Article
The relationship between chronic obstructive pulmonary disease and lung cancer in African American patients.
Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Clinical Lung Cancer (impact factor:
2.94).
11/2011;
13(2):149-56.
DOI:10.1016/j.cllc.2011.09.006
Source: PubMed
- Citations (19)
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Cited In (0)
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Article: Systematic evaluation of genetic variants in the inflammation pathway and risk of lung cancer.
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ABSTRACT: Inflammatory responses to environmental exposures, such as tobacco smoke, may play a role in lung carcinogenesis. To test this hypothesis, we studied genetic polymorphisms in the inflammation pathway in relation to lung cancer risk. We evaluated a panel of 59 single nucleotide polymorphisms (SNP) in 37 inflammation-related genes among non-Hispanic Caucasian lung cancer cases (N=1,553) and controls (N=1,730) from Houston, Texas. Logistic regression was used to assess associations with lung cancer under a dominant genetic model adjusted for sex, age, and smoking. Haplotypes were estimated with the expectation-maximization algorithm. False-positive report probabilities (FPRP) were calculated for significant associations. Interleukin 1 beta (IL1B) C3954T was associated with lung cancer [odds ratio (OR), 1.27; 95% confidence interval (95% CI), 1.10-1.47; FPRP 0.148]. Two IL1A SNPs (C-889T and Ala(114)Ser) were also related to lung cancer (OR, 1.18-1.22), although FPRPs were higher. One IL1A-IL1B haplotype, containing only the IL1B 3954T allele, was associated with elevated lung cancer risk (OR, 1.80; 95% CI, 1.24-2.61). These associations were stronger in heavy smokers, particularly for IL1B C3954T (OR, 1.59; 95% CI, 1.28-1.97; FPRP 0.004). Lung cancer risk was unrelated to polymorphisms in IL1 receptor or antagonist genes. Associations with lung cancer were also seen for SNPs in granulocyte macrophage colony stimulating factor and peroxisome proliferator-activated factor-delta, but FPRPs were high. IL1A and IL1B polymorphisms are associated with increased lung cancer risk, especially among heavy smokers. IL1A and IL1B are critical signals in initiating inflammation. Our results suggest that a dysregulated inflammatory response to tobacco-induced lung damage promotes carcinogenesis.Cancer Research 08/2007; 67(13):6520-7. · 7.86 Impact Factor -
Article: Measurement and impact of co-morbidity in elderly patients with advanced non-small cell lung cancer treated with chemotherapy. A phase II study of weekly paclitaxel.
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ABSTRACT: Aging is associated with an increasing of comorbidity and at the time of lung cancer diagnosis patients present one or more other serious disease. The aim of the study is to evaluate tolerability, response and survival of weekly paclitaxel in elderly patients with advanced NSCLC and concomitant diseases. Patients with advanced NSCLC who were poor candidates to platinum-based therapy because of age >65 years and coexistent illnesses received weekly paclitaxel over 1 hour at a dose of 80 mg/m2. Comorbidity was evaluated according to the Charlson scale, Kaplan-Feinstein index and the Cumulative Illness Rating Scale. A total of 57 patients (median age, 74 years; range, 65-84) were included. The overall response rate was 44%. Median survival was 7.8 months. Grade 3-4 toxicity was uncommon: neutropenia 1.8%, thrombocytopenia 1.8%, neuropathy 7%, hypersensitivity reaction 1.8%. Comorbidity indexes were useful to characterize better the population of elderly patients, but did not define a subgroup with worse prognosis. The low toxicity profile and efficacy of low-dose weekly paclitaxel justified its usage in this group of poor prognosis elderly patients with advanced NSCLC and comorbidities. A comorbidity index should be introduced in prospective oncological studies in the elderly to ensure compatibility.Acta Oncologica 01/2007; 46(3):367-73. · 3.33 Impact Factor -
Article: Gene expression profiling of human lung tissue from smokers with severe emphysema.
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ABSTRACT: The mechanism by which inhaled smoke causes the anatomic lesions and physiologic impairment of chronic obstructive pulmonary disease remains unknown. We used high-density microarrays to measure gene expression in severely emphysematous lung tissue removed from smokers at lung volume reduction surgery (LVRS) and normal or mildly emphysematous lung tissue from smokers undergoing resection of pulmonary nodules. Class prediction algorithms identified 102 genes that accurately distinguished severe emphysema from non-/mildly emphysematous lung tissue. We also defined a number of genes whose expression levels correlated strongly with lung diffusion capacity for carbon monoxide and/or forced expiratory volume at 1 s. Genes related to oxidative stress, extracellular matrix synthesis, and inflammation were increased in severe emphysema, whereas expression of endothelium-related genes was decreased. To identify candidate genes that might be causally involved in the pathogenesis of emphysema, we linked gene expression profiles to chromosomal regions previously associated with chronic obstructive pulmonary disease in genome-wide linkage analyses. Unsupervised hierarchical clustering of the LVRS samples revealed distinct molecular subclasses of severe emphysema, with body mass index as the only clinical variable that differed between the groups. Class prediction models established a set of genes that predicted functional outcome at 6 mo after LVRS. Our findings suggest that the gene expression profiles from human emphysematous lung tissue may provide insight into pathogenesis, uncover novel molecular subclasses of disease, predict response to LVRS, and identify targets for therapeutic intervention.American Journal of Respiratory Cell and Molecular Biology 01/2005; 31(6):601-10. · 5.13 Impact Factor
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Keywords
114 African Americans
African American population
African Americans
Airflow obstruction
COPD diagnosis
CT evidence
joint occurrence
Karmanos Cancer Center
lung cancer
lung cancer diagnosis
lung cancer risk
medical care
medical records
normal spirometry
population-based case-control studies
previous diagnosis
selected group
significant number
spirometry-diagnosed COPD
treatment modality