Abstract:Among lung cancers, a substantial shift over time has occurred in the recorded frequency of adenocarcinoma (AdC) relative to that of squamous cell carcinoma (SqCC). This is evident in many countries, and also in those who have never smoked. We attempted to address the extent to which this increase is real, or an artefact of changing diagnostic practices. We reviewed studies re-evaluating diagnoses using more up-to-date criteria, and studies applying standard criteria to cases collected over a long period. We a… Show more
“…Sources of bias and compensation are discussed separately below. Detailed consideration of the data on lung cancer rate trends is beyond the scope of this paper, although the interested reader might wish to refer to publications of mine suggesting alternative explanations for the trends (Lee, 2016;Lee & Gosney, 2016;Lee & Sanders, 2004).…”
Section: Discussionmentioning
confidence: 99%
“…While there is an unfortunate lack of data relating tar level (rather than filter/plain use) to histological type of lung cancer it is clear that this claim has little foundation for a number of reasons. Apart from the lack of evidence of an increased risk of adenocarcinoma in filter compared to plain cigarette smokers (Brooks et al, 2005;Lee et al, 2012;Lee & Sanders, 2004;Marugame et al, 2004;Papadopoulos et al, 2011), it is also clear that there has been a rise in relative frequency of adenocarcinoma to squamous carcinoma in non-smokers and persuasive evidence that changes in methods for classification of histological type have contributed to the observed increase in relative frequency (Lee & Gosney, 2016).…”
Despite evidence that smokers substantially compensate for reduced cigarette yields, the results clearly show lower risks in lower tar smokers. Limitations of the evidence are discussed, but seem unlikely to affect this conclusion.
“…Sources of bias and compensation are discussed separately below. Detailed consideration of the data on lung cancer rate trends is beyond the scope of this paper, although the interested reader might wish to refer to publications of mine suggesting alternative explanations for the trends (Lee, 2016;Lee & Gosney, 2016;Lee & Sanders, 2004).…”
Section: Discussionmentioning
confidence: 99%
“…While there is an unfortunate lack of data relating tar level (rather than filter/plain use) to histological type of lung cancer it is clear that this claim has little foundation for a number of reasons. Apart from the lack of evidence of an increased risk of adenocarcinoma in filter compared to plain cigarette smokers (Brooks et al, 2005;Lee et al, 2012;Lee & Sanders, 2004;Marugame et al, 2004;Papadopoulos et al, 2011), it is also clear that there has been a rise in relative frequency of adenocarcinoma to squamous carcinoma in non-smokers and persuasive evidence that changes in methods for classification of histological type have contributed to the observed increase in relative frequency (Lee & Gosney, 2016).…”
Despite evidence that smokers substantially compensate for reduced cigarette yields, the results clearly show lower risks in lower tar smokers. Limitations of the evidence are discussed, but seem unlikely to affect this conclusion.
“…The mortality and morbidity associated with lung cancer represent a serious threat to human health ( 26 ). Lung cancer patients often have an irritating cough, expectoration, hemoptysis, and other symptoms during the early stages of the disease, and its development is related to factors such as tumor location and pathological type ( 27 ). Lung cancer is divided into non-small cell and small cell lung cancer, with non-small cell lung cancer accounting for ~80% of all cases.…”
Interleukin-24 (IL-24) is a tumor-suppressor gene that has been documented in human melanoma cells. IL-24 has marked antitumor activities on various types of human cancer, but its underlying mechanism remains unclear. In the present, we investigated the effects of human IL-24 (hIL-24) on the chemotherapy resistance of lung cancer cells. The cisplatin (DDP)-resistant lung carcinoma cell line A549/DDP was subjected to adenovirus-mediated transfection with the human IL-24 gene (Ad-hIL-24). The growth-inhibitory and apoptotic effects of Ad-hIL-24 on A549/DDP cells were observed, and the expression levels of AKT, phosphorylated-AKT (p-AKT) and P-glycoprotein (P-gp) were detected. Ad-hIL-24 significantly decreased the levels of p-AKT and P-gp, and effectively inhibited A549/DDP cell growth. Furthermore, A549/DDP cells exhibited a significantly increased rate of apoptosis, as well as G2/M-phase arrest, following transfection with Ad-hIL-24, and these effects were increased in cells treated with Ad-IL-24 combined with DDP when compared with those treated with Ad-hIL-24 or DDP alone. These results suggest that hIL-24 can reverse the DDP resistance of lung cancer cells, and that the associated mechanism involves the induction of apoptosis and G2/M-phase arrest through the phosphoinositide3-kinase (PI3K)/AKT signaling pathway, as well as a decrease in drug resistance through P-gp expression.
The rising incidence of adenocarcinoma of the lung is alarming. The cancer registry data do not allow risk factor analysis. In the international discussion, the introduction of filter cigarettes as well as the changing composition of cigarettes has been hypothesized as being responsible. Further epidemiologic studies are strongly needed.
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