| 61. |
- Van der Heyden, J H A, et al.
(författare)
-
Socioeconomic inequalities in lung cancer mortality in 16 European populations.
- 2009
-
Ingår i: Lung Cancer. - : Elsevier BV. - 0169-5002 .- 1872-8332. ; 63:3, s. 322-330
-
Tidskriftsartikel (refereegranskat)abstract
- Important socioeconomic inequalities exist in lung cancer mortality in Europe. They are consistent with the geographical spread of the smoking epidemic. In the next decades socioeconomic inequalities in lung cancer mortality are likely to persist and even increase among women. In Southern European countries we may expect a reversal from a positive to a negative association between socioeconomic status and lung cancer mortality. Continuous efforts are necessary to tackle socioeconomic inequalities in lung cancer mortality in all European countries.
|
|
| 62. |
- Willén, Linda, 1979-, et al.
(författare)
-
Educational level and management and outcomes in non-small cell lung cancer. A nationwide population-based study
- 2019
-
Ingår i: Lung Cancer. - : ELSEVIER IRELAND LTD. - 0169-5002 .- 1872-8332. ; 131, s. 40-46
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives: We examined associations between educational level and clinical presentation, patterns of management and mortality in patients with non-small cell lung cancer (NSCLC) in Sweden, a country with a National Health Care System. Materials and Methods: We identified 39,671 patients with a NSCLC diagnosis 2002-2016 in Lung Cancer Data Base Sweden (LCBaSe), a population-based research database. In analyses adjusted for comorbidity and other prognostic factors, odds Ratios (OR) and hazard Ratios (HR) were estimated to examine associations between patients' educational level and aspects of management and mortality. Results: Stage at diagnosis and waiting times did not differ between educational groups. In multivariable analysis, the likelihood to undergo PET/CT and assessment in a multidisciplinary team setting were higher in patients with high compared to low education (aOR 1.14; CI 1.05-1.23 and aOR 1.22; CI 1.14-1.32, respectively). In patients with early stage IA-IIB disease, the likelihood to undergo stereotactic radiotherapy was elevated in patients with high education (aOR 1.40; CI 1.03-1.91). Both all-cause (aHR 0.86; CI 0.77-0.92) and cause specific mortality (aHR 0.83; CI 0.74-0.92) was lower in patients with high compared to low education in early stage disease (IA-IIB). In higher stage NSCLC no differences were observed. Patterns were similar in separate assessments stratified by sex and histopathology. Conclusions: While stage at diagnosis and waiting times did not differ between educational groups, we found socioeconomic differences in diagnostic intensity, multidisciplinary team assessment, stereotactic radiotherapy and mortality in patients with NSCLC. These findings may in part reflect social gradients in implementation and use of novel diagnostic and treatment modalities. Our findings underscore the need for improved adherence to national guidelines.
|
|
| 63. |
- Winkler, Volker, et al.
(författare)
-
Predicting lung cancer deaths from smoking prevalence data
- 2011
-
Ingår i: Lung Cancer. - Clare : Elsevier. - 0169-5002 .- 1872-8332. ; 74:2, s. 170-177
-
Tidskriftsartikel (refereegranskat)abstract
- Reliable data on lung cancer burden is not available from most developing countries as cancer registration is lacking. In a previously proposed model to estimate lung cancer deaths in those countries using smoking prevalence data, we estimated the current yearly number of lung cancer deaths in Ethiopia as 3356, a figure far above the WHO estimate of 1343 and the GLOBOCAN of 748. Our aim was to further develop and validate our estimation procedure. We included additional data on risk estimates for lung cancer mortality of ex-smokers and an approximation of duration of smoking into our model and reanalysed study results on non-smoker mortality, thus building two improved models. For validation the number of lung cancer deaths in Germany (2006), the UK (2006), Canada (2004), and Utah, USA (2000) were estimated based on all three models and compared to the observed number of deaths in these countries. We found that the refined model with a modified estimate of lung cancer mortality rates in non-smokers and a more detailed incorporation of smoking dose categories estimates rather well the observed lung cancer deaths in the above countries. With this model, the updated estimate of yearly lung cancer deaths in Ethiopia is 2946 deaths, close to the previous reported estimate. If Ethiopian lung cancer mortality rates in never-smokers and smoking relative risks are the same as in industrialised countries, our models suggests that WHO lung cancer deaths may be underestimated in Ethiopia.
|
|
| 64. |
|
|
| 65. |
|
|
| 66. |
|
|
| 67. |
|
|
| 68. |
|
|
| 69. |
|
|
| 70. |
- Hansen, Lasse Tengbjerg, et al.
(författare)
-
DNA Repair Rate and Etoposide (VP16) Resistance of Tumor Cell Subpopulations derived from a Single Human Small Cell Lung Cancer
- 2003
-
Ingår i: Lung Cancer. - : Elsevier. - 0169-5002. ; 40:2, s. 157-64
-
Tidskriftsartikel (refereegranskat)abstract
- Two human small cell lung cancer (SCLC) subpopulations, CPH 54A, and CPH 54B, established from the same patient tumor by in vitro cloning, were investigated. The tumor was classified as intermediate-type SCLC. The cellular sensitivity to ionizing radiation (IR) was previously determined in the two sublines both in vivo and in vitro. Here we measured the etoposide (VP16) sensitivity together with the induction and repair of VP16- and IR-induced DNA double-strand breaks (DSBs). The two subpopulations were found to differ significantly in sensitivity to VP16, with the radioresistant 54B subline also being VP16 resistant. In order to explain the VP16 resistant phenotype several mechanisms where considered. The p53 status, P-glycoprotein, MRP, topoisomerase IIα, and Mre11 protein levels, as well as growth kinetics, provided no explanations of the observed VP16 resistance. In contrast, a significant difference in repair of both VP16- and IR-induced DSBs, together with a difference in the levels of the DSB repair proteins DNA-dependent protein kinase (DNA-PKcs) and RAD51 was observed. The VP16- and radioresistant 54B subline exhibited a pronounced higher repair rate of DSBs and higher protein levels of both DNA-PKcs and RAD51 compared with the sensitive 54A subline. We suggest, that different DSB repair rates among tumor cell subpopulations of individual SCLC tumors may be a major determinant for the variation in clinical treatment effect observed in human SCLC tumors of identical histological subtype.
|
|
