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Gaskin, Janet. "Radon and Lung Cancer." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39003.
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Background: Lung cancer was the fifth leading cause of mortality globally in 2010, and the leading cause of cancer mortality in Canada, representing 26% of all cancer deaths for both men and women in 2017. Radon is a very modifiable environmental exposure that is the second most important cause of lung cancer.
Objectives: The objectives of this thesis are to quantify the lung cancer burden associated with residential radon and to identify the most cost effective mitigation options to reduce residential radon in Canada.
Methods: The global burden of lung cancer mortality attributable to radon in 2012 was estimated from the 66 countries for which a representative national radon survey was available, using several different models for excess relative risk (ERR) of lung cancer from radon studies. Cost-utility analyses are conducted for 20 practical radon interventions scenarios to reduce residential radon exposures in new and existing housing in Canada, each province/territory and 17 census metropolitan areas. A societal perspective and a lifetime horizon are adopted. A Markov cohort model and a discrete event simulation are used to model residents by household, based on a period-life table analysis, at a discount rate of 1.5%.
Results: The estimates of the global median PAR were consistent, ranging from 16.5% to 13.6% for the three ERR models based on miners, and the mean estimates of PAR for Canada ranged from 16.3% to 14.6%. It is very cost effective to install radon preventive measures in new construction compared to no radon control in all regions across Canada. At a radon mitigation threshold of 100 Bq/m3, the sequential analysis recommends the combination of the activation of preventive measures in new housing with the mitigation of existing housing at current testing and mitigation rates for cost effectiveness thresholds between 51,889 and 92,072 $/QALY for Canada, between 27,558 and 85,965 $/QALY for Manitoba, and between 15,801 and 36,547 $/QALY for the Yukon. The discounted ICER for screening and mitigation of existing housing at current rates relative to no radon control measures is 62,451 (66,421) $/QALY using a Markov cohort model (discrete event simulation model) for mitigation of housing above a threshold of 200 Bq/m3, and is 58,866 (59,556) $/QALY using a Markov cohort model (discrete event simulation model) for mitigation of housing above a threshold of 100 Bq/m3.
Conclusions: Cost effective residential radon interventions should be implemented across Canada to reduce exposures to this very modifiable cause of lung cancer and to help reduce the increasing lung cancer burden in an ageing Canadian population.
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Thomas, Akesh, zainab Fatima, and Girendra resident Hoskere. "Lung Cancer in Tennessee." Digital Commons @ East Tennessee State University, 2021. https://dc.etsu.edu/asrf/2021/presentations/69.
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Introduction
Lung cancer is the most common cause of cancer-related death in the United States (US). Tobacco smoking is a well-recognized cause of lung cancer. About 2% of the United States (US) population lives in Tennessee (TN). Nearly 21 % of TN adults are current smokers as per 2019 data, compared to 14% across the US. The percentage of smokers has historically been high in TN and its surroundings. This can be attributed to the area's socio-economic and cultural characteristics, along with large areas of tobacco farming in the region. This increases the risk of lung cancer in the TN population. Surveillance Epidemiology and End Results Program (SEER) is a collection of cancer registries across the US, covering about 35% of the US population (TN cancer registry is not a part of SEER). Our study compares lung cancer incidence and characteristics in the TN cancer registry with the SEER 18 registry.
Materials and Methods
Data were collected from the TN cancer registry and SEER separately for lung and bronchial cancer. Data was analyzed for different histological subtypes, age groups, gender, stage at diagnosis, and rural/urban residence. Stata and Microsoft Excel were used in data analysis. A Chi-square test was used to calculate the statistical significance.
Results
From 2008 to 2017, 58644 cases of lung cancer were reported in the Tennessee cancer registry. During the same period, 519112 cases were reported in the SEER registry. The most frequent histological subtype of lung cancer in TN and SEER was adenocarcinoma (frequency of 17,503 Vs. 182346), followed by squamous cell carcinoma and small cell carcinoma. Most cancers in TN and SEER were diagnosed at stage of distant metastasis (46% vs. 52% ), followed by regional metastasis, localized, and in situ (Image1). The frequency of lung cancer diagnosis was high among those older than 65 in TN and SEER (64% vs. 69%). Males had a higher incidence of lung cancer in both registries. Most lung cancers were reported in the urban area in both registries. Chronic obstructive pulmonary disease was the most commonly reported secondary diagnosis (3,099), followed by pleural effusion in the TN database; the comparable data were not available in SEER. Relative survival at 12 months and five years for lung cancer in TN were 46.6 % and 19.5 % (Vs. 46.4% and 19.9% in SEER)
Discussion and Conclusion
If both registries were perfect, then lung and bronchial cancer incidence will be 9241 and 6048 per million in ten years in TN and SEER, respectively. But after careful analysis, we conclude that such analysis will be erroneous. The proportion of different histological types, stage at diagnosis, age groups, and gender were in the same order in both groups. Although chi-square test values are significant for all the variables, we infer no conclusion considering the data's inherent bias. Further in-depth analysis of the data is required.
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Ruiz, Rossana, Marco Galvez-Nino, Ebert Poquioma, Abel Limache-García, Edgar Amorin, Mivael Olivera, Natalia Valdiviezo, et al. "Lung Cancer in Peru." Elsevier Inc, 2020. http://hdl.handle.net/10757/652438.
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Peru is a South American nation with a growing and aging population of 31 million people with a life expectancy at birth of 76.7 years. The country is divided into 25 regions, 79% of the population is urban, and Lima, the capital, concentrates more than a third of the population.1 Although Peru is an upper-middle-income country, health expenditure represents only 5.1% of the gross domestic product, which is lower than the average of Latin America and the Caribbean (LATAM) (8.56%).2 Out-of-pocket health expenditure is 30.9%.3 Peru has a comprehensive National Cancer Plan and two population-based cancer registries in Lima and Arequipa.Revisión por pares
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Salvati, Valentina. "Development of effective lung cancer therapies based on lung cancer stem cella targeting." Doctoral thesis, Università di Catania, 2015. http://hdl.handle.net/10761/4035.
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Il carcinoma polmonare non a piccole cellule (NSCLC) rappresenta circa l 80% di tutti i tumori al polmone ed è il cancro più comune e più mortale al mondo.
Il trattamento convenzionale per il NSCLC in stadio avanzato è stato basato per molto tempo sull uso della chemioterapia, ma con basso impatto sulla sopravvivenza .
Una migliore comprensione dei meccanismi molecolari coinvolti nel processo di tumorigenesi e una maggiore capacità nell identificazione di specifiche alterazioni genetiche come bersagli terapeutici, hanno portato ad un significativo avanzamento verso lo sviluppo di terapie più efficaci.
Il recettore del fattore di crescita dell epidermide (EGFR) è spesso over-espresso nel NSCLC ed è considerato un promettente bersaglio terapeutico per il trattamento di questo tumore.
La presenza di mutazioni nel gene EGFR sono un importante predittore di risposta agli inibitori dell EGFR. Sebbene gli inibitori dell EGFR di prima generazione hanno mostrato incoraggianti risposte cliniche nei tumori al polmone, quasi tutti i pazienti sviluppano resistenza al trattamento nel corso del tempo.
La resistenza ai trattamenti potrebbe dipendere anche dalla presenza delle cellule staminali tumorali (CSCs), una sottopopolazione di cellule intrinsecamente resistenti. Così, lo studio delle cellule staminali tumorali del polmone, potrebbe essere uno strumento efficace per l identificazione e validazione di bersagli terapeutici innovativi contribuendo all'introduzione di importanti miglioramenti nell ambito dell oncologia clinica.
Pertanto, la terapia mirata verso l EGFR continua ad evolvere in seguito alla scoperta della sensibilità agli inibitori tirosin-chinasici da parte di pazienti caratterizzati da mutazioni attivanti del gene EGFR. Tuttavia, circa il 10-20% dei pazienti privi della mutazione dell EGFR, beneficiano anch essi del trattamento con gli inibitori TKIs, suggerendo che potrebbero esistere altri determinanti di risposta al trattamento, indipendenti dalla mutazione del recettore.
