Yu, Kai Shing. / "November 2010." / Thesis (M.Phil.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 103-114). / Abstracts in English and Chinese. / Abstract --- p.2 / 中文摘要 --- p.6 / List of Contents --- p.9 / List of Table --- p.12 / Abbreviation --- p.13 / Acknowledgement --- p.14 / Chapter Chapter 1: --- Introduction --- p.15 / Chapter 1.1 --- Epidemiology of lung cancer --- p.15 / Chapter 1.2 --- Overview of significant prognostic factors for patients with NSCLC --- p.18 / Chapter 1.2.1 --- Tumor related factors --- p.19 / Chapter 1.2.2 --- Patient related factors --- p.21 / Chapter 1.3 --- Overview of significant prognostic factors for SCLC patients --- p.22 / Chapter Chapter 2: --- Literature Review --- p.25 / Chapter 2.1 --- Prevalence of co-morbidity among lung cancer patients --- p.25 / Chapter 2.2 --- Impact of co-morbidity on non small cell lung cancer patients --- p.28 / Chapter 2.3 --- Impact of co-morbidity on small cell lung cancer patients --- p.36 / Chapter 2.4 --- Summary of evidence from literature review --- p.40 / Chapter Chapter 3: --- Aim and Objectives --- p.42 / Chapter 3.1 --- General aim --- p.42 / Chapter 3.2 --- Specific objectives --- p.42 / Chapter 3.3 --- Main hypothesis --- p.42 / Chapter Chapter 4: --- Methodology --- p.43 / Chapter 4.1 --- Research design --- p.43 / Chapter 4.2 --- Study population --- p.43 / Chapter 4.3 --- Sample size estimation --- p.45 / Chapter 4.4 --- Data collection --- p.47 / Chapter 4.4.1 --- Demographic information --- p.47 / Chapter 4.4.2 --- Co-morbidity --- p.51 / Chapter 4.4.3 --- Adverse symptoms --- p.51 / Chapter 4.4.4 --- Disease characteristics --- p.52 / Chapter 4.4.5 --- Baseline laboratory findings --- p.53 / Chapter 4.4.6 --- Treatment data --- p.53 / Chapter 4.4.7 --- Follow up --- p.53 / Chapter 4.5 --- Statistical analyses --- p.54 / Chapter Chapter 5: --- Results --- p.56 / Chapter 5.1 --- Description of cohort --- p.56 / Chapter 5.2 --- Baseline characteristics --- p.58 / Chapter 5.3 --- Symptom presentation --- p.62 / Chapter 5.4 --- Histological characteristics --- p.64 / Chapter 5.5 --- Treatment characteristics --- p.67 / Chapter 5.6 --- Haematological characteristics of study population --- p.69 / Chapter 5.7 --- Prevalence of co-morbidity --- p.71 / Chapter 5.8 --- Overall survival --- p.74 / Chapter 5.8.1 --- Univariate and multivariate survival analysis for SCLC patients --- p.75 / Chapter 5.8.2 --- Univariate and multivariate survival analysis for NSCLC patients --- p.77 / Chapter 5.8.3 --- In-depth analyses for the Impact of co-morbidity on lung cancer survival --- p.79 / Chapter 5.8.4 --- Selected underlying causes of death --- p.84 / Chapter Chapter 6: --- Discussion --- p.85 / Chapter 6.1 --- Prognostic factors --- p.85 / Chapter 6.2 --- Prevalence of co-morbidity --- p.89 / Chapter 6.3 --- Impact of co-morbidity on lung cancer survival --- p.92 / Chapter 6.4 --- Strengths and limitations of this study --- p.97 / Chapter Chapter 7: --- Conclusions --- p.101 / Chapter Chapter 8: --- Implications and Recommendations for medial practice --- p.102 / References --- p.103

Lin, Hualiang. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2011. / Includes bibliographical references (leaves 140-177). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.

