centre for Inflammation Research, University of Edinburgh, Edinburgh


Gieling RG, Babur M, Mamnani L, et al.
Antimetastatic effect of sulfamate carbonic anhydrase IX inhibitors in breast carcinoma xenografts.
J Med Chem. 2012; 55(11):5591-600 [PubMed]
A panel of compounds belonging to the underexposed sulfamate class of carbonic anhydrase (CA, EC 4.2.1.1) inhibitors was generated that displayed high specificity at nanomolar levels for the tumor-associated CA IX/XII isoforms. Three of the specific CA IX/XII inhibitors showed a positive response in in vitro assays for tumor cell migration and spreading. One of them, 4-(3'-(3″,5″-dimethylphenyl)ureido)phenyl sulfamate (S4), was taken forward into the orthotopic MDA-MB-231 (breast carcinoma) model in mice. Treatment with a 10 mg/kg maintenance dosage of S4 given daily on a "5 days on, 2 days off" regimen reduced metastatic tumor burden in the lung while not affecting primary tumor growth or mouse condition. CA inhibitors of the sulfamate class specifically targeting the tumor-associated isoforms are potential candidates in antimetastatic therapy.
Hypoxia and Therapeutics Group, School of Pharmacy and Pharmaceutical Sciences, University of Manchester, Manchester
Research funded by:


Wang W, Hodkinson P, McLaren F, et al.
Small cell lung cancer tumour cells induce regulatory T lymphocytes, and patient survival correlates negatively with FOXP3+ cells in tumour infiltrate.
Int J Cancer. 2012; 131(6):E928-37 [PubMed]
Small cell lung cancer (SCLC) kills at least one person every 2 hr in the United Kingdom. Some patients do relatively well but most have rapidly progressive disease. There is no effective treatment and overall 2-year survival is less than 5%. Patients with SCLC have poorly understood local and systemic immune defects and can be immunocompromised. As CD4(+) T lymphocytes coordinate and regulate immunity, a better understanding of interactions between SCLC tumour cells and CD4(+) T cells may lead to effective molecular immunotherapy. We show that some, but not all, SCLC tumour cell lines secrete molecules that induce IL-10 secretion by and de novo differentiation of functional CD4(+)CD25(+)FOXP3(+)CD127(lo)Helios(-) regulatory T (Treg) cells in healthy blood lymphocytes. FOXP3(+) T cells were found in SCLC tumour biopsies, and patients with higher ratios of FOXP3(+) cells in tumour infiltrates have a worse survival rate. The inhibitory effect of SCLC tumour cells was not affected by blocking IL-10 receptor or TGF-β signalling but was partially reversed by blocking IL-15, which is reported to be involved in human Treg cells induction. IL-15 was secreted by SCLC cells that inhibited CD4(+) T-cell proliferation and was present in SCLC biopsy tumour cells. These novel findings demonstrate that SCLC tumour cells can induce CD4(+) T-cell-mediated immunosuppression. This gives a potential mechanism by which SCLC tumour cells may downregulate local and systemic immune responses and contribute to poor patient survival. Our data suggest that IL-15 and Treg cells are potential new therapeutic targets to improve immune response and patient survival in SCLC.
Department of Respiratory Medicine and Allergy, King's College London, London
Research funded by:


Navani N, Brown JM, Nankivell M, et al.
Suitability of endobronchial ultrasound-guided transbronchial needle aspiration specimens for subtyping and genotyping of non-small cell lung cancer: a multicenter study of 774 patients.
Am J Respir Crit Care Med. 2012; 185(12):1316-22 [PubMed] Free Access to Full Article
RATIONALE: The current management of advanced non-small cell lung cancer (NSCLC) requires differentiation between squamous and nonsquamous subtypes as well as epidermal growth factor receptor (EGFR) mutation status. Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) is increasingly used for the diagnosis and staging of lung cancer. However, it is unclear whether cytology specimens obtained with EBUS-TBNA are suitable for the subclassification and genotyping of NSCLC.
OBJECTIVES: To determine whether cytology specimens obtained from EBUS-TBNA in routine practice are suitable for phenotyping and genotyping of NSCLC.
METHODS: Cytological diagnoses from EBUS-TBNA were recorded from 774 patients with known or suspected lung cancer across five centers in the United Kingdom between 2009 and 2011.
MEASUREMENTS AND MAIN RESULTS: The proportion of patients with a final diagnosis by EBUS-TBNA in whom subtype was classified was 77% (95% confidence interval [CI], 73-80). The rate of NSCLC not otherwise specified (NSCLC-NOS) was significantly reduced in patients who underwent immunohistochemistry (adjusted odds ratio, 0.50; 95% CI, 0.28-0.82; P = 0.016). EGFR mutation analysis was possible in 107 (90%) of the 119 patients in whom mutation analysis was requested. The sensitivity, negative predictive value, and diagnostic accuracy of EBUS-TBNA in patients with NSCLC were 88% (95% CI, 86-91), 72% (95% CI, 66-77), and 91% (95% CI, 89-93), respectively.
CONCLUSIONS: This large, multicenter, pragmatic study demonstrates that cytology samples obtained from EBUS-TBNA in routine practice are suitable for subtyping of NSCLC and EGFR mutation analysis and that the use of immunohistochemistry reduces the rate of NSCLC-NOS.
The Centre for Lung Carcinogenesis and Regeneration, University College London, London
Research funded by:


Hoggart C, Brennan P, Tjonneland A, et al.
A risk model for lung cancer incidence.
Cancer Prev Res (Phila). 2012; 5(6):834-46 [PubMed]
Risk models for lung cancer incidence would be useful for prioritizing individuals for screening and participation in clinical trials of chemoprevention. We present a risk model for lung cancer built using prospective cohort data from a general population which predicts individual incidence in a given time period. We build separate risk models for current and former smokers using 169,035 ever smokers from the multicenter European Prospective Investigation into Cancer and Nutrition (EPIC) and considered a model for never smokers. The data set was split into independent training and test sets. Lung cancer incidence was modeled using survival analysis, stratifying by age started smoking, and for former smokers, also smoking duration. Other risk factors considered were smoking intensity, 10 occupational/environmental exposures previously implicated with lung cancer, and single-nucleotide polymorphisms at two loci identified by genome-wide association studies of lung cancer. Individual risk in the test set was measured by the predicted probability of lung cancer incidence in the year preceding last follow-up time, predictive accuracy was measured by the area under the receiver operator characteristic curve (AUC). Using smoking information alone gave good predictive accuracy: the AUC and 95% confidence interval in ever smokers was 0.843 (0.810-0.875), the Bach model applied to the same data gave an AUC of 0.775 (0.737-0.813). Other risk factors had negligible effect on the AUC, including never smokers for whom prediction was poor. Our model is generalizable and straightforward to implement. Its accuracy can be attributed to its modeling of lifetime exposure to smoking.
Department of Epidemiology and Biostatistics, Imperial College London, St Mary's Campus, Paddington, London


Schmidt-Hansen M, Baldwin DR, Hasler E
What is the most effective follow-up model for lung cancer patients? A systematic review.
J Thorac Oncol. 2012; 7(5):821-4 [PubMed]
INTRODUCTION: In the U.K. more than 40,000 people are diagnosed with lung cancer every year and an estimated 65,000 people are living with lung cancer. The most effective follow-up strategy for these patients is undetermined. This article reports a systematic review of studies comparing different follow-up strategies for patients with lung cancer.
METHODS: We searched Medline, Premedline, Embase, Cochrane Library, Cinahl, BNI, Psychinfo, Amed, Web of Science (SCI & SSCI), and Biomed Central and included any original study published in English comparing one type of follow-up strategy to another in patients with lung cancer who had received treatment with curative or palliative intent and/or best supportive care. Studies were included if there were 50 patients or more per follow-up group.
RESULTS: Of the four included studies that compared different follow-up strategies in patients with lung cancer, one was a randomized controlled trial and three were retrospective. The studies all examined different follow-up strategies and tended to be marked by various limitations. No formal data synthesis was therefore possible. However, in one article there was some evidence that regular review was associated with less emergency-department crisis attendances than symptom-generated review.
CONCLUSIONS: The included studies were marked by a number of methodological compromises. On the basis of the reported body of evidence it is therefore not possible to make any firm conclusions about the most effective follow-up strategy but the review has identified a need for urgent research into all aspects of follow-up.
Researcher, National Collaborating Centre for Cancer, Cardiff


