Publications
664 results found
Thway K, Jordan S, Fisher C, et al., 2015, Updates in the approach to intrathoracic sarcomas, HISTOPATHOLOGY, Vol: 67, Pages: 755-770, ISSN: 0309-0167
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- Citations: 15
Raghu G, Wells A, Nicholson AG, et al., 2015, CONSISTENT EFFECT OF NINTEDANIB ON DECLINE IN FVC IN PATIENTS ACROSS SUBGROUPS BASED ON HRCT DIAGNOSTIC CRITERIA: RESULTS FROM THE INPULSIS (R) TRIALS IN IPF, Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A60-A61, ISSN: 0040-6376
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- Citations: 1
Freidin MB, Freydina DV, Leung M, et al., 2015, Circulating Tumor DNA Outperforms Circulating Tumor Cells for KRAS Mutation Detection in Thoracic Malignancies, CLINICAL CHEMISTRY, Vol: 61, Pages: 1299-1304, ISSN: 0009-9147
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- Citations: 83
Walsh SLF, Wells AU, Sverzellati N, et al., 2015, Relationship between fibroblastic foci profusion and high resolution CT morphology in fibrotic lung disease, BMC Medicine, Vol: 13, ISSN: 1741-7015
BackgroundFibroblastic foci profusion on histopathology and severity of traction bronchiectasis on highresolution computed tomography (HRCT) have been shown to be predictors of mortality in patients with idiopathic pulmonary fibrosis (IPF). The aim of this study was to investigate the relationship between fibroblastic foci (FF) profusion and HRCT patterns in patients with a histopathologic diagnosis of usual interstitial pneumonia (UIP), fibrotic non-specific interstitial pneumonia (NSIP) and chronic hypersensitivity pneumonitis (CHP).MethodsThe HRCT scans of 162 patients with a histopathologic diagnosis of UIP or fibrotic NSIP (n = 162) were scored on extent of groundglass opacification, reticulation, honeycombing, emphysema and severity of traction bronchiectasis. For each patient, a fibroblastic foci profusion score based on histopathologic appearances was assigned. Relationships between extent of fibroblastic foci and individual HRCT patterns were investigated using univariate correlation analysis and multivariate linear regression.ResultsIncreasing extent of reticulation (P < 0.0001) and increasing severity of traction bronchiectasis (P < 0.0001) were independently associated with increasing FF score within the entire cohort. Within individual multidisciplinary team diagnosis subgroups, the only significant independent association with FF score was severity of traction bronchiectasis in patients with idiopathic pulmonary fibrosis (IPF)/UIP (n = 66, r2 = 0.19, P < 0.0001) and patients with chronic hypersensitivity pneumonitis (CHP) (n = 49, r2 = 0.45, P < 0.0001). Furthermore, FF score had the strongest association with severity of traction bronchiectasis in patients with IPF (r2 = 0.34, P < 0.0001) and CHP (r2 = 0.35, P < 0.0001). There was no correlation between F
Alton EWFW, Armstrong DK, Ashby D, 2015, Repeated nebulisation of non-viral CFTR gene therapy in patients with cystic fibrosis: a randomised, double-blind, placebo-controlled, phase 2b trial, The Lancet Respiratory Medicine, Vol: 3, Pages: 684-691, ISSN: 2213-2600
BackgroundLung delivery of plasmid DNA encoding the CFTR gene complexed with a cationic liposome is a potential treatment option for patients with cystic fibrosis. We aimed to assess the efficacy of non-viral CFTR gene therapy in patients with cystic fibrosis.MethodsWe did this randomised, double-blind, placebo-controlled, phase 2b trial in two cystic fibrosis centres with patients recruited from 18 sites in the UK. Patients (aged ≥12 years) with a forced expiratory volume in 1 s (FEV1) of 50–90% predicted and any combination of CFTR mutations, were randomly assigned, via a computer-based randomisation system, to receive 5 mL of either nebulised pGM169/GL67A gene–liposome complex or 0·9% saline (placebo) every 28 days (plus or minus 5 days) for 1 year. Randomisation was stratified by % predicted FEV1 (<70 vs ≥70%), age (<18 vs ≥18 years), inclusion in the mechanistic substudy, and dosing site (London or Edinburgh). Participants and investigators were masked to treatment allocation. The primary endpoint was the relative change in % predicted FEV1. The primary analysis was per protocol. This trial is registered with ClinicalTrials.gov, number NCT01621867.FindingsBetween June 12, 2012, and June 24, 2013, we randomly assigned 140 patients to receive placebo (n=62) or pGM169/GL67A (n=78), of whom 116 (83%) patients comprised the per-protocol population. We noted a significant, albeit modest, treatment effect in the pGM169/GL67A group versus placebo at 12 months' follow-up (3·7%, 95% CI 0·1–7·3; p=0·046). This outcome was associated with a stabilisation of lung function in the pGM169/GL67A group compared with a decline in the placebo group. We recorded no significant difference in treatment-attributable adverse events between groups.InterpretationMonthly application of the pGM169/GL67A gene therapy formulation was associated with a significant, albeit modest, benefit in FEV1 compared with placebo at 1 yea