Questo progetto, quindi, è stato focalizzato sull analisi della via di segnale dell EGFR e sullo studio della sensibilità delle cellule staminali tumorali di polmone e di modelli murini da esse derivati, agli inibitori dell EGFR, al fine di identificare possibili biomarcatori predittivi di risposta agli TKIs, in cellule prive della mutazione dell EGFR.
Questo studio ha portato all identificazione della fosforilazione dell EGFR al residuo tirosina 1068, ma non 1173, come potenziale marcatore di risposta all Erlotinib nelle cellule staminali tumorali di polmone e negli xenografts da esse derivati.
Inoltre, anche linee cellulari commerciali di polmone sensibili all Erlotinib, esprimevano pEGFR-tyr-1068 indipendentemente dalla mutazione dell EGFR, così, l espressione di pEGFR-tyr1068 nelle cellule staminali tumorali di polmone è risultata essere associata ad una risposta positiva al trattamento con l Erlotinib.
La valutazione, mediante immunoistochimica, dello stato di fosforilazione dell EGFR in pazienti con mutazione e senza mutazione del recettore, ha portato a correlare solo pEGFR-tyr1068 e non pEGFR-tyr1173, con la mutazione dell EGFR.
In base a questi dati, quindi, è possibile ipotizzare che l identificazione del livello di fosforilazione dell EGFR al residuo tirosina 1068 nei tumori dei pazienti, permetterebbe di individuare tumori con e senza mutazione dell EGFR ma caratterizzati da attivazione del recettore, in grado probabilmente di rispondere in modo positivo al trattamento con l Erlotinib.
Questi studi potrebbero avere importanti implicazioni terapeutiche per il trattamento dei tumori al polmone e potrebbero permettere ai pazienti con NSCLC di essere selezionati per terapie più efficaci e meno tossiche.
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Şeşen, Mustafa Berkan. "Lung cancer assistant : a hybrid clinical decision support application in lung cancer treatment selection." Thesis, University of Oxford, 2013. https://ora.ox.ac.uk/objects/uuid:e0dd01e4-3f18-49ed-89af-5e81894d4967.
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We describe an online clinical decision support (CDS) system, Lung Cancer Assistant (LCA), which we have developed to aid the clinicians in arriving at informed treatment decisions for lung cancer patients at multidisciplinary team (MDT) meetings. LCA integrates rule-based and probabilistic decision support within a single platform. To our knowledge, this is the first time this has been achieved in the context of CDS in cancer care. Rule-based decision support is achieved by an original ontological guideline rule inference framework that operates on a domain-specific module of Systematized Nomenclature of Medicine-Clinical Terms (SNOMED-CT), containing clinical concepts and guideline rule knowledge elicited from the major national and international guideline publishers. It adopts a conventional argumentation-based decision model, whereby the decision options are listed along with arguments derived by matching the patient records to the guideline rule base. As an additional feature of this framework, when a new patient is entered, LCA displays the most similar patients to the one being viewed. Probabilistic inference is provided by a Bayesian Network (BN) whose structure and parameters have been learned based on the English Lung Cancer Database (LUCADA). This allows LCA to predict the probability of patient survival and lay out how the selection of different treatment plans would affect it. Based on a retrospective patient subset from LUCADA, we present empirical results on the treatment recommendations provided by both functionalities of LCA and discuss their strengths and weaknesses. Finally, we present preliminary work, which may allow utilising the BN to calculate survival odd ratios that could be translated into quantitative degrees of support for the guideline rule-based arguments. An online version of LCA is accessible on http://lca.eng.ox.ac.uk.
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Turner, Nicola Jane. "Cancer in older people : studies in lung cancer." Thesis, University of Leeds, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.399662.
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OLSSON, MILLA, and CAROLINE ROSELL. "Telemedicine for Lung Cancer Patients." Thesis, KTH, Skolan för datavetenskap och kommunikation (CSC), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-136951.
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Den svenska sjukvården står idag för ett antal utmaningar om den skall fortsatt kunna erbjuda god service som vårdgivare och vara attraktiv som arbetsgivare. Bland annat diskuteras frågor som förvärrad platsbrist, läkarbrist samt avstånd till specialistsjukvård. På Karolinska Universitetssjukhuset i Solna ligger Radiumhemmet och där behandlas bland annat lungcancerpatienter. Där diskuteras huruvida telemedicin kan vara en möjlig väg för att lösa ovanstående problem. Denna uppsats utreder på vilket sätt telemedicin kan användas på Radiumhemmet för lungcancerpatienter. För att kunna utreda en telemedicinsk lösnings möjligheter på Radiumhemmet genomfördes intervjuer och fokusgrupper med personalen. Externa experter från sjukvården och industri intervjuades och ett besök gjordes på barnsjukhuset Childrens Healthcare of Atlanta, USA, där man har kommit långt i användningen av telemedicin. Det finns delar av verksamheten på Radiumhemmet där telemedicin skulle kunna bidra till att skapa möjligheter till en tätare kontakt mellan patient och vårdpersonal. Detta i syfte att lugna oroliga patienter och hjälpa till med lättare symptombedömningar och på så sätt minska väntetiderna. Genom de undersökningar som utfördes upptäcktes dock även svagheter i en telemedicinsk lösning avsedd för lungcancerpatienter. Patientgruppen ofta är äldre med liten erfarenhet av datorer och sjukdomen är allvarlig. Det krävs personlig kontakt och fysiska undersökningar, men i vilken utsträckning är individuellt. Telemedicin kanske inte kan ses som en absolut lösning för de problem som råder i sjukvården idag när det kommer till lungcancerpatienter, men väl som ett komplement. Om lungcancerpatienter är den optimala målgruppen är ifrågasättbart men att telemedicin kan underlätta i den svenska sjukvården står klart.Nowadays the health care system in Sweden is faced with several challenges like shortage of space, physicians and long distances to specialized health care. A possible solution for this being discussed at the lung cancer department of Karolinska University 2 Hospital is the use of telemedicine. If implemented it would be part of the followup treatment. The objective of our research is to find out if this technology can help improve the health care. In order to investigate the opportunity for a telemedicine solution, we collected qualitative data from multiple different sources. This included two doctors specialized in lung cancer, and a focus group with nurses from Radiumhemmet. We also conducted interviews with relevant individuals outside the hospital including Nirav Desai who is the Founder and CEO of Hands On Telehealth; furthermore, we visited the Children’s Healthcare of Atlanta based in Atlanta, Georgia where telemedicine is used on a daily basis. Thanks to the carried out research, we have discovered that telemedicine could be used in certain scenarios and contribute towards a more frequent contact between the patient and the medical professionals. Thus, this new technique could help nurses execute lighter symptoms assessment remotely and reduce waiting times. We also discovered some inconveniences in a telemedicine solution designed for lung cancer patients. We personally do not think they are the best target group for such a solution since the patients are mostly the elderly with little computer experience. Also the disease is severe and requires physical examinations where the telemedicine existing today would not improve the care giving. To all intents and purposes, telemedicine might not be the only and ultimate solution for the problems identified within healthcare for lung cancer patients at Radiumhemmet, but it can work well as a supplement. 3
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Basran, Parminder S. "Optimisation of lung cancer treatment." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq22568.pdf.
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Tinnemans, Monique Maria Franciska Johanna. "Cytokinetic analysis of lung cancer." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1996. http://arno.unimaas.nl/show.cgi?fid=7289.
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Richards, Elizabeth. "Molecular profiling of lung cancer." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24546.
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Cisplatin is a first line chemotherapeutic agent for lung cancer however, although patients may respond to therapy, resistance often develops with tumour recurrence and disease progression. Somatic alterations in the tumour may alter therapeutic responses. Consequently a model of cisplatin resistance in lung cancer derived A549 cells has been created to examine the genomic changes that occur as chemo-resistance develops. Drug resistance was induced in A549 cells through multiple rounds of cisplatin dosage and recovery over two different time courses. The concentration of cisplatin required to inhibit growth (inhibitory concentration [IC] value) was calculated at each round and cycles were continued until the IC value increased at least four-fold. Cells were harvested and total RNA extracted for whole transcriptome microarray analysis. Data was analysed using R statistics and associated packages, Affy, Limma, Mfuzz and WGCNA. A five-fold increase in IC value was generated over successive doses in both regimes, accompanied by highly significant changes in gene expression. To explore these changes, temporal expression clustering and extensive network analyses were performed across the rounds of cisplatin dosing, as well as an untreated cell culture time course that acted as a comparison to the two treated regimes. The results gathered from this robust model suggest that differences in dose and frequency of chemotherapy may affect genomic changes at specific loci that confer cisplatin resistance. Interesting and relevant pathways and genes have been discovered. In combination with analyses on a small patient cohort, these results have provided insights into the mechanism of cisplatin resistance and have highlighted new clinical biomarkers of potential use in prognosis of patients undergoing cancer treatment.
