Inflammation in the development of lung cancer: epidemiological evidence.
The lung is a site for repeated or chronic inflammatory insults. Epidemiologic research has provided evidence to support the hypothesis that tissue damage caused by inflammation can initiate or promote the development of lung cancer, possibly in conjunction with tobacco use. For example, some studies suggest an increased risk of lung cancer among persons with lung infections, such as tuberculosis, bacterial pneumonia, or inflammatory lung diseases. Elevated serum levels of C-reactive protein, an inflammation marker, are associated with heightened lung cancer risk. Recent studies also demonstrate increased lung cancer risk among immunosuppressed individuals infected with HIV. Other research indicates an association between genetic polymorphisms in the inflammation pathway, which might modulate the inflammatory response and lung cancer risk.
Engels
Eric A
EA
Infections & Immunoepidemiology Branch, Division of Cancer Epidemiology & Genetics, National Cancer Institute, 6120 Executive Blvd, EPS 7076, Rockville, MD 20892, USA. engelse@exchange.nih.gov
D001249:Asthma / Q000150:complications / Q000453:epidemiology; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D015658:HIV Infections / Q000150:complications / Q000453:epidemiology; D006801:Humans; D008175:Lung Neoplasms / Q000453:epidemiology* / Q000209:etiology / Q000235:genetics; D011014:Pneumonia / Q000150:complications / Q000453:epidemiology*; D018410:Pneumonia, Bacterial / Q000150:complications / Q000453:epidemiology; D011024:Pneumonia, Viral / Q000150:complications / Q000453:epidemiology; D011110:Polymorphism, Genetic; D012307:Risk Factors
D015415:Biomarkers; D002097:C-Reactive Protein