Access to abstract permanently restricted to Ball State community only / Access to thesis permanently restricted to Ball State community only / Department of Chemistry

Lung cancer is one of the most important causes of 'avoidable deaths' globally and is responsible for approximately 900,000 deaths per year. However, lung cancer rates tend to be higher for males than for females and the disease also varies geographically, as rates are far higher in developed countries compared to developing countries. Scotland has the highest rate of lung cancer of any country where lung cancer data is available. However, explaining the spatial distribution of this disease is difficult because lung cancer has a number of known causes that operate at a range of different spatial scales. This is further complicated by the lag time between the period of exposure to a risk factor and the date of diagnosis. This thesis examines the causes of lung cancer across Scotland, using lung cancer registrations for the period 1988 to 1991. Exploratory methods are presented for examining the geographical distribution of the disease in small areas using methods of age-standardisation and cluster detection to identify areas with unusual rates. Estimates of the key risk factors potentially associated with lung cancer are calculated for the same small areas. These include estimates of smoking behaviour, air pollution levels in 1971 and 1991, radon gas potential, coal mining activity, quarrying activity and area deprivation. The risk factors are incorporated into a set of regression models to examine which factors are significant in explaining lung cancer incidence. Finally, the residual values derived from the optimum model of lung cancer incidence in Scotland are examined to identify areas where lung cancer incidence is particularly high and low. This study revealed that there were marked geographical differences in lung cancer rates, with higher rates in the large urban areas, especially Glasgow, and also the more deprived areas of Scotland. Smoking was consistently significant in explaining lung cancer incidence for all cohorts, types of lung cancer and urban-rural areas. The estimated air pollution levels in 1971 were also found to be significant, but the 1991 estimates were not. Exposure to radon was only significant in explaining lung cancer in the younger age groups. However, the coal mining and quarrying variables did not independently influence the incidence of the disease. Area deprivation and measure of urbanness both had a significant effect on lung cancer incidence in Scotland that was independent of the key risk factors. The analysis of the residual values showed that, having controlled for the key risk factors, lung cancer incidence is higher than expected in rural rather than urban areas.

Background: Providing unpaid care for a spouse, partner, relative or friend is a day-to-day reality. Carers in the context of cancer have a similar profile to carers in the UK. Lung Cancer is a low profile cancer but yet is the second most common cancer in Scotland associated with social deprivation, poverty, therapeutic nihilism, and stigma. The significant contribution by carers of people affected by cancer has resulted in their recognition as “partners in the delivery of care”.   Aim: To explore the experiences of the diagnosis and treatment of lung cancer from a carer’s perspective.   Methods: Unstructured interviews were undertaken with 15 carers of relatives with a lung cancer diagnosis. The individual with lung cancer identified carers. Data were analysed using a qualitative design and analysis in the grounded theory tradition.  Findings: Analysis of data from the carers indicated that whilst carers are engulfed by the cancer experience and face barriers and deficits of care, they have illustrated and demonstrated that they have their own assets, which are further enhanced by community and societal resources. Five categories were identified and a sense of carer resilience emerged. Subsequently the theory developed was fostering carer resilience in lung cancer care.     Discussion: Resilience emerged in carers at a time of increasing interest within the wider context of health and social care. Although resilience is not a new concept there are a lack of studies including carers in a cancer context and until now none in lung cancer. Resilience cannot and should not be fostered by one professional group and therefore an opportunity exists for collaboration between agencies involved in the provision of services for carers of relatives with cancer. The limitations of the study are acknowledged.   Conclusion: The findings from this study have implications for practice beyond healthcare and as Scotland embarks upon health and social care integration it is perhaps an opportune time to develop that. Findings highlighted the potential, strengths, interests, abilities and capacity of carers rather than their limitations. Future research could look specifically at resilience in carers of relatives with lung cancer in addition to testing interventions to enhance carers’ resilience.