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Bingula, Rea. "Non-small cell lung cancer, immunity and microbiota : laying ground for the gut-lung-lung cancer axis in human subjects." Thesis, Université Clermont Auvergne (2017-2020), 2019. http://www.theses.fr/2019CLFAS009.
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Le cancer du poumon est la principale cause de décès par cancer dans le monde. En dépit de la variété de traitements disponibles, tels que la chirurgie, la chimiothérapie, la radiothérapie et l’immunothérapie, la survie moyenne à 5 ans est de 60 %. L’une des raisons sous-jacente est une très grande variabilité de réponse au traitement, expliquée par les antécédents génétiques du patient et depuis peu par son microbiote. Le terme « microbiote » regroupe les bactéries, les archées, les champignons, les virus et les protistes qui colonisent notre organisme. Des études utilisant des modèles animaux montrent que le microbiote intestinal joue un rôle crucial dans la réponse de l’hôte au traitement, via la stimulation du système immunitaire. Dans ce contexte, plusieurs « axes de communication » entre le site intestinal et les sites tumoraux distaux commencent à émerger, y compris l’axe « intestin-poumon ». Cependant, le microbiote pulmonaire, qui pourrait directement influencer la réponse tumorale et interagir avec le microbiote intestinal, est pour l’heure peu caractérisé. Afin de développer cette idée d’un axe « intestin, poumon et cancer du poumon », nous avons inclus dans notre étude 18 patients atteints d’un cancer du poumon non à petites cellules (CBNPC) admissibles à la chirurgie. Nous avons analysé leurs microbiotes par séquençage à haut débit à partir de quatre échantillons différents de poumon (tissu sain, tissus péritumoral et tumoral et fluide de lavage broncho-alvéolaire LBA) mais également à partir d’échantillons de salive et de fèces. Nous avons également analysé plusieurs marqueurs immunitaires (infiltration lymphocytaire des tumeurs, profils Th et neutrophiles, cytokines dans le LBA et le sang), des marqueurs inflammatoires et enfin les acides gras à chaînes courtes dans les fèces. Une caractérisation détaillée de ces quatre types d’échantillons de poumons nous a permis de montrer que le microbiote du LBA présente une communauté nettement distincte de celle du tissu pulmonaire. Les tumeurs des lobes inférieurs prédisant le plus mauvais pronostic, nous avons décidé d’étudier le lien entre l’emplacement des tumeurs et la composition du microbiote. Les microbiotes du tissu péritumoral et du LBA ont été identifiés comme étant les plus impactés en terme d’abondance et de diversité ; la tumeur est quant à elle moins impactée. Cependant nous avons observé que le phylum des Firmicutes, décrit comme étant élevé dans les maladies pulmonaires obstructives chroniques, est plus abondant dans le microbiote des lobes inférieurs du poumon. Par conséquent, nous pouvons émettre l’hypothèse que l’augmentation des Firmicutes et les variations importantes du microbiote dans le tissu péritumoral pourraient être associés à une agressivité accrue des tumeurs du lobe inférieur. Nous avons ensuite démontré que la présence de ganglions lymphatiques (GL) métastatiques, marqueur d’un pronostic négatif dans le NSCLC, influence considérablement le microbiote local de par le profil respiratoire du tissu. Nous avons en effet observé que les bactéries anaérobies étaient plus abondantes dans les tumeurs en présence de LN métastatiques. Les bactéries aérobies sont quant à elles plus représentées dans les tumeurs sans GL métastatiques. Nous avons cependant observé la situation inverse dans les tissus extratumoraux. L’hypothèse avancée est celle d’une migration bactérienne en fonction des préférences de conditions de croissance, directement liées aux caractéristiques de la tumeur. Ceci nous permet de proposer plusieurs biomarqueurs pour la détection de GL métastatique, facilitant ainsi leur détection sans imposer de biopsie. Enfin, nous montrons que le microbiote du LBA est d’avantage associé à la réponse immunitaire locale et est indépendant de la présence de GL métastatique. Les recherches à venir porteront sur l’exploration de l’interaction entre le microbiote pulmonaire, l’immunité systémique et le microbiote intestinalLung cancer is the main cause of death by cancer worldwide. Despite the variety of available treatments, including surgery, chemotherapy, radiotherapy, and immune therapy, the average 5-year survival is 60%. One of the underlying reasons is a very high variability in patients’ susceptibility to treatment, explained by genetic background and since recently – our microbiota. The term microbiota includes bacteria, archaea, fungi, viruses and protists that inhabit our organism. The studies in animal models show that the gut microbiota (focused on bacteria) has a crucial role in host’s responsiveness to therapy through the stimulation of immune system. In this light, several “communication axes” between the gut and distal tumour sites have started to develop, including the “gut-lung” axis. However, the resident microbiota in the lungs that could directly influence the tumour response and interact with the gut microbiota has been scarcely characterised. To enable further development of the idea of the “gut-lung-lung cancer” axis, we included 18 non-small cell lung cancer (NSCLC) patients eligible for surgery and analysed the microbiota from four different lung samples (non-malignant, peritumoural and tumour tissue and bronchoalveolar lavage fluid; BAL), saliva and faeces by high-throughput sequencing. We also analysed several immune markers, as lymphocytic tumour infiltrate, Th and neutrophil profiles and cytokines in BAL and blood, and inflammatory markers in faeces along with short-chain fatty acids. Focusing first on the lungs, we show that BAL microbiota represents a significantly distinct community compared to lung tissue microbiota by providing detailed characterisation of the four different lung samples. Since tumours in lower lobes are reported as the ones with the worse prognosis, we investigated how the lobe location affected the microbiota composition. Peritumoural tissue and BAL microbiota were identified as the most affected in both abundance and diversity, and tumour as the least affected. However, phylum Firmicutes, previously reported as elevated in chronic obstructive pulmonary disease compared to controls, was found more abundant in microbiota from lower lung lobes. Therefore, we propose that both increase in Firmicutes and extensive changes in peritumoural tissue could be associated to increased aggressiveness of the lower lobe tumours. Next, we show that the presence of metastatic lymph nodes (LN), negative prognostic marker in NSCLC, significantly influence the local tissue microbiota in relation to its respiratory profile. We reported that anaerobic bacteria were more abundant within the tumour in the presence of metastatic LN, and aerobic bacteria within the one without it. Moreover, exactly inverse was observed for the same bacteria in extratumoural tissues. Along with migratory hypothesis depending on the bacterial preference for growth conditions shaped by tumour’s features, we propose several biomarkers for detection of metastatic LN that might facilitate their detection without imposing LN biopsy. Finally, we showed that BAL microbiota is the most associated to the local immune response and independent of the presence of metastatic LN. Future research will focus on the exploration of the interaction between the lung microbiota, systemic immunity and the gut microbiota
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Grewal, Amardeep Singh. "Prevalence and Outcome of Lung Cancer in Lung Transplant Recipients." Thesis, Harvard University, 2015. http://nrs.harvard.edu/urn-3:HUL.InstRepos:17295910.
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Lung transplant is the only available therapy for patients with advanced lung disease. The goal of this study was to examine the prevalence, origin, management and outcome of lung cancer in recipients of lung transplant at the Brigham and Women’s Hospital.
We conducted a retrospective chart review of all lung transplantations in our institution from January 1990 until June 2012. The prevalence of lung cancer in the explanted lung was 6 (1.2%) of 462 and all cases were in subjects with lung fibrosis. All 4 subjects with lymph node involvement died of causes related to the malignancy. Nine (1.9%) of 462 patients were found to have bronchogenic carcinoma after lung transplant. The median time to diagnosis after lung transplant was 28 months with a range from 9 months to 10 years. Median survival was 8 months, with tumors involving lymph nodes or distant metastases associated with a markedly worse prognosis (median survival 7 months) than stage I disease (median survival 27 months).