Lu SK, Anbunathan H, Popat S, et al., 2015, Molecular Landscape of Malignant Mesothelioma from Whole Exome Sequencing, Publisher: ELSEVIER SCIENCE INC, Pages: S253-S253, ISSN: 1556-0864
Nicholson AG, 2015, Approach to the Diagnosis of Rare and Unusual Lung Tumours, 8th Joint Meeting of the British-Division of the International-Academy-of-Pathology and the Pathological-Society-of-Great-Britain-and-Ireland, Publisher: WILEY-BLACKWELL, Pages: S5-S5, ISSN: 0022-3417
Viola P, Villegas IA, Robertus JL, et al., 2015, Mediastinal Biopsies: Small Biopsies for Challenging Cases - A Single Centre Review, 8th Joint Meeting of the British-Division of the International-Academy-of-Pathology and the Pathological-Society-of-Great-Britain-and-Ireland, Publisher: WILEY-BLACKWELL, Pages: S35-S35, ISSN: 0022-3417
De Sa VK, Prieto T, Olivieri ER, et al., 2015, HAases and HAS in Lung/Bronchial Pre-Neoplastic Lesions: Impact on Prognosis, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S347-S347, ISSN: 1556-0864
Cufari ME, Proli C, Phull M, et al., 2015, Increasing Incidence of Non-Smoking Lung Cancer: Presentation of Patients with Early Disease to a Tertiary Institution in the UK, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S793-S794, ISSN: 1556-0864
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- Citations: 1
Cufari ME, Proli C, Phull M, et al., 2015, Increasing Incidence of Non-Smoking Lung Cancer: Presentation of Patients with Early Disease to a Tertiary Institution in the UK, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S220-S220, ISSN: 1556-0864
Travis WD, Brambilla E, Nicholson AG, et al., 2015, The 2015 World Health Organization Classification of Lung Tumors <i>Impact of Genetic</i>, <i>Clinical and Radiologic Advances Since the 2004 Classification</i>, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: 1243-1260, ISSN: 1556-0864
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- Citations: 2710
Travis WD, Brambilla E, Burke AP, et al., 2015, Introduction to The 2015 World Health Organization Classification of Tumors of the Lung, Pleura, Thymus, and Heart, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: 1240-1242, ISSN: 1556-0864
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- Citations: 547
Luciano G, Viola P, Al Sahaf M, et al., 2015, Is It Possible to Distinguish between Second Primary vs. Metastasis in Resectable Synchronous Nodules with the Same Histotype of Lung Cancer?, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S261-S261, ISSN: 1556-0864
Alton EWFW, Armstrong DK, Ashby D, 2015, Repeated nebulisation of non-viral CFTR gene therapy in patients with cystic fi brosis: a randomised, double-blind, placebo-controlled, phase 2b trial (vol 3, pg 684, 2015), LANCET RESPIRATORY MEDICINE, Vol: 3, Pages: E33-E33, ISSN: 2213-2600
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- Citations: 2
Cufari ME, Proli C, Phull M, et al., 2015, Is the Development of Primary Lung Adenocarcinoma Simply Due To 'Bad Luck'?, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S737-S737, ISSN: 1556-0864
Viola P, Maurya M, Croud J, et al., 2015, A Validation Study for the Use of ROS-1 Immunohistochemistry in Screening for ROS-1 Translocations in Lung Cancer, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S694-S694, ISSN: 1556-0864
Viola P, Devaraj A, Lim E, et al., 2015, Pathology-Imaging Agreement in Distinguishing Separate Primary Tumours and Intrapulmonary Metastasis in Staging of Multiple Lung Cancers, Publisher: ELSEVIER SCIENCE INC, Pages: S261-S262, ISSN: 1556-0864
Gennatas S, Anbunathan H, Montero A, et al., 2015, Validation of a Specific Missense GTF2I Mutation in More Indolent Thymic Epithelial Tumours, Publisher: ELSEVIER SCIENCE INC, Pages: S403-S403, ISSN: 1556-0864
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- Citations: 1
Viola P, Vroobel K, Jordan S, et al., 2015, Clinicopathological Features of Primary Intra-Thoracic Follicular Dendritic Cell Sarcomas, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: S750-S750, ISSN: 1556-0864
