The Open Lung Cancer Journal最新文献

{"title":"Elderly Patients with Advanced Non-Small Cell Lung Cancer: What Treatment?","authors":"A. Rossi","doi":"10.2174/1876819901104010004","DOIUrl":"https://doi.org/10.2174/1876819901104010004","url":null,"abstract":"Advanced non-small cell lung cancer (NSCLC) in elderly patients is an increasingly common problem which the practitioner of oncology must face. There is no consensus on the cut-off age for defining the elderly. However, 70 years may be the most appropriate because the incidence of age-related changes starts to increase after this boundary. Important concerns in evaluating the treatment of elderly patients are the presence of comorbidities and the progressive physiologic reduction of hepatic, renal and bone-marrow functions which could have a negative impact on the degree of toxicity. To individualize treatment choice within a group of elderly NSCLC patients of the same chronological age, it would be important to perform a comprehensive geriatric assessment (CGA) which would allow to subdivide elderly patients into three main categories: fit, pre-frail and frail. Fit older patients have similar prognosis and a similar treatment tolerance and outcome compared to their younger counterparts. On the other hand, pre-frail patients experience significant treatment related toxicity and usually are offered a single-agent chemotherapy whose choice should take into account the expected toxicity profile of the agent, pharmacokinetics, organ function and co-morbidities. For the third category of patients only best supportive care or individualized approaches are recommended. Overall, only prospective trials, specifically addressed to elderly NSCLC patients selected through an adequate CGA at baseline, let us opt for the best treatment to be administered to each elderly patient.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"4 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2011-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129377473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pulmonary Endothelial Impairment During Gefitinib Therapy: A Preliminary Assessment with Iodine-123-Metaiodobenzylguanidine (123IMIBG) Scintigraphy","authors":"T. Koizumi, Kazuhisa Urushihata, T. Fujii, K. Kubo","doi":"10.2174/1876819901104010001","DOIUrl":"https://doi.org/10.2174/1876819901104010001","url":null,"abstract":"Iodine-123-metaiodobenzylguanidine ( 123 I-MIBG) kinetics in the lung could serve as a novel diagnostic tool to evaluate endothelial damage. Interstitial lung disease (ILD) associated with gefitinib, an epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI), has been reported as a serious adverse effect. This study was performed to examine the possibility that gefitinib induces pulmonary endothelial damage. Serial 123 I-MIBG scintigraphy was performed in 5 patients with non-small cell lung cancer before and one month after initiation of gefitinib treatment. Anterior planar images were acquired 15 min after injection of 123 I-MIBG and the total lung to upper mediastinum ratio (L/M) was calculated in both lungs. None of the patients developed ILD during the study. There were no significant differences in the values of L/M before and after gefitinib therapy. These findings suggest that gefitinib has little influence on the pulmonary endothelium in patients with no signs of ILD.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"2 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2011-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125453950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circulating DNA as a Biomarker for Early Detection of Cancer: A Brief Update with an Emphasis on Lung Cancer~!2010-06-09~!2010-08-03~!2010-09-06~!","authors":"R. E. Cabral","doi":"10.2174/1876819901003010038","DOIUrl":"https://doi.org/10.2174/1876819901003010038","url":null,"abstract":"In most cases, early detection and treatment of cancer are prerequisites for full recovery. However, its early detection continues to be extremely difficult since its characteristic symptoms rarely manifest at the onset of disease. The development of highly sensitive, specific biomarkers also capable of reflecting pathological changes is, therefore, of the upmost importance. Lung cancer, for example, is most frequently diagnosed during the late metastatic stage so that, as a result, malignant neoplasms in the lung are among the leading causes of cancer-related deaths worldwide. Circulating DNA is a non-invasive diagnostic assay that has been greatly improved for the purposes of diagnosis, prognosis, and treatment of cancer. In the current review, we discuss recent data concerning circulating tumor-derived DNA as a tool for early detection, diagnosis, and follow-up. Given the scope of this review, the focus will be on lung cancer, one of the most prolific and lethal cancers affecting humanity today.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"90 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121507945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anemia in Elderly Sudanese Lung Cancer Patients Treated with Chemotherapy~!2010-05-06~!2010-06-28~!2010-07-20~!","authors":"F. Hassan","doi":"10.2174/1876819901003010034","DOIUrl":"https://doi.org/10.2174/1876819901003010034","url":null,"abstract":"Statistical Analysis: Analysis of data obtained by independent sample test (t-test) was performed for equality of these mean probability value. Results: Prior treatment pre cycle I; 56.2% of patients were normal, 38.8% with mild anemia and 5.0% were had a moderate anemia. Post cycle I treatment; the normal were declined to only 9.0% and mild anemia were the highest percentage 55% followed by 28.5% for moderate anemia and 7.5% showed severe anemia. Post cycle II about 27.5% of patient showed normal hemoglobin while the majority of them 72.5% had moderate anemia. Conclusion: A correlation of hemoglobin values after completion of therapy to overall treatment was found as a decline in range of (1 to 2 g/dl). Anemia has been demonstrated to be a predictive indicator of response to chemo radiotherapy in lung tumors.