While stage I disease is associated with improved survival in this cohort, survival is still not comparable to that of the general population, likely influenced by the need for aggressive immune suppression.
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Li, Xinjun. "Familial risks for cancer with reference to lung cancer /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-007-9/.
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Moore, S. "The social construction of lung cancer : an analysis of representations of lung cancer in UK media." Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/372913/.
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Lung cancer is a commonly occurring cancer in the United Kingdom. However, little attention has been directed at understanding meanings in relation to the disease, and how these are socially constructed. This thesis examines representations of lung cancer in media stories to explore how the disease is constructed and with what effects. Drawing on a social constructionist approach, media stories are understood as public places or sites in which meanings about the world are produced and reproduced through language and discourse. Media portrayals of lung cancer are examined for their content and how they may function to construct meanings and knowledge about lung cancer and people who develop the disease. Media portrayals of breast cancer are used to compare and contrast how the two diseases are portrayed in order to identify differences that may have implications for the construction of meanings. The analysis identifies that media stories draw heavily on discourses that associate lung cancer with death and smoking. It is suggested that stories also draw on wider cultural discourses in which health and dying are constructed as moral issues. As a consequence, lung cancer is constructed as a potentially blameworthy death and thereby unworthy of public attention and support. In contrast, media stories about breast cancer draw on discourses that associate the disease with survival and factors that suggest women as ‘at risk’ rather than the cause of the disease. As a consequence, breast cancer is constructed as an indiscriminate threat and, as such, worthy of public attention. The thesis argues that media representations are illustrative of the social processes and conditions involved in the production and sustenance of lung cancer stigma.
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Hillinger, Sven. "Immune targeted therapy for lung cancer /." Zürich, 2006. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253405.
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Buttery, Robert Christians. "Integrin affinity modulation and lung cancer." Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/29025.
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Recent work has shown that the transmembrane protein CD98 is able to influence the affinity with which β1 integrins bind to extracellular ligands. The first part of this thesis presents confocal microscopy and co-immunoprecipitation experiments that confirm the physical juxtaposition of the two proteins within the cell membrane, suggesting a direct functional link between the two. It also demonstrated that cross-linking CD98 stimulates both phosphoinositide 3-kinase intracellular signalling and increased β1 integrin-dependent cellular adhesion. Because of the role of CD98 in integrin affinity modulation, the immunohistochemical expression of CD98 and its ligand, galectin-3, was studied in a variety of human ling diseases including lung cancers. The major finding of this work was a striking distinction between high expression of galectin-3 in non-small cell lung cancer and low expression in small cell lung cancer. This may hag significant implications for the differing clinical behaviours of these two groups of cancers. The final section of this thesis returns to describe experiments aimed at defining the molecular regulators of integrin affinity more clearly. A genetic screen of a cDNA library was undertaken to identify candidate genes coding for proteins able to rescue integrins from the low affinity state induced by the small signalling protein H-Ras. This identified a candidate cDNA 480, recognised to be part of a novel gene Nessie, which codes for a large protein with multiple transmembrane domains. Both 480 and Nessie appear to have the ability to rescue integrin affinity from H-Ras suppression.
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Tran, Vanessa Hoang Medical Sciences Faculty of Medicine UNSW. "Breath biomarkers associated with lung cancer." Publisher:University of New South Wales. Medical Sciences, 2009. http://handle.unsw.edu.au/1959.4/43717.
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Lung cancer (LC) is often diagnosed at advanced stage and as a result, survival rates are low. Recent studies describe exhaled breath and exhaled breath condensate (EBC) as a potential non-invasive method of sampling the airways for assessing inflammation of the respiratory system, and possibly for the early detection of LC. It was hypothesised that higher concentrations of markers and protein will be present in the EBC of LC patients compared to those of normal controls and healthy smokers, and may aid in assessing lung status. Methods: The gaseous phase of breath was investigated for volatile organic compound (VOC) patterns using an electronic nose (eNose) system, in addition to off-line measurements of carbon monoxide (CO) and nitric oxide (NO) levels. The aqueous phase, EBC, was collected during tidal breathing through a glass collection device cooled to 4??C by ice. Nitrite/nitrate (NOx) and pH levels were determined by a fluorescent modification of the Griess method, and silicon chip sensor pH meter, respectively. Protein levels in EBC were examined with a bicinchoninic acid (BCA) assay, silver staining and PAGE techniques, while the levels of tumour markers, CYFRA 21-1 and CEA, were quantified by enzyme-linked immunosorbent assays (ELISA). Results: The eNose machine was not able to produce characteristic VOC profiles from exhaled breath unique to each study group, while no significant difference was observed for mean NOx concentrations in the LC group when compared to other subjects (p=0.8824). Higher protein levels were found in the EBC of LC patient compared to normal controls (p=0.0204), with subsequent measurements of elevated CEA levels observed in the LC group when compared to non-smokers and smokers (p=0.023). Conclusion: This study showed that protein can be detected in the exhaled breath condensate of patients, with a significantly elevated amount in the samples from newly diagnosed LC patients. The mechanism for these differences remains to be determined but may be related to inflammatory changes within the airway, such as vascular protein leakage and release of mediators. Future work may aim to identify the upregulated proteins, and focus on proteomics and tissue microarrays to explore candidate proteins.
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Hochstenbag, Monique. "Imaging in clinical lung cancer staging." [Maastricht] : Maastricht : UPM, Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 2003. http://arno.unimaas.nl/show.cgi?fid=8287.
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Buys, Timon Paul Hermus. "Clonal evoluation and lung cancer pharmacogenomics." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/9532.
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Background: Lung cancer is the world's leading cause of cancer death, with a 5 year
survival rate of ~16%. Several factors contribute to this poor prognosis: the limited detection of disease at treatable stages, the high metastatic potential of any primary tumour, and the variable effectiveness of chemotherapy. We applied high resolution whole genome profiling technologies to uncover genes associated with specific lung cancer phenotypes and to delineate clonal relationships between tumours.
Hypotheses: (i) Shared genetic features in tumours from the same patient are evidence
of a common progenitor. (ii) Continuing clonal evolution facilitates selection for
resistance genes during drug exposure. (iii) Drug response can be predicted for pretreatment lung cancer by evaluating specific gene changes.
Materials/Methods: DNA alteration data from non-small cell lung cancers (NSCLC) were
integrated with mRNA/protein expression data to identify genes contributing to
tumourigenesis. Fine-mapped DNA alteration boundaries were used to evaluate clonality, discriminating multiple primary tumours from intrapulmonary metastasis. Subsequently, this approach was applied to define chemoresistance gene candidates in cells grown under drug selection. Genome alteration data for early stage lung tumours
were also analyzed to define gene changes driving post-treatment recurrence in patients.
Results: We optimized collection of and genomic analysis for clinical lung cancer,
identifying novel oncogene candidates (including genes contributing to tumour
invasion). In addition, we successfully used DNA alteration boundaries to discriminate
clonally-related tumours and define ongoing clonal evolution in both tumours and cancer
cell lines, providing evidence in support of our first two hypotheses. We also identified
dysregulated genes and gene pathways associated with post-treatment recurrence for
clinical lung cancer. These last data suggest that chemoresistance may be an intrinsic process for the majority of cells in a pre-treatment tumour, lending support to our third hypothesis. Significantly, we also detected distinct recurrence-associated gene changes within tumour histology subgroups, indicating that NSCLC may not be treatable as a single disease entity.
Conclusions: Global analysis of DNA alterations is an effective means for defining clonal relationships between tumours. Further, tumour phenotypes such as chemoresistance are governed by complex activation of a variety of gene networks.
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Wilkinson, Pauline. "Lung cancer in Ireland : 1991-1992." Thesis, Queen's University Belfast, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336721.
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Dial, Christian W. "Adaptive Radiation Therapy for Lung Cancer." VCU Scholars Compass, 2014. http://scholarscompass.vcu.edu/etd/3579.