Leung EY, Scott HR, McMillan DC
Clinical utility of the pretreatment glasgow prognostic score in patients with advanced inoperable non-small cell lung cancer.
J Thorac Oncol. 2012; 7(4):655-62 [PubMed]
INTRODUCTION: Traditional tumor-based staging systems provide limited information on the best treatment option for individual patients with advanced inoperable non-small cell lung cancer (NSCLC). The Glasgow prognostic score (GPS) reflects the host systemic inflammatory response and is a validated independent prognostic factor in these patients. The aim of this study was to examine the clinical application of the pretreatment GPS in a mature cohort of patients with inoperable NSCLC.
METHODS: The data of 261 patients with inoperable NSCLC were collected prospectively and before treatment. Information on patient demographics, body mass index, performance status (PS), the modified Glasgow prognostic score (mGPS), the prognostic index, and treatment received were included.
RESULTS: The majority of patients were aged 65 years or older (68%), were men (59%), had a body mass index more than 20 (89%), and an Eastern Cooperative Oncology Group performance status (ECOG-PS) 0 or 1 (54%). Most patients had a pretreatment mGPS = 1 (62%) and pretreatment prognostic index = 1 (56%). During the follow-up period, 248 (95%) patients died, 246 from their disease. The median survival was 8 months. On multivariate analysis, age (p = 0.001), ECOG-PS (p < 0.05), mGPS (p < 0.0001), and tumor stage (p < 0.0001) were independently associated with cancer-specific survival. Using 5-year cancer-specific mortality as an end point, the area under the receiver operator curve was 0.735 (95% confidence interval [CI], 0.566-0.903; p = 0.024) for the mGPS, 0.669 (95% CI, 0.489-0.848; p = 0.106) for ECOG-PS, and 0.622 (95% CI, 0.437-0.807; p = 0.240) for tumor, node, metastasis stage. Patients with an increased mGPS were more likely to have a poorer ECOG-PS (p < 0.05), an increased white cell count (p < 0.05), and received palliative treatment (p < 0.05).
CONCLUSION: The pretreatment mGPS is a useful and important predictor of cancer-specific survival in patients with inoperable NSCLC. Basing clinical assessment on the mGPS has implications for the routine monitoring and treatment of the patients.
University Department of Surgery, Faculty of Medicine-University of Glasgow, Royal Infirmary, Glasgow


Dibben SM, Holt RJ, Davison TS, et al.
Implications for powering biomarker discovery studies.
J Mol Diagn. 2012 Mar-Apr; 14(2):130-9 [PubMed]
This study examined variations in gene expression between FFPE blocks within tumors of individual patients. Microarray data were used to measure tumor heterogeneity within and between patients and disease states. Data were used to determine the number of samples needed to power biomarker discovery studies. Bias and variation in gene expression were assessed at the intrapatient and interpatient levels and between adenocarcinoma and squamous samples. A mixed-model analysis of variance was fitted to gene expression data and model signatures to assess the statistical significance of observed variations within and between samples and disease states. Sample size analysis, adjusted for sample heterogeneity, was used to determine the number of samples required to support biomarker discovery studies. Variation in gene expression was observed between blocks taken from a single patient. However, this variation was considerably less than differences between histological characteristics. This degree of block-to-block variation still permits biomarker discovery using either macrodissected tumors or whole FFPE sections, provided that intratumor heterogeneity is taken into account. Failure to consider intratumor heterogeneity may result in underpowered biomarker studies that may result in either the generation of longer gene signatures or the inability to identify a viable biomarker. Moreover, the results of this study indicate that a single biopsy sample is suitable for applying a biomarker in non-small-cell lung cancer.
Almac Diagnostics, Craigavon