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114206180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adjuvant Platinum-Based Chemotherapy vs Observation in Non-Small Cell Lung Cancer: Meta-analysis of Trials with Intermediate- and Long-Term Follow-Up","authors":"E. Ibrahim, J. Zekri, H. Abdelrahman","doi":"10.2174/1876819901003010017","DOIUrl":"https://doi.org/10.2174/1876819901003010017","url":null,"abstract":"","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"56 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123924035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Study of Lung Epithelial Atypia in Regard to the Effect of Smoking and Traffic-Related Air Pollution in Sudan","authors":"H. Ahmed, Twhida Mahdi Rezgalla","doi":"10.2174/1876819901003010010","DOIUrl":"https://doi.org/10.2174/1876819901003010010","url":null,"abstract":"Background: Lung cancer risk in association with smoking was well established, but its association with traffic- related air pollution still unclear. To determine the relationship between exposure to smoking and air pollutants and lung epithelial atypia, we assessed using cytological method; cytological changes in sputum specimens. Methods: Sputum specimens were obtained from 300 apparently healthy volunteers, living in the city of Khartoum. Of the 300 study subjects, 150 were Traffic policemen (they were exposed to traffic-related air pollution (ascertained as Cases)) and 150 were non-exposed (ascertained as Controls). Results: Dysplasia was detected in nine individuals, of whom seven were cases and two were controls. All the nine individuals with dysplasia were smokers. Consequently, the risk of dysplasia associated with smoking was found to be statistically significant (P<0.02). Notably, there were 84 individuals with metaplasia, of whom, 58(69%) were identified among cases and the remaining 26(31%) were among controls. As a result, the risk of metaplasia associated with smoking and traffic-related air pollution was found to be statistically significant (P<0.001). In respect to the duration of exposure to traffic-related-air pollution among cases, metaplasia increases with the increasing of exposure (P<0001). Conclusion: Exposure to traffic was also associated with borderline elevated risks for developing dysplasia and high risks of development of metaplasia. Sputum cytology may provide a useful method in the assessment of lung atypical changes.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"18 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132865471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence for Epigenetic Changes in the Estrogen Receptor Alpha Promoter in Lymphangioleiomyomatosis (LAM)~!2010-01-05~!2010-03-12~!2010-05-11~!","authors":"D. Noonan, D. Lou","doi":"10.2174/1876819901003010001","DOIUrl":"https://doi.org/10.2174/1876819901003010001","url":null,"abstract":"Lymphangioleiomyomatosis (LAM) is a rare but often fatal disease, characterized by the abnormal proliferation of smooth muscle cells of the lung. LAM occurs almost exclusively in women and its pathology correlates with mutations in the tuberous sclerosis complex 2 (TSC2) gene and expression of the hormone estrogen. One of the hallmarks of LAM lesions is the anomalous expression of the intracellular receptor for estrogens, ER , and the distinct gender specificity of LAM would support the hypothesis that this anomalous expression of ER plays an essential role in the pathology of the disease. Our previous studies have defined a direct link between the TSC2 gene product tuberin and estrogen signaling through ER . The objectives of this study were to investigate epigenetic changes in the ER promoter as a mechanism for upregulation of ER expression in LAM disease. The results of this study provide evidence for: a) use of multiple ER promoters in human airway smooth muscle cells and LAM- associated cell lines, b) epigenetic changes in the promoter of the ER gene in LAM-associated cell lines and LAM lesions, and c) differential binding of histone deacetylase 1 and methyl-CpG binding proteins in human airway smooth muscle and LAM cells. These studies cumulatively suggest the upregulation of ER expression associated with LAM disease may in part be a consequence of demethylation at the ER promoter.