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Prognosis for lung cancer patients remains poor. For those receiving radiation therapy, local control and survival have been shown to improve with increased doses; however, deliverable dose is often limited by associated toxicity. Therefore, methods that reduce dose to normal tissues and allow isotoxic escalation are desirable. Adaptive radiation therapy seeks to improve treatment by modifying the initial plan throughout delivery, and has been shown to decrease normal tissue dose. Studies to date suggest a trend of increasing benefit with increases in replanning frequency; however, replanning is costly in terms of workload and past studies implement at most weekly adaptation. The purpose of this thesis is to quantify the benefit associated with daily replanning and characterize the tradeoff between replanning frequency and adaptive benefit. A software tool is developed to facilitate planning studies and to introduce complimentary methods for evaluating adaptive treatments. Synthetic images and contours are xii generated for each fraction of a typical fractionation schedule using principal component analysis and a novel method of sampling coefficients that preserves temporal trends in the data (e.g. tumor regression). Using the synthetic datasets, a series of adaptive schedules ranging from no adaption to daily replanning are simulated and compared to quantify adaptive benefits and characterize tradeoffs with frequency. Daily replanning resulted in significant reductions in all normal tissue planning metrics when compared to no adaptation, and incremental reductions were observed with each increase in replanning frequency while the magnitude of average reductions decreased with each step. Modest correlation between absolute change in planning target volume over the course of treatment and reductions in both mean lung dose and mean esophageal dose were observed.
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Rattican, Debra. "Symptom Clusters in Lung Cancer Patients." VCU Scholars Compass, 2012. http://scholarscompass.vcu.edu/etd/352.
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SYMPTOM CLUSTERS IN LUNG CANCER PATIENTS By Debra Rattican, PhD, RN A dissertation submitted in partial fulfillment of the requirements for the degree of Doctor of Philosophy at Virginia Commonwealth University. Virginia Commonwealth University, 2012 Major Director: Debra E. Lyon, PhD. Professor and Chair Family and Community Health Nursing The purpose of the study was to examine selected relationships among symptoms common to individuals with lung cancer. The specific aims were: 1) To examine the relationship between the symptoms of dyspnea and anxiety in patients with lung cancer. 2) To examine the relationships among the symptoms of dyspnea, anxiety, and symptom cluster components (depressive symptoms, fatigue, pain) in patients with lung cancer. 3) To examine the correlation between functional ability and quality of life in patients with lung cancer. 4) To explore the relationships among the symptoms of dyspnea, anxiety, and symptom cluster components (depressive symptoms, fatigue, pain) in patients with lung cancer and patients’ functional ability. 5) To explore the relationships among the symptoms of dyspnea, anxiety, and symptom cluster components (depressive symptoms, fatigue, pain) in patients with lung cancer and patients’ quality of life. Data were gathered through online survey and analyzed using descriptive, correlation, principal component analysis, exploratory factor analysis, and forward stepwise regression techniques. A strong positive correlation was found between dyspnea and anxiety (both anxiety in general and anxiety at the time the survey was completed. While results of this study cannot provide conclusive evidence of the existence of a symptom cluster composed of depressive symptoms, fatigue, and pain, the results are consistent with other studies in this area. Significant positive correlations among these three symptoms indicate that this is a possible symptom cluster experienced by lung cancer patients in general. This study provides preliminary data on how these symptoms are related and how they affect functional ability, or the ability to perform routine activities of daily living (ADLS) and instrumental activities of daily living (IADLS), and quality of life in patients with lung cancer. Further study is needed on to better understand the symptom experience of these individuals in order to develop robust interventions targeting effective symptom management.
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Kurtyka, Courtney A. "Novel Therapeutic Strategies in Lung Cancer." Scholar Commons, 2014. https://scholarcommons.usf.edu/etd/5363.
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Lung cancer is the leading cause of cancer-related death and the second most diagnosed cancer in the United States. Unfortunately, many patients either do not have any common mutations for which there are already targetable agents, or they eventually become resistant to these compounds. As such, there is a high demand for new, effective methods of treating this disease as well as predicting patient prognosis and potential benefit from chemotherapy. In this work, numerous strategies for treating lung cancer are explored.
The first method described here is through the use of a pan-early 2 factor (E2F) inhibitor, HLM006474, which is shown to synergize with paclitaxel in non-small cell lung cancer (NSCLC). Next, we explored the creation and utilization of an E2F signature that is prognostic and predictive of early-stage NSCLC patient benefit from adjuvant chemotherapy (ACT). The third project examined possible targets to enhance sensitivity to cisplatin in NSCLC lacking Kirsten rat sarcoma viral oncogene homolog (KRAS) and epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma receptor tyrosine kinase (ALK) fusions (triple-negative), for which cisplatin is one of the few treatment options. These studies led to the identification of a kinase that is overexpressed in NSCLC and whose knockdown sensitizes cells to platinum agents.
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Lee, Richard. "An improved system for lung cancer diagnosis using lung cell images." Diss., Online access via UMI:, 2006.
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Tian, Fei. "Effect of the Hedgehog Pathway inhibitor GDC-0449 in lung cancer cells and lung cancer stem cells." Diss., Ludwig-Maximilians-Universität München, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-156374.
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The cancer stem cell hypothesis implicates that tumor cell population is heterogeneous with relatively well-differentiated cells and poorly-differentiated cells. Only the small population of tumourigenic poorly-differentiated CSCs can escape the normal limits of self-renewal and has the ability to proliferate and maintain the malignant growth of the tumor.
One characteristic of stem cell is that the ability to exclude DNA dyes, such as Hoechst 33342 via the over-expression of ATP-binding cassette transporters (ABC transporters) on the cell membrane. It makes the detecting of the stem cell possible. After the Hoechst 33342 staining, stem cells extrude this dye and show a typical profile of low fluorescence in Hoechst red versus Hoechst blue bivariate dot plots. These low Hoechst 33342 stained cells are named as side population (SP) cells. This characteristic has enabled purification and characterization of CSCs when carried out alone or in combination with stem cell surface markers.
The CSC hypothesis could have a fundamental influence on cancer therapy. CSCs have shown significant substantial resistance to conventional chemotherapy in contrast to the differentiated cancer cells. It is essential to design a complete therapy strategy first to reduce or minimize proliferating cell mass and then to differentiate or eliminate CSCs, so that the relapses of metastatic cancers could be prevented.
This work aimed at investigating if Hedgehog pathway inhibitor GDC-0449 is effective in the lung cancer cell lines HCC (adeno-carcinoma) and H1339 (small cell lung carcinoma) and also the cisplatin resistant lung cancer cells, and if possible effects of GDC-0449 are mediated via SPs. Furthermore, the effect of GDC-0449 on the calcium homeostasis was also investigated.
GDC-0449 showed dose-dependent inhibitory effects on cell growth in both HCC and H1339 cells. The combination of GDC-0449 and cisplatin gave an additional inhibitory effect. GDC- 0449 could also inhibit the cell growth in cisplatin resistant HCC and H1339 cells.
SP cells as cancer stem-cell-like cells could be found in HCC and H1339 cells. Only the SP cells showed the repopulation ability but not the non-SP cells. GDC-0449 could inhibit the SP cell fraction in both HCC and H1339 cells. So the inhibitory effect of GDC-0449 on cell growth may be mediated via SP.
GDC-0449 affected the expression of the Hh pathway components in both HCC and H1339 cells. In HCC cells, GDC-0449 inhibited the activity of the Hh pathway and the down- regulation of Shh, Patched and Gli-1 could be shown. In H1339 cells, GDC-0449 could also inhibit the pathway activity and decrease the expression of Gli-1 in an autocrine pattern due to the over-expression of Shh. The inhibition of Hh pathway increased the expression of Bmi-1 to compensate the loss of Hh pathway function. The Hh pathway activity could be detected only in SP cells from HCC and H1339 cells.
The application of GDC-0449 on HCC and H1339 naïve and cisplatin resistant cells increased [Ca2+]c by decreasing [Ca2+]ER. GDC-0449 induced Ca2+ release from ER into cytoplasm in HCC and H1339 naïve and cisplatin resistant cells. The Ca2+ overload could lead to apoptosis, which was related to the cell growth inhibitory effect of GDC-0449 in lung cancer cells. The expression of SERCA and IP3R was not detectably influenced by GDC-0449. The effect of GDC-0449 on lung cancer cell Ca2+ -regulating machinery was not via the alternation of the expression of ER Ca2+ regulating channels.