Freidin MB, Bhudia N, Lim E, et al.
Impact of collection and storage of lung tumor tissue on whole genome expression profiling.
J Mol Diagn. 2012 Mar-Apr; 14(2):140-8 [PubMed] Free Access to Full Article
Gene expression profiling could assist in revealing biomarkers of lung cancer prognosis and progression. The handling of biological samples may strongly influence global gene expression, a fact that has not been addressed in many studies. We sought to investigate the changes in gene expression that may occur as a result of sample processing time and conditions. Using Illumina Human WG-6 arrays, we quantified gene expression in lung carcinoma samples from six patients obtained at chest opening before and immediately after lung resection with storage in RNAlater [T1a((CO)) and T1b((LR))], after receipt of the sample for histopathology, placed in RNAlater [T2a((HP))]; snap frozen [T2b((HP.SF))]; or snap frozen and stored for 1 week [T2c((HP.SFA))], as well as formalin-fixed, paraffin-embedded (FFPE) block samples. Sampling immediately after resection closely represented the tissue obtained in situ, with only 1% of genes differing more than twofold [T1a((CO)) versus T1b((LR))]. Delaying tissue harvest for an average of 30 minutes from the operating theater had a significant impact on gene expression, with approximately 25% of genes differing between T1a((CO)) and T2a((HP)). Many genes previously identified as lung cancer biomarkers were altered during this period. Examination of FFPE specimens showed minimal correlation with fresh samples. This study shows that tissue collection immediately after lung resection with conservation in RNAlater is an optimal strategy for gene expression profiling.
National Heart and Lung Institute, Imperial College London, London


Krebs MG, Hou JM, Sloane R, et al.
Analysis of circulating tumor cells in patients with non-small cell lung cancer using epithelial marker-dependent and -independent approaches.
J Thorac Oncol. 2012; 7(2):306-15 [PubMed]
INTRODUCTION: Epithelial circulating tumor cells (CTCs) are detectable in patients with non-small cell lung cancer (NSCLC). However, epithelial to mesenchymal transition, a widely reported prerequisite for metastasis, may lead to an underestimation of CTC number. We compared directly an epithelial marker-dependent (CellSearch) and a marker-independent (isolation by size of epithelial tumor cells [ISET]) technology platform for the ability to identify CTCs. Molecular characteristics of CTCs were also explored.
METHODS: Paired peripheral blood samples were collected from 40 chemonäive, stages IIIA to IV NSCLC patients. CTCs were enumerated by Epithelial Cell Adhesion Molecule-based immunomagnetic capture (CellSearch, Veridex) and by filtration (ISET, RareCell Diagnostics). CTCs isolated by filtration were assessed by immunohistochemistry for epithelial marker expression (cytokeratins, Epithelial Cell Adhesion Molecule, epidermal growth factor receptor) and for proliferation status (Ki67).
RESULTS: CTCs were detected using ISET in 32 of 40 (80%) patients compared with 9 of 40 (23%) patients using CellSearch. A subpopulation of CTCs isolated by ISET did not express epithelial markers. Circulating tumor microemboli (CTM, clusters of ≥ 3 CTCs) were observed in 43% patients using ISET but were undetectable by CellSearch. Up to 62% of single CTCs were positive for the proliferation marker Ki67, whereas cells within CTM were nonproliferative.
CONCLUSIONS: Both technology platforms detected NSCLC CTCs. ISET detected higher numbers of CTCs including epithelial marker negative tumor cells. ISET also isolated CTM and permitted molecular characterization. Combined with our previous CellSearch data confirming CTC number as an independent prognostic biomarker for NSCLC, we propose that this complementary dual technology approach to CTC analysis allows more complete exploration of CTCs in patients with NSCLC.
Clinical and Experimental Pharmacology Group, Paterson Institute for Cancer Research, University of Manchester
Research funded by:


McQueen AS, Scott J
CT staging of colorectal cancer: what do you find in the chest?
Clin Radiol. 2012; 67(4):352-8 [PubMed]
AIM: To clarify the chest computed tomography (CT) findings in patients with a new diagnosis of colorectal adenocarcinoma.
MATERIALS AND METHODS: Patients diagnosed with colorectal cancer (CRC) over a 3-year period were retrospectively studied. All CT examinations were performed within a single NHS Trust using the same CT system and protocol. Two primary outcomes were assessed: the presence of pulmonary metastases and the identification of a significant, unexpected chest abnormality.
RESULTS: Five hundred and fourteen out of 568 (90.5%) CRC patients underwent complete CT staging. Thirty-one patients (6%) had lung metastases, of which four (0.8%) were isolated. Three hundred and fifty-three (68.7%) had no evidence of pulmonary metastases, but 130 (25.3%) had indeterminate lung nodules (ILNs). The ILNs of 12 patients were subsequently confirmed as metastases on follow-up. A major non-metastatic finding (pulmonary embolism or synchronous primary malignancy) was found in 15/514 patients (3%).
CONCLUSIONS: Thoracic CT altered the initial TNM stage in fewer than 1% of CRC patients, but the detection of significant incidental chest disease and the establishment of an imaging baseline are useful outcomes of this imaging strategy. One-quarter of all staging examinations demonstrated ILNs.
Department of Radiology, Freeman Hospital, Newcastle upon Tyne


Jamal-Hanjani M, Spicer J
Epidermal growth factor receptor tyrosine kinase inhibitors in the treatment of epidermal growth factor receptor-mutant non-small cell lung cancer metastatic to the brain.
Clin Cancer Res. 2012; 18(4):938-44 [PubMed]
Brain metastases are a common and devastating consequence of disease progression in patients with non-small cell lung cancer (NSCLC). The epidermal growth factor receptor (EGFR) inhibitors erlotinib and gefitinib have shown efficacy in patients with NSCLC and brain metastases. The cerebrospinal fluid (CSF) exposure to these drugs is a small fraction of the plasma levels achieved with standard doses, but disruption of the blood-brain barrier in the presence of central nervous system metastases is likely to lead to locally increased drug concentration, and dose escalation to boost CSF exposure has documented clinical efficacy. The use of gefitinib and erlotinib in this setting is reviewed here, including evidence from case reports, case series, and single-arm phase II trials. High response rates in the brain are seen in patients with EGFR mutation, or in populations in which this genotype is expected. By contrast, activity in the context of documented wild-type EGFR in disease metastatic to the brain is not common. These drugs may potentiate the effectiveness of radiotherapy to the brain, and their use may also delay development of disease within the brain.
Guy's Hospital, London