Further studies were done to investigate the mechanism responsible for 1-BI-induced apoptosis in NCI-H460. It was found that 1-BI stimulated the expression of pro-apoptotic p53, Bax and cytosolic NF-kB p65 subunit but decreased pERK in NCI-H460 cells. The active forms of caspase 3 and caspase 9 were detected by Western blot, accompanied by an increase in caspase 3 activity. Reactive oxygen species (ROS) was highly generated at 24 hours after the treatment and the mitochondrial membrane potential was significantly decreased at 48 and 72 hours. The application of either N-acetyl cysteine (NAC) or glutathione (GSH) attenuated the cell growth inhibition caused by 1-BI. NCI-H460 cells pretreated with NAC showed a decrease in ROS production and p65 protein but an increase in pERK. / Taken together, these findings suggest that the inhibition of THXS suppresses lung cancer cell growth by promoting either G1 cell cycle arrest or apoptosis. The status of p53 is critical for both cell cycle arrest and apoptosis in 1-BI-mediated growth inhibition, which is evident by enhanced apoptosis detected in p53-transfected NCI-H23 and DMS 114 cells and G1 cell cycle in lung cancer cells treated with PFT-alpha. The 1-BI-induced growth-inhibitory pathway is associated with the generation of ROS, alteration of mitochondrial membrane potential, down-regulation of pERK and p65. / The result showed that THXS expressed in all of the three lung cancer cell lines (NCI-H23, DMS 114 and NCI-H460). The activity of THXS was also reflected by the presence of THXS metabolite thromobxane B2 (TXB2) in the cells, which was detected by ELISA. 1-Benzylimidazole (1-BI), a specific THXS inhibitor, suppressed the lung cancer cell proliferation measured by MTT assay. 1-BI treatment caused G1 phase arrest and enhanced the level of cyclin dependent kinase inhibitor p27 in a time-dependent manner in NCI-H23 and DMS 114 cells. It markedly increased DNA fragmentation in NCI-H460 cells. The findings suggest that 1-BI inhibits cell growth by arresting cell cycle and inducing cell death. Annexin V/PI staining revealed that the cell death induced by I-BI was mainly in the format of apoptosis. Further experiments showed that the I-BI-induced apoptosis could be enhanced by the introduction of p53 into NCI-H23 and DMS 114 cells, and such enhancement was associated with a decrease in mitochondrial membrane potential. This result suggests that the p53 may play a positive role in apoptosis induced by 1-BI through changing of the mitochondrial membrane potential. The role of p53 in I-BI-mediated apoptosis was further confirmed by the experiment of the p53 inhibition. Pifithrin-alpha hydrobromide (PFT-alpha), a p53 specific inhibitor, suppressed the 1-BI-induced p53 protein expression and increased G1 cell cycle arrest. / Thromboxane A2 (TXA2) is a potent arachidonate metabolite in the cyclooxygenase-2 (COX-2) pathway, which is produced by a member of cytochrome P450 (CYP) superfamily called thromboxane synthase (THXS). Recent studies have showed that thromboxane and THXS are associated with cancer cell migration, angiogenesis, tumor metastasis and cancer proliferation but there is limited information on their role in lung cancer development. This thesis is to test the hypothesis that inhibition of THXS could alter lung cancer cell growth. / Leung, Kin Chung. / Adviser: George G. Chen. / Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3319. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 130-144). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

In conclusion, our study has demonstrated that TGZ, a synthetic PPARgamma ligand, inhibits lung cancer cells growth through cell-cycle arrest, increased cell differentiation and induction of apoptosis. In this pathway, the activation of ERK by TGZ plays a central role in promoting apoptosis, which appears to be mediated via a mitochondria-related mechanism and functions in a PPARgamma-dependent manner. The interaction between PPARgamma and ERK may create an auto-regulatory and positive feedback loop to enhance the effect of ERK whereas the activation of Akt may generate a negative regulation to control the degree of apoptosis occurred in lung cancer cells. TGZ may counteract NNK function to inhibit lung cancer cell growth in the PPARgamma-dependent manner. / Lung cancer is the world's leading cause of cancer death. Currently there is not an acceptable adjuvant or palliative treatment modalities that have been conclusively shown to prolong survival in lung cancer. Therefore, translational research to improve outcomes with this disease is critical. Peroxisome proliferator-activated receptor-gamma (PPARgamma) is a member of the nuclear hormone receptor superfamily of ligand-activated transcription. PPARgamma ligands have been demonstrated to inhibit growth of cancer cells. The role of the PPARgamma in cell differentiation, cell cycle arrest and apoptosis