Common Familial Component in Lung Cancer and Chronic Obstructive Pulmonary Disease

Cohen, Bernice H.

doi:10.1016/s0140-6736(78)90030-2

Cited by 11 publications

(16 citation statements)

References 14 publications

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“…Several studies in the 1970s and 1980s reported higher rates of airflow obstruction in first degree relatives of patients with COPD than in control subjects. [20][21][22] For example, Kueppers et al found that the mean FEV 1 in siblings of patients with COPD (90% of predicted) was significantly lower than in the siblings of matched control subjects (103% of predicted). 23 Additional studies have shown familial aggregation for chronic bronchitis.…”

Section: Role Of Other Genetic Factors In Copdmentioning

confidence: 99%

Chronic obstructive pulmonary disease * 1: Susceptibility factors for COPD the genotype-environment interaction

Sandford

Silverman²

2002

Thorax

137

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Section: Role Of Other Genetic Factors In Copdmentioning

confidence: 99%

Chronic obstructive pulmonary disease * 1: Susceptibility factors for COPD the genotype-environment interaction

Sandford

Silverman²

2002

Thorax

137

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“…Further, in the context that chronic obstructive pulmonary disease (COPD), a disease that starts in the small airways(13,18–21), is a risk factor for lung cancer independent of smoking (22–26), we asked whether CSTA is up-regulated in the SAE of smokers with COPD beyond that of smokers per se , and whether this up-regulation is also dependent on genetic variation. In view of the fact that both smoking and COPD are stronger risk factors for SCC than for adenocarcinoma of the lung, and that most SCCs are derived from large airways(15,27–30)we also examined CSTA expression in large airway epithelium (LAE) samples obtained in a subset of the study subjects, and compared our CSTA gene expression data to publicly available lung cancer microarray data derived using comparable methodologies (31), to see if CSTA is discordantly expressed in SCC and adenocarcinoma of the lung, relative to the SAE and LAE.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Cystatin A Expression in Human Airway Epithelium Related to Genotype, Smoking, COPD, and Lung Cancer

et al. 2011

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Cystatin A (gene: CSTA), is up-regulated in non-small-cell lung cancer(NSCLC) and dysplastic vs normal human bronchial epithelium. In the context that chronic obstructive pulmonary disease (COPD), a small airway epithelium (SAE) disorder, is independently associated with NSCLC(especially squamous cell carcinoma, SCC), but only occurs in a subset of smokers, we hypothesized that genetic variation, smoking and COPD modulate CSTA gene expression levels in SAE, with further up-regulation in SCC. Gene expression was assessed by microarray in SAE of 178 individuals [healthy nonsmokers (n=60), healthy smokers (n=82), and COPD smokers (n=36)], with corresponding large airway epithelium (LAE) data in a subset (n=52). Blood DNA was genotyped by SNP microarray. Twelve SNPs upstream of the CSTA gene were all significantly associated with CSTA SAE gene expression(p<0.04 to 5 × 10 −4). CSTA gene expression levels in SAE were higher in COPD smokers (28.4 ± 2.0) than healthy smokers (19.9 ± 1.4, p<10−3), who in turn had higher levels than nonsmokers(16.1 ± 1.1, p<0.04). CSTA LAE gene expression was also smoking-responsive (p<10−3). Using comparable publicly available NSCLC expression data, CSTA was up-regulated in SCC vs LAE (p<10−2) and down-regulated in adenocarcinoma vs SAE (p <10−7). All phenotypes were associated with significantly different proportional gene expression of CSTA to cathepsins. The data demonstrate that regulation of CSTA expression in human airway epithelium is influenced by genetic variability, smoking, and COPD, and is further up-regulated in SCC, all of which should be taken into account when considering the role of CSTA in NSCLC pathogenesis.

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“…The results were compared with values obtained in a matched control group because it is important to select such a group by factors that can probably influence immunocapacity as well as the development and occurence of lung cancer (Wal et al, 1966;Cohen et al, 1977).…”

Section: Discussionmentioning

confidence: 99%

The primary immune response of patients with different stages of squamous-cell bronchial carcinoma.

Jansen¹,

The²,

Gast³

et al. 1978

Thorax

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Common Familial Component in Lung Cancer and Chronic Obstructive Pulmonary Disease

Cited by 11 publications

References 14 publications

Chronic obstructive pulmonary disease * 1: Susceptibility factors for COPD the genotype-environment interaction

Chronic obstructive pulmonary disease * 1: Susceptibility factors for COPD the genotype-environment interaction

Modulation of Cystatin A Expression in Human Airway Epithelium Related to Genotype, Smoking, COPD, and Lung Cancer

The primary immune response of patients with different stages of squamous-cell bronchial carcinoma.

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