de Sa VK, Rocha TP, Moreira AL, et al., 2015, Hyaluronidases and hyaluronan synthases expression is inversely correlated with malignancy in lung/bronchial pre-neoplastic and neoplastic lesions, affecting prognosis, Brazilian Journal of Medical and Biological Research, Vol: 48, Pages: 1039-1047, ISSN: 1678-4510
We collected a series of 136 lung/bronchial and 56 matched lung parenchyma tissue samples from patients who underwent lung/bronchial biopsies and presented invasive carcinoma after lung surgery. The lung/bronchial samples included basal cell hyperplasia, squamous metaplasia, moderate dysplasia, adenomatous hyperplasia, severe dysplasia, squamous cell carcinoma and adenocarcinoma. Matched lung parenchyma tissue samples included 25 squamous cell carcinomas and 31 adenocarcinomas. Immunohistochemistry was performed to analyze for the distribution of hyaluronidase (Hyal)-1 and −3, and hyaluronan synthases (HAS)-1, −2, and −3. Hyal-1 showed significantly higher expression in basal cell hyperplasia than in moderate dysplasia (P=0.01), atypical adenomatous hyperplasia (P=0.0001), or severe dysplasia (P=0.03). Lower expression of Hyal-3 was found in atypical adenomatous hyperplasia than in basal cell hyperplasia (P=0.01) or moderate dysplasia (P=0.02). HAS-2 was significantly higher in severe dysplasia (P=0.002) and in squamous metaplasia (P=0.04) compared with basal cell hyperplasia. HAS-3 was significantly expressed in basal cell hyperplasia compared with atypical adenomatous hyperplasia (P=0.05) and severe dysplasia (P=0.02). Lower expression of HAS-3 was found in severe dysplasia compared with squamous metaplasia (P=0.01) and moderate dysplasia (P=0.01). Epithelial Hyal-1 and −3 and HAS-1, −2, and −3 expressions were significantly higher in pre-neoplastic lesions than in neoplastic lesions. Comparative Cox multivariate analysis controlled by N stage and histologic tumor type showed that patients with high HAS-3 expression in pre-neoplastic cells obtained by lung/bronchial biopsy presented a significantly higher risk of death (HR=1.19; P=0.04). We concluded that localization of Hyal and HAS in lung/bronchial pre-neoplastic and neoplastic lesions was inversely related to malignancy, which implied that visualizing these factors could be
Freidin MB, Freydina DV, Fernandez AM, et al., 2015, Application of RNA in situ hybridisation for identification of circulating tumour cells, JOURNAL OF CLINICAL PATHOLOGY, Vol: 68, Pages: 669-U89, ISSN: 0021-9746
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- Citations: 2
Cane P, Linklater KM, Nicholson AG, et al., 2015, Morphological and genetic classification of lung cancer: variation in practice and implications for tailored treatment, HISTOPATHOLOGY, Vol: 67, Pages: 216-224, ISSN: 0309-0167
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- Citations: 6
Bush A, Cunningham S, de Blic J, et al., 2015, European protocols for the diagnosis and initial treatment of interstitial lung disease in children, Thorax, Vol: 70, Pages: 1078-1084, ISSN: 1468-3296
Interstitial lung disease in children (chILD) is rare, and most centres will only see a few cases/year. There are numerous possible underlying diagnoses, with specific and non-specific treatment possibilities. The chILD-EU collaboration has brought together centres from across Europe to advance understanding of these considerations, and as part of this process, has created standard operating procedures and protocols for the investigation of chILD. Where established consensus documents exist already, for example, for the performance of bronchoalveolar lavage and processing of lung biopsies, these have been adopted. This manuscript reports our proposals for a staged investigation of chILD, starting from when the condition is suspected to defining the diagnosis, using pathways dependent on the clinical condition and the degree of illness of the child. These include the performance of genetic testing, echocardiography, high-resolution CT, bronchoscopy when appropriate and the definitive investigation of lung biopsy, in order to establish a precise diagnosis. Since no randomised controlled trials of treatment have ever been performed, we also report a Delphi consensus process to try to harmonise treatment protocols such as the use of intravenous and oral corticosteroids, and add-on therapies such as hydroxychloroquine and azithromycin. The aim is not to dictate to clinicians when a therapeutic trial should be performed, but to offer the possibility to collaborators of having a unified approach when a decision to treat has been made.