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"68 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2010-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132794648","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Adaptation of Lung Tumor Cell Lines with Increasing Concentrations of Nitric Oxide Donor","authors":"J. Radosevich, K. Elseth, B. Vesper, G. Tarján, G. Kenneth, Haines Iii","doi":"10.2174/1876819900902010035","DOIUrl":"https://doi.org/10.2174/1876819900902010035","url":null,"abstract":"The free radical nitric oxide (NO) is known to play an important role in the biology of human cancers, including lung cancer. However, it is still not clear how elevated amounts of nitric oxide affect tumor development and propagation. Herein we develop an in vitro model system to study these effects in lung tumor cells. Two cell lines—one human lung adenocarcinoma (A549) and one mouse adenocarcinoma (LP07) cell line—were adaptively grown in increasing concentrations of the NO donor DETA-NONOate over several months. Both cell lines were successfully adapted to high levels of NO (HNO). Experiments validated the adaptation occurred as a result of the exogenous NO produced by the DETA-NONOate, and was not merely a response to the chemical composition of DETA-NONOate. No morphological differences were observed between cells that were adapted to the HNO and cells which did not undergo the adaptation process (i.e., \"parent cells\"). Parent cells were unable to survive when placed directly in media containing high levels of DETA-NONOate, suggesting that the adapted cells underwent a biological change enabling them to survive and grow in a HNO environment. The adapted cells were found to grow faster than the parent cells under both normal growth conditions and stressful growth conditions (serum-less media, growth on soft agar) even when the DETA-NONOate was removed from the HNO culture media. These adapted cell lines can serve as a novel tool for use in future experiments designed to better understand the role nitric oxide plays in lung cancer.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"36 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127572141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenoid Cystic Carcinoma (ACC) of the Tracheo-Bronchial Tree Treated with Laser Therapy and Irradiation: Report of Two Cases","authors":"G. Lay, M. Amichetti, M. Dessì, S. Orrù, R. Versace","doi":"10.2174/1876819900902010031","DOIUrl":"https://doi.org/10.2174/1876819900902010031","url":null,"abstract":"Adenoid cystic carcinoma (ACC) of the tracheo-bronchial tree is an uncommon tumor. ACC is generally diagnosed as a lesion involving the trachea; endobronchial involvement is extremely rare. At present, surgical resection and reconstruction followed or not by post-operative irradiation is considered as the therapy of choice for definitive cure. Endoscopic treatment of these tumors is uncommonly reported in the literature. We report two cases of ACC of the tracheo-bronchial tree successfully treated by laser and post-operative irradiation.","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"121620606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Theoretical Approach to the Deposition of Cancer-Inducing Asbestos Fibers in the Human Respiratory Tract","authors":"R. Sturm","doi":"10.2174/1876819900902010001","DOIUrl":"https://doi.org/10.2174/1876819900902010001","url":null,"abstract":"In the study presented here a stochastic model predicting the deposition of variably shaped asbestos fibers in the human respiratory tract is introduced. Deposition calculations are commonly based on the concept of the aerodynamic diameter. Besides Brownian diffusion, inertial impaction, and sedimentation, also interception representing the capture of particles at the carinal ridges of single airway bifurcations is considered as main deposition mechanism for the computa- tion of regional and local deposition fractions. Concerning total deposition in the human respiratory tract, fibers with a cy- lindrical diameter, termed dp, smaller than 0.1 � m exhibit lower deposition fractions than comparable spheres, whilst fi- bers with dp greater than 0.1 � m show higher deposition fractions than spheres. The fiber aspect ratiohas only an insig- nificant influence on total deposition, i.e. total deposition fractions of fibers with � = 10 and � = 100 differ by 2 to 10 %. Regarding regional deposition, the fiber diameter represents a controlling factor insofar, as fibrous particles with dp = 0.1 � m are preferably deposited in the bronchioles and alveoli, whereas fibers with dp = 10 � m are exclusively accumulated in the extrathoracic region. Only deposition behavior of fibers with dp = 1 � m is more complex, since valuable particle frac- tions deposit in all compartments of the lungs. Local (i.e. generation-by-generation) deposition of fibrous particles is char- acterized by a deposition peak at airway generation 19 in the case of fibers with dp = 0.1 � m. The deposition maximum is subject to a continuous dislocation towards more proximal airway generations with increasing dp. Therefore, particles with dp = 10 � m are chiefly deposited in the first three bronchial airway generations. Differences of fiber deposition between sitting and light-work breathing conditions may be evaluated is insignificant in most cases. Only fibrous particles with dp = 1 � m significantly change their deposition behavior with increasing inhalative flow rate in the way that proximal depo- sition is remarkably enhanced at the cost of bronchiolar and alveolar deposition. In general, any increase of the inhalative flow rate Q causes a successive dislocation of fiber deposition from distal to proximal compartments of the human respi- ratory tract. The results obtained from the theoretical approach lead to the conclusion that thin fibers with variable length tend to deposit in the pulmonary region of the lung, where they represent a remarkable hazard for mesothelioma. Thick fi- bers are preferentially accumulated in the proximal bronchi and therefore may induce bronchial lung cancer (adenocarci- noma).","PeriodicalId":108490,"journal":{"name":"The Open Lung Cancer Journal","volume":"66 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2009-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"117011284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}