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Brena, Romulo Martin. "Aberrant DNA methylation in human non-small cell lung cancer." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1172083621.
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陳潔盈 and Kit-ying Loucia Chan. "Expression analysis of Candidate cancer genes in non-small cell lung cancer." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011163.
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Cong, Chunling. "Statistical Analysis and Modeling of Breast Cancer and Lung Cancer." Scholar Commons, 2010. http://scholarcommons.usf.edu/etd/3563.
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The objective of the present study is to investigate various problems associate with breast cancer and lung cancer patients. In this study, we compare the effectiveness of breast cancer treatments using decision tree analysis and come to the conclusion that although certain treatment shows overall effectiveness over the others, physicians or doctors should discretionally give different treatment to breast cancer patients based on their characteristics. Reoccurrence time of breast caner patients who receive different treatments are compared in an overall sense, histology type is also taken into consideration. To further understand the relation between relapse time and other variables, statistical models are applied to identify the attribute variables and predict the relapse time. Of equal importance, the transition between different breast cancer stages are analyzed through Markov Chain which not only gives the transition probability between stages for specific treatment but also provide guidance on breast cancer treatment based on stating information.
Sensitivity analysis is conducted on breast cancer doubling time which involves two commonly used assumptions: spherical tumor and exponential growth of tumor and the analysis reveals that variation from those assumptions could cause very different statistical behavior of breast cancer doubling time.
In lung cancer study, we investigate the mortality time of lung cancer patients from several different perspectives: gender, cigarettes per day and duration of smoking. Statistical model is also used to predict the mortality time of lung cancer patients.
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Sarvi, Sana. "Small cell lung cancer and cancer stem cell-like cells." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9542.
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Small cell lung cancer (SCLC) is a highly aggressive malignancy with extreme mortality and morbidity. Although initially chemo- and radio-sensitive, almost inevitable recurrence and resistance occurs. SCLC patients often present with metastases, making surgery not feasible. Current therapies, rationally designed on underlying pathogenesis, produce in vitro results, however, these have failed to translate into satisfactory clinical outcomes. Recently, research into cancer stem cells (CSCs) has gained momentum and form an attractive target for novel therapies. Based on this concept, CSCs are the cause of neoplastic tissue development that are inherently resistant to chemotherapy, explaining why conventional therapies can shrink the tumour but are unable to eliminate the tumour completely, leading to eventual recurrence. Here I demonstrate that SCLC H345 and H69 cell lines contain a subset of cells expressing CD133, a known CSC marker. CD133+ SCLC sub-population maintained their stem cell-like phenotype over a prolonged period of culture, differentiated in appropriate conditions and expressed the embryonic stem cell marker Oct-4 indicating their stem-like phenotype. Additionally, these cells displayed augmented clonogenic efficacy, were chemoresistant and tumorigenic in vivo, distinct from the CD133- cells. Thus, the SCLC CD133 expressing cells fulfil most criteria of CSClike definition. The molecular mechanisms associated with CD133+ SCLC chemoresistance and growth is unknown. Up-regulated Akt activity, a known promoter of resistance with survival advantage, was observed in CD133+ SCLC cells. Likewise, these cells demonstrated elevated expression of Bcl-2, an anti-apoptotic protein compared to their negative counterpart explaining CD133+ cell chemoresistance phenotype. Additionally, CD133+ cells revealed greater expression of neuropeptide receptors, gastrin releasing peptide (GRP) and V1A receptors compared to the CD133- cells. Addition of exogenous GRP and arginine vasopressin (AVP) to CD133+ SCLC cells promoted their clonogenic growth in semi-solid medium, illustrating for the first time neuropeptide dependent growth of these cells. A novel peptide (peptide-1) was designed based on the known structure of the substance P analogues that have shown benefit in animal models and in early clinical trials. This compound inhibited the growth of SCLC cells in in vitro with improved potency and stability compared to previous analogues and reduced tumorigenicity in vivo. Interestingly, peptide-1 was more effective in CD133+ cells due to increased expression of neuropeptide receptors on these cells. In conclusion, my results show that SCLC cells retain a sub-population of cells that demonstrate CSC-like phenotype. Preferential activation of Akt and Bcl-2 survival pathways and enhanced expression of neuropeptide receptors contribute to CD133+ SCLC chemoresistance and growth. Therefore, it can be proposed that CD133+ cells are the possible cause of SCLC development, treatment resistance and disease recurrence. Despite being chemoresistant, CD133+ cells demonstrated sensitivity to peptide-1. The identification of such new analogue that demonstrates efficacy towards resistant CD133+ SCLC cells is a very exciting step forward in the identification of a potential new therapy for resistant disease.
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De, Souza Nicosha. "Molecular epidemiology of lung cancer in the Liverpool Lung Project (LLP) cohort." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/2006199/.
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The primary aim of the project was to evaluate the epidemiological and genetic susceptibility factors associated with lung cancer, in the Liverpool Lung Project (LLP) population. The associated datasets available for research with the LLP dataset (questionnaire) were: Office of National Statistics (ONS), Health Episode Statistics (HES) data with comorbidity data, single nucleotide polymorphism (SNP) data of 570 cases from Liverpool, 3000 controls from the 1958 Birth Cohort. The epidemiological (HES) data was used to study the effect of Charlson (CCI) and Elixhauser comorbidity index (ECI) on the incidence of lung cancer using the Cox proportional hazard regression and use the same HES data to design a 5-year sex specific incidence model for lung cancer with crucial covariates. The ECI and CCI were significant in both univariate and multivariate analyses adjusted for age at the start of the study, sex and smoking pack years. The developed models had a good discriminatory power (AUCmale = 0.73; AUCfemale = 0.77) when internally validated using a 10-fold cross validation. The genetic data for the LLP lung cancer cases was used in several contexts: i) to identify SNPS associated with lung cancer under a range of allelic models (additive, dominant, recessive and genotypic), using the Wellcome trust 1958 Birth Cohort as a control dataset; ii) to identify SNPs associated with cause specific and overall survival in lung cancer patients, utilising the Cox proportional hazard model with adjustment for various covariates; and iii) to identify gene pathways that are associated with lung cancer survival using the random forest survival method. SNPs within the genes PRDM11, ZNF382 and HMGA2 were identified in the genome wide case-control study when using the additive, dominant or genotypic models, whereas the recessive model identified the gene ITIH2. Significant SNPs (p≤10-6) associated with cause-specific survival in early stage cases were rs10230420 (WIPF3), rs3746619 and rs3827103 (both in MC3R). In advanced stage cases, significant SNPs were rs1868110 (NEK10) and rs2206779 (AF357533). For the overall survival analysis, significant SNPs were rs10230420 (WIPF3), rs2056533 (ZBTB20) and rs6708630 (CYS1) in early stage cases, whereas rs1868110 (NEK10) and rs2206779 (AF357533) were significantly associated with overall survival in advanced stage NSCLC cases. The pathway analysis using the random survival forest method was undertaken on 18 pathways for both cause-specific and overall survival of lung cancer cases. The results were consistent with apoptosis, base excision repair and mismatch repair being pathways influencing survival.
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Chan, Kit-ying Loucia. "Expression analysis of Candidate cancer genes in non-small cell lung cancer /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38480360.
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Keller, Elizabeth Greer. "Novel chemotherapeutics against lung and colon cancer." Click here for download, 2010. http://proquest.umi.com.ps2.villanova.edu/pqdweb?did=1961333981&sid=1&Fmt=2&clientId=3260&RQT=309&VName=PQD.
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Maltt, N. D. "Diagnosis of lung cancer by raman spectroscopy." Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492488.
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lung cancer patients from 'at risk' controls and 'at risk' control subjects from healthy control subjects. Porphyrin-containing substances were higher in the 'at risk' controls than either the healthy controls or the lung cancer patients. Additionally the induced sputum from the three groups was analysed using Surface-enhanced Desorption-Ionization Time-of-flight mass spectrometry which also distinguished the three groups. A mini fibre optic probe was used in conjunction with shifted subtracted Raman spectroscopy to analyse normal and malignant ex vivo lung tissue from 7 patients, obtained from lung cancer surgical resections and could classify the two types of tissue perfectly. In conclusion, Raman spectroscopy has the potential to diagnose lung cancer, predict prognosis and elucidate the chemical changes associated with carcinogenesis.