McGrath EE, Warriner D, Anderson P
The insertion of self expanding metal stents with flexible bronchoscopy under sedation for malignant tracheobronchial stenosis: a single-center retrospective analysis.
Arch Bronconeumol. 2012; 48(2):43-8 [PubMed]
OBJECTIVE: To describe a 10-year experience of inserting Ultraflex™ self-expanding metal stents (SEMS) under sedation using flexible bronchoscopy for the treatment of malignant tracheobronchial stenosis in a tertiary referral centre.
METHODS: Medical notes were retrospectively reviewed for all patients who underwent SEMS insertion between 1999 and 2009.
RESULTS: A data analysis of 68 patients who had Ultraflex™ SEMS inserted under sedation was completed. Thirty three males and 35 females with a mean age of 67.9 years (range 35-94) presented with features including dyspnea/respiratory distress (39 patients), stridor (16 patients) and hemoptysis/dyspnea (13 patients). Etiology of stenosis included lung cancer (46 patients) esophageal cancer (14 patients) and other malignancies (8 patients). Mean dose of midazolam administered was 5mg (range 0-10mg). The trachea was the most common site of stent insertion followed by the right and left main bronchus, respectively. Adjuvant laser therapy was applied at some stage in 31% of all cases, and chemotherapy and/or radiotherapy was administered to at least 64% of patients with malignant disease. Hemoptysis and stent migration were the most frequent complications (5 and 4 patients, respectively). The mean survival time of stented non-small cell lung cancer (NSCLC) patients was 214 days (range 5-1233) and that of esophageal malignancy was 70 days (range 12-249). Mean pack-year history of individuals with lung cancer requiring stent insertion was 37 (range 2-100).
CONCLUSION: Ultraflex stents offer a safe and effective therapy for patients who are inoperable or unresectable that otherwise would have no alternative therapy. It has an immediate beneficial effect upon patients, not only through symptom relief but, in some, through prolongation of life. Survival data is no worse than other studies using different varieties of stents and insertion techniques indicating its longer-term efficacy. Moreover, this report highlights the feasibility of performing this procedure successfully in a respiratory unit, without the need for general anesthesia.
Department of Respiratory Medicine, Northern General Hospital, Sheffield


O'Brien ME, Myerson JS, Coward JI, et al.
A phase II study of ¹⁸F-fluorodeoxyglucose PET-CT in non-small cell lung cancer patients receiving erlotinib (Tarceva); objective and symptomatic responses at 6 and 12 weeks.
Eur J Cancer. 2012; 48(1):68-74 [PubMed]
BACKGROUND: The aim of this study was to assess if (18)F-fluorodeoxyglucose (FDG) Positron Emission Tomography (PET)-CT scanning could minimise the time non-responding patients were exposed to erlotinib (Tarceva).
METHODS: Patients were selected for clinical factors that would predict response to erlotinib. A FDG PET-CT and diagnostic contrast-enhanced (traditional) CT scan were carried out at baseline, and then a FDG PET-CT at 6 weeks and a traditional CT at 12 weeks were repeated. The primary end-point was rate of early progression in patients after 6 weeks, of which a minimum 12 out of 35 were required to make the study worthwhile. The responses at 6 (PET-CT) and 12 weeks (traditional CT) were compared and correlated with symptomatic response at both these time points.
RESULTS: Forty seven patients were recruited with 38 and 33 patients assessable by FDG PET-CT at 6 weeks and traditional CT at 12weeks, respectively. There was good correlation between Partial response (PR) at both time points and all 10 patients who had a PR at 12 weeks had a PR at 6 weeks. Of the 13 patients with progressive disease (PD) at 12 weeks, seven had PD at 6 weeks and could have had their treatment stopped early. No evaluable patient with stable disease (SD) (8/38) or PD (9/38) on FDG PET-CT at 6 weeks went on to have a later response. Symptomatic response at 6 or 12 weeks did not correlate well with objective response on scanning at either time point.
CONCLUSIONS: The primary end-point of this study was met as >12 (15/38) patients could have stopped treatment early on the basis of the FDG PET-CT scan result. A FDG PET-CT evaluable response of SD or PD at 6 weeks does predict future lack of response. No correlation was found between response and symptomatic response at either 6 or 12 weeks.
Royal Marsden Hospital, Downs Road, Sutton, Surrey SM2 5PT