Kerr KM, Tsao M-S, Nicholson AG, et al., 2015, Programmed Death-Ligand 1 Immunohistochemistry in Lung Cancer <i>In what state is this art</i>?, JOURNAL OF THORACIC ONCOLOGY, Vol: 10, Pages: 985-989, ISSN: 1556-0864
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- Citations: 221
Sheard S, Nicholson AG, Edmunds L, et al., 2015, Pulmonary light-chain deposition disease: CT and pathology findings in nine patients, CLINICAL RADIOLOGY, Vol: 70, Pages: 515-522, ISSN: 0009-9260
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- Citations: 31
Gopinath PP, Ali A, Van Tornout F, et al., 2015, Chronic silicone embolism syndrome due to PIP breast implant leakage - a new entity?, HISTOPATHOLOGY, Vol: 66, Pages: 904-906, ISSN: 0309-0167
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- Citations: 7
Green AC, Marx A, Stroebel P, et al., 2015, Type A and AB thymomas: histological features associated with increased stage, HISTOPATHOLOGY, Vol: 66, Pages: 884-891, ISSN: 0309-0167
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- Citations: 18
Yancheva SG, Velani A, Rice A, et al., 2015, Bombesin staining in neuroendocrine cell hyperplasia of infancy (NEHI) and other childhood interstitial lung diseases (chILD), Histopathology, Vol: 67, Pages: 501-508, ISSN: 1365-2559
Aims:We have analysed levels of bombesin-positive neuroendocrine cells (NECs) in neuroendocrine cell hyperplasia of infancy (NEHI) and other childhood interstitial lung diseases (chILDs) in order to validate proposed histological criteria for NEHI and investigate its aetiology.Methods and results:The extent of bombesin-positive cells within airway epithelium was analysed in lung biopsies from seven patients diagnosed with NEHI, including two classified previously as non-diagnostic, and other chILDs (n = 64) with age ranges of 1 month–18 years. NECs were counted and calculated as a percentage of airways containing NECs, average percentage of NECs per airway, percentage of airways with >10% NECs and number of neuroendocrine bodies (NEBs). Correlation with age and gender was also undertaken. Patients with NEHI had the highest average percentage of bombesin-positive NECs per airway compared to other chILDs. However, NEH was also seen in many other chILDs, and appears to be most prominent in disorders associated with lung immaturity such as histological patterns associated with surfactant protein-related disorders and pulmonary interstitial glycogenosis.Conclusions:NEH may, to a degree, be a marker of airway immaturity rather than the direct cause of NEHI. This possibility is supported by the fact that the number of bombesin-positive NECs decreased with age in this cohort, independent of disease type. The average percentage of bombesin-positive NECs per airway appears to be the best histological criterion for assessing the extent of NECs in the context of NEHI.
Lim E, Nicholson AG, Padley S, et al., 2015, Never smoker with ground glass opacities on CT, LANCET RESPIRATORY MEDICINE, Vol: 3, Pages: 328-328, ISSN: 2213-2600
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- Citations: 1
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