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Tomai, Evangelia. "Gap junctional communication in lung cancer cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0017/MQ54488.pdf.
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Smit, Egbert Frederik. "Aspects of palliative chemotherapy for lung cancer." [S.l. : [Groningen : s.n.] ; University Library Groningen] [Host], 1990. http://irs.ub.rug.nl/ppn/292220588.
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Oosterhout, Anselmus Gerardus Maria van. "Small cell lung cancer and brain metastasis." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1995. http://arno.unimaas.nl/show.cgi?fid=6643.
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Seute, Tatjana. "Neurologic complications in small cell lung cancer." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Universiteit Maastricht [host], 2008. http://arno.unimaas.nl/show.cgi?fid=9520.
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Belderbos, Josepha Sophia Antonia. "Radiotherapy in lung cancer: a moving field." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2007. http://dare.uva.nl/document/45315.
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Wu, Mau-Ching. "Mouse models of human lung cancer development." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624711.
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Lake, Sarah Louise. "Genetic analysis of LPHH1 in lung cancer." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404506.
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This thesis contends that the monarch-centred view of the masque, which has prevailed since the publication in the 1960s and 1970s of Stephen Orgel's seminal works on the genre, needs to be challenged in the light of recent scholarship on the cultural agency of other members of the royal family. In my introduction I argue that while the New Historicism has been crucial in elucidating the theatricalization of power in the early Stuart court, its insistence on the inevitability of the collusion between art and sovereign power needs to be questioned. The masque has long been seen as a monolithic and univocal celebration of monarchical power, despite the fact that it was promoted at court not by King James but by other members of the royal family. Adopting a loosely chronological approach, this thesis retells the story of the 'Jacobean' court masque by recovering the role played in the commissioning and performance of masques by James's wife, his children, and his male favourites. The chapters set out to hear voices other than that of the King, and discover that, while panegyric was part of each masque, it was rarely as unequivocal as traditional criticism has suggested. On the contrary, the annual masques were frequently appropriated to express the oppositional agendas of factions at court, and above all, of members of James's own family. I argue that Queen Anne set a precedent for the disruptive use of the masque which she exploited to present herself as independent from the King, and to emphasise her importance as the mother of the royal children. Prince Henry, and later Prince Charles, both used the masque to contest the pacifist policies of the King, while Buckingham's success as a favourite was linked to his skilful exploitation of the masques as an integral part of his self-fashioning. Above all by shifting the focus away from King James to consider the more active participation in the masque of other members of the royal family, this thesis offers a possibility of moving beyond the current impasse of the subversion / containment debate to a more nuanced reading of the culture of the early Stuart court which recognises the delicate process of negotiation and accommodation in which the masquers and their audiences were engaged.
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Salem, Ahmed. "Validating non-invasive therapeutic lung cancer biomarkers." Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/validating-noninvasive-therapeutic-lung-cancer-biomarkers(edeb97f1-b1d4-43a3-bafb-8c7e1fa9d8c7).html.
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Lung cancer is the leading cause of cancer death and a priority research area. There is an unmet need to develop biomarkers to enable patient selection and stratification in future lung cancer trials. This thesis aimed to validate non-invasive therapeutic lung cancer biomarkers. The investigated biomarkers were derived from imaging techniques used in routine healthcare (computed tomography and [18F]fludeoxyglucose (FDG) positron emission tomography (PET)) and research-domain imaging methods of hypoxia (multi-parametric magnetic resonance imaging (MRI) and [18F]fluoroazomycin arabinoside (FAZA) PET) and proliferation ([18F]fluorothymidine (FLT) PET), along with circulating biomarkers. These biomarkers were derived from one randomized controlled trial and 3 prospective pilot studies. I report for the first time the outcome of early limited stage (LS)- small cell lung cancer (SCLC), staged using the tumour, node and metastasis (TNM) staging system, within a randomized controlled trial. Early (TNM stage I-II) LS-SCLC patients achieve long-term survival with minimal acute side-effects following chemoradiotherapy and prophylactic cranial irradiation. This study guides patient management and benchmarks achievable outcomes in the era of modern radiotherapy. I report on the effects of different [18F]FAZA PET acquisition and analysis procedures on image parameters, comparing hypoxic volumes and fractions using fixed (>1.4, >1.2) and image-derived thresholds in non-small cell lung cancer (NSCLC) patients. I also investigate, for the first time, image repeatability and compare findings with a tissue-based hypoxia assessment in a patient subset, thus providing new [18F]FAZA PET validation data for the optimal application of this modality to derive potential hypoxia biomarkers. I present the world first oxygen-enhanced (OE) MRI clinical study to evaluate repeatability and show pharmacodynamic treatment effect, providing new technical and biological validation data for OE-MRI NSCLC hypoxia biomarkers. These results suggest that OE-MRI is feasible, well-tolerated, repeatable and has potential clinical utility as a biomarker in future NSCLC hypoxia-targeted therapy trials and radiotherapy dose painting studies. I present a pilot study that evaluated, to my knowledge, the largest blood biomarker panel in lung cancer patients. I show that baseline IL-1b and neutrophil count and early-treatment CYFRA 21-1 predict lung cancer radiotherapy response. CYFRA 21-1 and VCAM-1 correlated with [18F]FLT PET, highlighting for the first time a potential role of blood biomarkers as imaging surrogates. A trial proposal to investigate nimorazole (a hypoxic radiosensitizer) in TNM stage II-III NSCLC patients is presented. One of the trial aims is to validate (and ultimately qualify) [18F]FAZA PET, building on the thesis results. In summary, this thesis presents important new validation data for a range of therapeutic lung cancer biomarkers.
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Gray, Eoin. "Validating and updating lung cancer prediction models." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/19206/.
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Lung cancer is a global disease that affect millions of individuals worldwide. Additionally, the disease is beset with a poor 5-year survival rate, a direct consequence of a low early stage diagnosis rate. In an attempt to improve lung cancer prognosis, individuals at high risk of developing lung cancer should be identified for periodic screening. Prediction models are devised to predict an individual’s risk of developing a disease over a specified time period. These can be used to identify high risk individuals and be made publically available to allow individuals’ to be conscience of their own risk. While prediction models have multiple uses it is imperative the models demonstrate a good standard of performance consistently when reviewed. The project conducted a systematic review, analysing previously published lung cancer prediction models. The review identified that there had been inadequate reporting of the existing models and when these models have been validated this had not been consistent across different publications. As a consequence models have not been consistently considered as a selective screening tool. The project then validated the prediction models using datasets from the International Lung Cancer Consortium. The validation identified the leading models which will allow a more targeted focus on these models in future research. This could culminate in the model being implemented as a clinical utility. The final stage reviewed methods to update a single prediction model or aggregate multiple prediction models into a meta-model. A literature review identified and evaluated the different methods, discussing how different methods can be successful in different scenarios. The methods were also reviewed for their suitability updating selected lung cancer prediction models, and appropriate methods were identified. These were then applied to create updated lung cancer models which were validated to assess which methods were successful at improving the performance and robustness of lung cancer prediction models. As lung cancer research develops, particularly into researching genetic markers that may explain lung cancer risk, these factors could be incorporated into already successful prediction models using appropriate model updating methods that were identified in our research.
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Taylor, Fiona. "Biomarkers of lung cancer risk and progression." Thesis, University of Sheffield, 2019. http://etheses.whiterose.ac.uk/22855/.