Hubner RA, Riley RD, Billingham LJ, Popat S
Excision repair cross-complementation group 1 (ERCC1) status and lung cancer outcomes: a meta-analysis of published studies and recommendations.
PLoS One. 2011; 6(10):e25164 [PubMed] Free Access to Full Article
PURPOSE: Despite discrepant results on clinical utility, several trials are already prospectively randomizing non-small cell lung cancer (NSCLC) patients by ERCC1 status. We aimed to characterize the prognostic and predictive effect of ERCC1 by systematic review and meta-analysis.
METHODS: Eligible studies assessed survival and/or chemotherapy response in NSCLC or SCLC by ERCC1 status. Effect measures of interest were hazard ratio (HR) for survival or relative risk (RR) for chemotherapy response. Random-effects meta-analyses were used to account for between-study heterogeneity, with unadjusted/adjusted effect estimates considered separately.
RESULTS: 23 eligible studies provided survival results in 2,726 patients. Substantial heterogeneity was observed in all meta-analyses (I(2) always >30%), partly due to variability in thresholds defining 'low' and 'high' ERCC1. Meta-analysis of unadjusted estimates showed high ERCC1 was associated with significantly worse overall survival in platinum-treated NSCLC (average unadjusted HR = 1.61, 95%CI:1.23-2.1, p = 0.014), but not in NSCLC untreated with chemotherapy (average unadjusted HR = 0.82, 95%CI:0.51-1.31). Meta-analysis of adjusted estimates was limited by variable choice of adjustment factors and potential publication bias (Egger's p<0.0001). There was evidence that high ERCC1 was associated with reduced response to platinum (average RR = 0.80; 95%CI:0.64-0.99). SCLC data were inadequate to draw firm conclusions.
CONCLUSIONS: Current evidence suggests high ERCC1 may adversely influence survival and response in platinum-treated NSCLC patients, but not in non-platinum treated, although definitive evidence of a predictive influence is lacking. International consensus is urgently required to provide consistent, validated ERCC1 assessment methodology. ERCC1 assessment for treatment selection should currently be restricted to, and evaluated within, clinical trials.
Department of Medical Oncology, Christie NHS Foundation Trust, Manchester
Research funded by:


Newton RC, Kemp SV, Yang GZ, et al.
Imaging parenchymal lung diseases with confocal endomicroscopy.
Respir Med. 2012; 106(1):127-37 [PubMed]
BACKGROUND: "Optical biopsy" using bronchoscopic probe-based confocal endomicrosocopy (pCLE) provides real time images of the autofluorescent elastin scaffold of the healthy acinus.
OBJECTIVES: To establish how different parenchymal lung diseases (PLDs) alter the pCLE image, if intravenous fluorescein provides additional diagnostic information, and to assess pCLE's safety for investigating PLDs (UK REC: 09/H0708/18).
METHODS: 116 bronchopulmonary segments were examined in 38 patients and 4 healthy non-smoker volunteers. pCLE images were correlated with consensus multidisciplinary diagnosis from HRCT, bronchoalveolar lavage, and transbronchial/CT guided biopsies.
RESULTS: Severe emphysema is evident on pCLE imaging, with increased spacing between septal walls, sudden loss of fluorescence from bullae and a subsequent reticular pleural image. Other PLDs demonstrated marked loss of lobular autofluorescence and distinctiveness. In all diseases imaged, differentiation between septal wall and microvessel elastin is more difficult in diseased versus healthy acini. Smokers displayed a hyperfluorescent 15-30 micron cellular alveolar infiltrate - alveolar macrophages on in vitro BAL analysis. Varied intravenous fluorescein doses only create a hyperfluorescent foreground with bubbles. pCLE can cause pleuritic discomfort but there were no pneumothoraces. 3 patients had transient bleeding, and in vivo tearing of septal walls and microvessels abutting the probe was observed.
CONCLUSIONS: Marked emphysema is demonstrable from loss of elastic walls. The detail of high-resolution pCLE images is attenuated in other PLDs without further clarity from intravenous fluorescein. Nevertheless, pCLE is safe for PLD investigation. These findings form a basis for future work to harness pCLE's potential utility as part of a multiassessment modality for PLD diagnosis.
Hamlyn Institute for Robotic Surgery, Imperial College, London SW7 2AZ


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