has attracted increasing attention. Our study focused on the role of PPARgamma and its ligand troglitazone (TGZ) in the cell death of human lung cancer and the interaction between PPARgamma system and 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a major tobacco-specific carcinogen. / The epidemic of lung cancer is directly attributable to cigarette. However, it is still not completely known the molecular pathway of cigarette smoking in the pathogenesis of lung cancer. Among the carcinogenoic chemicals of cigarette smoking, 4-(N-Methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is the most potent, which induces lung cancer in all animal species tested. Unlike PPARgamma ligands, NNK can promote cell proliferationa and growth. It is interesting to know whether PPARgamma ligands can inhibit the growth-promoting function of NNK. To address this question, we used NCI-H23 lung cancer cells as the model to study how TGZ influenced the function of NNK. Results showed that NNK stimulated cell proliferation, induced the DNA binding activity of nuclear factor-kappaB (NF-kappaB), down-regulated Bad expression, and up-regulated PPARgamma protein expressions. Inhibition of NF-kappaB nuclear translocation led to the suppression of NNK-mediated Bad expression, indicating that NNK may regulate Bad expression through the activation of NF-kappaB. TGZ significantly inhibited cell proliferation induced by NNK. Though TGZ did not affect nuclear factor-kappaB (NF-kappaB) activity, it up-regulated Bad expression. Taken together, TGZ can efficiently inhibit the proliferation of lung cancer cells induced by NNK via Bad- and PPARgamma- related pathways, which may not be directly relevant to the activity of NF-kappaB. / To elucidate the mechanism responsible for the effect of PPARgamma and TGZ on lung cancer cells, we further studied the PPARgamma molecular pathway in NCIH23 treated by TGZ. The result demonstrated that TGZ induced PPARgamma and ERK1/2 accumulation in the nucleus, where the co-localization of both proteins was found. It showed that the activation of ERK1/2 resulted in apoptosis via the mitochondrial pathway, reflecting by reduction of mitochondria membrane potential, change in Bcl-2 family members, release of cytochrome c into cytosol, and activation of caspase 9. Both PPARgamma siRNA and U0126, a specific inhibitor of ERK1/2, were able to block these effects of TGZ, suggesting that apoptosis induced by TGZ was PPARgamma- and ERK1/2-dependent. Inhibition of ERK1/2 by U0126 also led to a significant decrease in the level of PPARgamma, indicating that there was probably a positive cross-talk between PPARgamma and ERK 1/2 or an auto-regulatory feedback mechanism to amplify the effect of ERK1/2 on cell growth arrest and apoptosis. In addition to ERK1/2, TGZ also activated Akt. Interestingly, inhibition of ERK1/2 prevented the activation of Akt whereas suppression of Akt had no effect on ERK1/2, suggesting that Akt was not necessary for TGZ-PPARgamma-ERK pathway. However, the inhibition of Akt promoted the release of cytochrome c. Thus, the activation of Akt may have a negative effect on apoptosis induced by TGZ. Wortmannin, a PI3K inhibitor, inhibited TGZ-induced ERK1/2 and Akt activation, indicating that PI3K may function at the up-stream of ERK and Akt. In conclusion, our study has demonstrated that TGZ induced apoptosis in NCI-H23 lung cancer cells via a mitochondrial pathway and this pathway was PPARgamma-and ERK1/2-dependent. / We first investigated the effect of PPARgamma ligand TGZ on two human lung cancer cells (NCI-H23 and CRL-2066) and one human lung normal cell (CCL-202). The results showed that in consistence with the loss of cell viability, TGZ induced apoptosis in CRL-2066 and NCI-H23 cells but not in CCL-202 cells. TGZ up-regulated PPARgamma expression in all these three lung cell lines, especially in the cancer cells. In association of the time-dependent inhibition of the cell proliferation, TGZ down-regulated the expression of Bcl-w and Bcl-2 but activated ERK1/2 and p38, suggesting that the growth-inhibitory effect of TGZ is associated with the reduction of Bcl-w and Bcl-2 and the increase of ERK1/2 and p38 activation. SAPK/JNK activation assay showed a decreased activity in all these three cell lines treated by TGZ. It was also demonstrated that TGZ was able to activate PPARgamma transcriptionally. We conclude that TGZ inhibits the growth of human lung cancer cells via the induction of apoptosis, at least in part, in a PPARgamma-relevant manner. / Li Mingyue. / "June 2006." / Advisers: George Gong Chen; Anthony Ping Chuen Yim. / Source: Dissertation Abstracts International, Volume: 67-11, Section: B, page: 6202. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2006. / Includes bibliographical references (p. 174-207). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstracts in English and Chinese. / School code: 1307.