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Lung cancer causes high mortality because most people present late with advanced disease that is not amenable to curative treatment. Screening high-risk groups with low dose CT imaging of the thorax has been shown to reduce lung cancer mortality by 20%, but at the cost of a high false positive rate. Population stratification with molecular biomarkers could improve the cost-benefit of lung cancer screening programmes and reduce false positives. Tumour cells shed DNA into the blood, enabling tumour-derived genetic alterations to be detected non-invasively by analysing circulating cell-free DNA (cfDNA). The aim of this study was to determine the screening and prognostic potential of total cfDNA levels and two genomic instability scores based on the detection of copy number aberrations in cfDNA samples of lung cancer cases and controls collected in the ReSoLuCENT study (A Resource for the Study of Lung Cancer Epidemiology in North Trent). Controls were identified as low or high risk for the development of lung cancer over five years using the Liverpool Lung Project risk model. CfDNA was extracted from the plasma of 52 untreated lung cancer cases, 32 high risk controls and 10 low risk controls and quantified total cfDNA levels by SYBR green real-time qPCR. Low coverage whole genome sequencing with Illumina HiSeq 2500 was completed for a subset of cases (N=62) and controls (N=40). Two published genomic instability scores were adapted and tested; the plasma genomic abnormality (PGA2) and the copy number aberration (CNA) score. Screening potential was evaluated by performing Receiver Operating Characteristic (ROC) curves to assess the ability of the test to discriminate between lung cancer cases and controls by calculating area under the curve (AUC). Logistic regression was used to further assess the ability of total cfDNA levels and genomic instability scores to predict case or control status. Prognostic value was determined by Kaplan Meir and Cox regression survival analyses. In this preliminary study, there was no difference in total cfDNA levels between early stage lung cancer cases and high risk controls. The PGA2 score was higher in high risk controls compared to lung cancer cases and was not further evaluated. In comparison, the CNA score had good discriminatory ability for high risk controls compared to all lung cancer cases (stage I-IV) with an AUC of 0.74 but poorer discriminatory ability for early stage cases (I-IIIA) with an AUC of 0.60. Although total cfDNA levels and CNA scores above the median value were associated with poor survival, both were statistically significant in univariable but not multivariable cox survival regression analyses. Therefore, total cfDNA levels and the CNA score had limited prognostic value when other factors were taken into account. Total cfDNA levels are not recommended as a screening tool because total levels lack specificity for cancer. The screening performance of the CNA score may be improved by targeting recurrent copy number aberrations and by combining the score with alternative tumour-derived genetic alterations in cfDNA such as point mutations or methylation changes.
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Forrest, Lynne Fiona. "Intervention-generated inequalities in lung cancer care." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2396.
Full textAbstract:
Lung cancer survival is poorer in more socio-economically deprived patient groups. It has been suggested that socio-economic inequalities in receipt of, and time to, treatment may contribute to inequalities in cancer outcome. Unintended variations in outcome that result from the way that interventions are organised and delivered have been described as intervention-generated inequalities. The aim of this thesis was to determine if there are socio-economic inequalities in lung cancer care and, if so, to identify where on the pathway of care these inequalities might occur: looking at receipt of treatment; referral, diagnostic and treatment time intervals; and survival. A systematic review and meta-analysis was conducted in order to examine the published evidence for socio-economic inequalities in lung cancer treatment. A secondary analysis of cancer registry data for 65,210 patients diagnosed between 1999-2010 with a primary diagnosis of lung cancer [ICD10 C33 and C34], linked to Hospital Episode Statistics and lung cancer audit data, was conducted. Logistic regression was used to examine the likelihood of receipt of treatment; of receiving timely referral, diagnosis and treatment within guidelines; and of being alive two years after diagnosis, by socio-economic position [SEP]. Cox regression was used to assess the likelihood of early referral, diagnosis and treatment and hazard of death, by SEP. Socio-economic inequalities in receipt of lung cancer surgery and chemotherapy, but not radiotherapy, were found in the systematic review and meta-analysis, and in the linked-data analysis. Socio-economic inequalities in the GP referral to first hospital appointment time interval were identified. Socio-economic inequalities in survival from lung cancer were statistically explained by socio-economic inequalities in receipt of treatment, but not by inequalities in timeliness of referral and treatment, in this cohort. However high levels of missing stage, performance status and co-morbidity data were a limitation. Research into the unexplained variance in treatment rates is required in order to develop interventions that address socio-economic inequalities in receipt of treatment and reduce socio-economic inequalities in survival.
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Macaulay, Valentine. "Growth regulation in small cell lung cancer." Thesis, Imperial College London, 1989. http://hdl.handle.net/10044/1/47547.
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Sinicropi-Yao, Sara Lu-Ming. "The Role of NOTCH1 in Lung Cancer." The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1522064811057979.
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Meikle, Claire K. "Platelet-Leukocyte Aggregation in Lung Cancer Patients." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco1555937904448281.
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Rupniewska, Ewa. "Targeting SRC family kinases in lung cancer." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9234.
Full textAbstract:
Lung cancer is the commonest cancer killer worldwide. This is mainly due to the rapid development of drug resistance and early metastatic dissemination of the disease. SRC family kinases (SFKs) are frequently over-expressed in various cancers and have been implicated in tumorigenesis through their ability to promote cancer cell proliferation, survival and invasiveness. Therefore, we sought to evaluate the involvement of SFKs in lung cancer biology and assess the possible therapeutic benefits of their inhibition, either alone or in combination with additional treatments. We demonstrate that SRC family kinases are over-expressed and activated in-vitro in a panel of lung cancer cell lines as compared to immortalised normal lung epithelial cells. SRC, FYN and LYN are expressed in a high proportion of lung cancer but not normal lung tissue sections. Furthermore, enhanced expression of LYN correlates with poor patients’ survival. Dasatinib is a novel SRC/ABL inhibitor which effectively blocks SFKs activity at nanomolar concentrations. Dasatinib reduces cell numbers in 10 out of 11 NSCLC cell lines tested, which correlates with a strong inhibition of DNA synthesis and cell proliferation, while apoptosis is moderately enhanced only in a few cell lines. Interestingly, dasatinib potently induces autophagy in all NSCLC cell lines tested. This appears to be a pro-survival mechanism as autophagy inhibition using chemical compounds or siRNA-mediated depletion of ATG5 sensitises NSCLC cells to dasatinib through enhanced apoptosis. Lastly, our results indicate that SFKs have both overlapping and isoform-specific functions in NSCLC cell biology, as demonstrated by the effects of siRNA-mediated knockdown of SRC, YES, FYN or LYN. Our results suggest that inhibition of SRC family kinases alone or in combination with autophagy inhibitors may be a beneficial therapeutic strategy in the management of lung cancer patients.
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Kvarnbrink, Samuel. "The importance og LRIG1 in lung cancer." Thesis, Umeå universitet, Onkologi, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-57834.
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Weber, Anika Maria. "Targeting ATM/ATR signalling in lung cancer." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:3117219f-5273-4dc7-9a28-c531c708663f.
Full textAbstract:
Cells respond to the induction of DNA damage with activation of the DNA damage response (DDR), a complex signalling network which orchestrates cell cycle arrest and DNA repair in order to maintain genomic stability and cell viability. Activation of these signalling pathways enables cancer cells to survive DNA damaging chemo- or radiotherapy and contributes to the development of therapy resistance. Therefore, components of the DDR have become attractive targets for chemo- or radiosensitisation. Furthermore, cancer cells frequently exhibit defects in certain DDR components and may, as a consequence, become highly dependent on remaining DDR pathways to survive DNA damage. Two apical mediators of the DDR are the serine/threonine protein kinases ATM and ATR. ATM is frequently mutated in non-small cell lung cancer (NSCLC), and defects in ATM may render the tumour cells dependent on ATR signalling for survival. In this study, we characterised the functional consequences of ATM mutations in NSCLC cell lines and established an immunohistochemistry-based assay to identify patients with loss of ATM expression. As a single agent, pharmacological ATR inhibition (ATRi) was selectively cytotoxic for cells deficient in both ATM and p53. Furthermore, ATRi in combination with either ATM or PARP inhibition selectively killed tumour cells with mutant p53. We show that following ATR inhibition, ATM and p53 perform critical cell cycle checkpoint functions, independently of each other. Our results suggest that while retained function in any of these pathways is sufficient to maintain cell viability, functional loss of ATM, ATR and p53 results in premature mitotic entry, chromosome fragmentation and mitotic catastrophe. We conclude that in NSCLC the functional status of both ATM and p53 determines the cellular response to ATR inhibition, and propose that a combination of ATR inhibition with ATM or PARP inhibition may have broad utility for the treatment of p53-mutated NSCLC.