Clinical Features of 5,628 Primary Lung Cancer Patients

Yang, Ping; Allen, Mark S.; Aubry, Marie Christine; Wampfler, Jason A.; Marks, Randolph S.; Edell, Eric S.; Thibodeau, Stephen N.; Adjei, Alex A.; Jett, James R.; Deschamps, Claude

doi:10.1378/chest.128.1.452

Cited by 379 publications

(272 citation statements)

References 19 publications

Supporting

Mentioning

245

Contrasting

Unclassified

Order By: Relevance

“…In contrast, lung function and prevalence of COPD were significantly different in the matched comparison (table 1). The demographic variables, staging and histological subtypes of the lung cancer cases in this study (tables 1 and 2) are comparable to a large series published from a cohort in the USA [19], suggesting that our lung cancer cohort is representative (histology: 17% small cell, 10% nonsmall cell, 43% adenocarcinoma, 24% squamous cell and 5% unknown histology; staging: 29% stage 1, 10% stage 2, 31% stage 3 and 30% stage 4).…”

Section: Discussionsupporting

confidence: 81%

COPD prevalence is increased in lung cancer, independent of age, sex and smoking history

Young¹,

Hopkins²,

Christmas³

et al. 2009

European Respiratory Journal

575

493

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) is a common comorbid disease in lung cancer, estimated to affect 40-70% of lung cancer patients, depending on diagnostic criteria. As smoking exposure is found in 85-90% of those diagnosed with either COPD or lung cancer, coexisting disease could merely reflect a shared smoking exposure. Potential confounding by age, sex and pack-yr smoking history, and/or by the possible effects of lung cancer on spirometry, may result in over-diagnosis of COPD prevalence.In the present study, the prevalence of COPD (pre-bronchodilator Global Initiative for Chronic Obstructive Lung Disease 2+ criteria) in patients diagnosed with lung cancer was 50% compared with 8% in a randomly recruited community control group, matched for age, sex and pack-yr smoking exposure (n5602, odds ratio 11.6; p,0.0001).In a subgroup analysis of those with lung cancer and lung function measured prior to the diagnosis of lung cancer (n5127), we found a nonsignificant increase in COPD prevalence following diagnosis (56-61%; p50.45). After controlling for important variables, the prevalence of COPD in newly diagnosed lung cancer cases was six-fold greater than in matched smokers; this is much greater than previously reported.We conclude that COPD is both a common and important independent risk factor for lung cancer.KEYWORDS: Chronic obstructive pulmonary disease, epidemiology, lung cancer, risk, spirometry A s only 10-15% of chronic smokers get lung cancer [1], host susceptibility factors have been implicated. Age, smoking history, family history and impaired lung function have been identified as key risk factors [2]. The question that then arises is: does the association between chronic obstructive pulmonary disease (COPD) and lung cancer come down to more than a shared smoking history?Cross-sectional studies show that the prevalence of COPD is 40-70% of those diagnosed with lung cancer [3,4], although prevalence is highly dependent on diagnostic criteria, age, sex and smoking exposure [5]. As none of these studies compared the prevalence of COPD in their lung cancer cohorts with a smoking cohort matched for these variables, the significance of this finding is uncertain. Moreover, none of these studies considered that lung cancer may itself cause an obstructive effect on spirometry. It is possible that potential confounding by age, sex and packyr smoking history on COPD prevalence, and/or the possible effects of lung cancer per se on spirometry, could result in over-diagnosis of COPD and a falsely increased association between COPD and lung cancer.

show abstract

Section: Discussionsupporting

confidence: 81%

COPD prevalence is increased in lung cancer, independent of age, sex and smoking history

Young¹,

Hopkins²,

Christmas³

et al. 2009

European Respiratory Journal

575

493

View full text Add to dashboard Cite

show abstract

“…The majority of patients are diagnosed with advanced and unresectable disease (stage IIIB/IV), which carries a 5-year survival rate of less than 5% [1]. Therefore, it is important to detect and treat lung cancer at an early stage.…”

Section: Introductionmentioning

confidence: 99%

Usefulness of Endobronchial Ultrasonography With a Guide Sheath and Virtual Bronchoscopic Navigation for Ground-Glass Opacity Lesions

Ikezawa

Shinagawa

Sukoh

et al. 2017

The Annals of Thoracic Surgery

View full text Add to dashboard Cite

show abstract

“…COX-2 inhibitors have been shown to inhibit tumor growth and metastasis in several animal models, including models of lung cancer (22). The current treatment strategies for advanced lung cancer include surgical resection, radiation, cytotoxic chemotherapy, and photodynamic therapy (5). In almost two thirds of cases, the cancer has already spread beyond localized disease at the time of diagnosis, limiting therapeutic options (23,24).…”

Section: Introductionmentioning

confidence: 99%

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Sharma

Meeran

Katiyar

2010

Molecular Cancer Therapeutics

View full text Add to dashboard Cite

Overexpression of cyclooxygenase-2 (COX-2) and prostaglandins (PG) is linked to a wide variety of human cancers. Here, we assessed whether the chemotherapeutic effect of grape seed proanthocyanidins (GSP) on non-small cell lung cancer (NSCLC) cells is mediated through the inhibition of COX-2 and PGE 2 /PGE 2 receptor expression. The effects of GSPs on human NSCLC cell lines in terms of proliferation, apoptosis, and expression of COX-2, PGE 2 , and PGE 2 receptors were determined using Western blotting, fluorescence-activated cell sorting analysis, and reverse transcription-PCR. In vitro treatment of NSCLC cells (A549, H1299, H460, H226, and H157) with GSPs resulted in significant growth inhibition and induction of apoptosis, which were associated with the inhibitory effects of GSPs on the overexpression of COX-2, PGE 2 , and PGE 2 receptors (EP1 and EP4) in these cells. Treatment of cells with indomethacin, a pan-COX inhibitor, or transient transfection of cells with COX-2 small interfering RNA, also inhibited cell growth and induced cell death. The effects of a GSP-supplemented AIN76A control diet fed to nude mice bearing tumor xenografts on the expression of COX-2, PGE 2 , and PGE 2 receptors in the xenografts were also evaluated. The growth-inhibitory effect of dietary GSPs (0.5%, w/w) on the NSCLC xenograft tumors was associated with the inhibition of COX-2, PGE 2 , and PGE 2 receptors (EP1, EP3, and EP4) in tumors. This preclinical study provides evidence that the chemotherapeutic effect of GSPs on lung cancer cells in vitro and in vivo is mediated, at least in part, through the inhibition of COX-2 expression and subsequently the inhibition of PGE 2 and PGE 2 receptors.Mol Cancer Ther; 9(3); 569-80. ©2010 AACR.

show abstract

Clinical Features of 5,628 Primary Lung Cancer Patients

Cited by 379 publications

References 19 publications

COPD prevalence is increased in lung cancer, independent of age, sex and smoking history

COPD prevalence is increased in lung cancer, independent of age, sex and smoking history

Usefulness of Endobronchial Ultrasonography With a Guide Sheath and Virtual Bronchoscopic Navigation for Ground-Glass Opacity Lesions

Proanthocyanidins Inhibit In vitro and In vivo Growth of Human Non–Small Cell Lung Cancer Cells by Inhibiting the Prostaglandin E2 and Prostaglandin E2 Receptors

Contact Info

Product

Resources

About