Yung, Kam Fai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2009. / Includes bibliographical references (leaves 107-129). / Abstracts in English and Chinese. / ABSTRACT --- p.ii / 摘要 --- p.iv / ACKNOWLEDGEMENTS --- p.vi / TABLE OF CONTENTS --- p.vii / PUBLICATION --- p.ix / LIST OF TABLES --- p.x / LIST OF FIGURES --- p.xi / LIST OF ABBREVIATIONS --- p.xii / Chapter SECTION I: --- BACKGROUND --- p.1 / Chapter CHAPTER 1: --- "The biology, diagnostics and management of lung cancer" --- p.2 / Chapter 1.1 --- "Basic biology, classification and diagnostics" --- p.2 / Chapter 1.1.1 --- Epidemiology and etiology of lung cancer --- p.2 / Chapter 1.1.2 --- Clinical Presentation and Diagnostics of Lung Cancer --- p.3 / Chapter 1.2 --- Treatment of lung cancer --- p.9 / Chapter 1.2.2 --- Radiotherapy --- p.10 / Chapter 1.2.3 --- Chemotherapy --- p.11 / Chapter CHAPTER 2: --- Epidermal Growth Factor Receptor Mutations in Lung Cancer --- p.13 / Chapter 2.1 --- The Epidermal Growth Factor Receptor --- p.13 / Chapter 2.2 --- Overexpression of EGFR in NSCLC --- p.14 / Chapter 2.3 --- The development of EGFR inhibitors --- p.15 / Chapter 2.3.1 --- Monoclonal Antibodies --- p.16 / Chapter 2.3.2 --- Small-molecule inhibitors --- p.17 / Chapter 2.3.2.1 --- Gefitinib --- p.17 / Chapter 2.3.2.2 --- Erlotinib --- p.19 / Chapter 2.3.2.3 --- Other small-molecule inhibitors --- p.20 / Chapter 2.4 --- Mutations of EGFR in NSCLC --- p.21 / Chapter 2.4.1 --- Activating Mutations conferring sensitivity to tyrosine kinase inhibitors --- p.21 / Chapter 2.4.2 --- Secondary mutations associated with resistance to tyrosine kinase inhibitors --- p.23 / Chapter 2.5 --- EGFR gene amplification --- p.24 / Chapter 2.6 --- Detection of EGFR mutations --- p.25 / Chapter 2.7 --- Aim of the thesis --- p.31 / Chapter SECTION II: --- DETECTION OF EGFR MUTATIONS IN TUMOR AND PLASMA SAMPLES BY MASS SPECTROMETRY AND DIGITAL PCR --- p.33 / Chapter CHAPTER 3: --- Detection of EGFR mutations by mass spectrometric methods --- p.34 / Chapter 3.1 --- Introduction --- p.34 / Chapter 3.1.1 --- Principles of Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) --- p.34 / Chapter 3.1.2 --- The MassARRAY Homogenous MassEXTEND (hME) assay --- p.35 / Chapter 3.1.3 --- The Single-Allele Base Extension Reaction (SABER) and the Allele-Specific Base Extension Reaction (ASBER) --- p.36 / Chapter 3.2 --- Materials and Methods --- p.36 / Chapter 3.2.1 --- The protocol for the detection of EGFR exon 21 point mutation by Mass Spectrometric Methods --- p.37 / Chapter 3.3 --- Results --- p.42 / Chapter 3.4 --- Discussion --- p.49 / Chapter CHAPTER 4: --- Evaluation of the detection limit and sensitivity of the digital PCR assays --- p.51 / Chapter 4.1 --- Introduction --- p.51 / Chapter 4.1.1 --- The theoretical basis of digital PCR quantification and the relationship with the Poisson distribution --- p.51 / Chapter 4.1.2 --- Assessment of Assay Detection Limit --- p.54 / Chapter 4.1.3 --- Comparing Digital PCR with sequencing after conformation sensitive gel electrophoresis (CSGE) --- p.59 / Chapter 4.2 --- Materials and Methods --- p.59 / Chapter 4.2.1 --- Design of digital PCR assay for the detection of EGFR exon21 L858R point mutation --- p.59 / Chapter 4.2.2 --- Design of digital PCR assay for the detection of EGFR exon19 deletion --- p.60 / Chapter 4.2.3 --- The protocols of digital PCR assays for EGFR mutation detection --- p.64 / Chapter 4.2.4 --- Single molecule detection test --- p.65 / Chapter 4.2.5 --- Artificial mixtures of mutant and wild-type DNA --- p.66 / Chapter 4.2.6 --- Sequencing after CSGE --- p.66 / Chapter 4.3 --- Results --- p.67 / Chapter 4.3.1 --- Results of the single molecule detection test and artificial mixture analysis --- p.67 / Chapter 4.3.2 --- Results of CSGE and sequencing compared with digital PCR --- p.73 / Chapter 4.4 --- Discussion --- p.75 / Chapter CHAPTER 5: --- Detection of EGFR mutations in prospectively collected tumor samples of NSCLC patients --- p.77 / Chapter 5.1 --- Introduction --- p.77 / Chapter 5.2 --- Materials and Methods --- p.78 / Chapter 5.2.1 --- Sample preparation and DNA extraction of tumor tissues --- p.78 / Chapter 5.3 --- Results --- p.79 / Chapter 5.4 --- Discussion --- p.82 / Chapter CHAPTER 6: --- Detection of EGFR mutations in prospectively collected plasma samples of NSCLC patients --- p.85 / Chapter 6.1 --- Introduction --- p.85 / Chapter 6.2 --- Materials and Methods --- p.87 / Chapter 6.2.1 --- Sample preparation and DNA extraction of plasma samples --- p.87 / Chapter 6.3 --- Results --- p.88 / Chapter 6.3.1 --- Digital PCR analysis of EGFR mutations in plasma samples of NSCLC patient --- p.88 / Chapter 6.3.2 --- Variations in plasma EGFR mutation concentration after TKI treatment --- p.93 / Chapter 6.4 --- Discussion --- p.96 / Chapter SECTION III: --- CONCLUDING REMARKS --- p.100 / Chapter CHAPTER 7: --- Conclusion and future perspectives --- p.101 / Chapter 7.1 --- Mass spectrometric analysis --- p.101 / Chapter 7.2 --- Microfluidics Digital PCR --- p.102 / Chapter 7.3 --- Future perspectives --- p.105 / References --- p.107

Orientador: Daniele Cristina Cataneo / Resumo: Objetivo: Comparar características epidemiológicas dos pacientes com diagnóstico de carcinoma broncogênico submetidos a tratamento cirúrgico com aqueles inoperáveis ao diagnóstico, identificar os fatores que levaram ao diagnóstico tardio e propor um novo protocolo de diagnóstico rastreamento. Métodos: estudo observacional retrospectivo, através de coleta de dados de prontuários de pacientes com diagnóstico de carcinoma broncogênico atendidos entre 2005 e 2018. Foram coletados dados clínicos, de exames laboratoriais, exames de imagem e terapêutica instituída. A amostra foi submetida análise descritiva de frequências. Em seguida foi dividida em dois grupos: operado e não operado, que foram comparados utilizando teste do qui quadrado e teste t, considerando significativo p < 0,05. As variáveis foram comparadas com a sobrevida utilizando os testes citados e o método de Kaplan-Meier para obtenção das curvas de sobrevida. Resultados: foram avaliados 230 pacientes com diagnóstico tomográfico ou anátomo-patológico de carcinoma broncogênico, tendo mais de 50% da amostra estadio avançado. Apenas 42 pacientes apresentavam doença operável ao diagnóstico. Nos dois grupos a massa pulmonar ao diagnóstico foi o achado de imagem mais frequente, visível na radiografia simples. No grupo inoperável, houve maior prevalência de sintomas e alterações laboratoriais associadas. A sobrevida foi impactada de forma negativa por alterações laboratoriais, tamanho do tumor e pior pontuação nos scores de pe... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Objective: to compare patients diagnosed with bronchogenic carcinoma who underwent surgical resection and those with inoperable disease at diagnosis, to identify factors leading to late diagnosis and to suggest a new diagnosis and screening protocol. Method: retrospective observational study, through data available in medical records from patients diagnosed with bronchogenic carcinoma between 2005 and 2018. We collected data regarding clinical features, laboratory exams, imaging exams and treatment. Data was analyzed using descriptive statistics and frequency distributions. Patients were also divided into two groups: operable and inoperable, and comparisons between these groups were made using Chi-square test and Student’s t test. We considered the differences significant when p < 0,05. All variables were compared to survival using the same tests and through the Kaplan-Meier Method. Results: we evaluated 230 patients who had tomographic or pathological diagnosis of bronchogenic carcinoma. More than 50% of the patients were in advanced stages of the disease, and only 42 patients had operable disease when diagnosed. In both groups, pulmonary mass was the most frequent alteration at diagnosis, and all were visible in chest radiograph. Among the patients in the inoperable group, symptoms and altered laboratory exams were more frequent. Presence of laboratory alterations, dyspnea, tumor size and worse punctuation in performance scores resulted in lower survival rates. Conclusion: ... (Complete abstract click electronic access below) / Mestre

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