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Lung Cancer Risk Following Detection of Pulmonary Scarring by Chest Radiography in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial—Invited Commentary

Lung Cancer Risk Following Detection of Pulmonary Scarring by Chest Radiography in the Prostate,... An association between cancer and chronic inflammation has been recognized for centuries. Hermann Boerhaave of Leiden (1668-1738) wrote that inflammation might lead to “scirrhus” (scar formation), and that scirrhus “may change to cancer under unfavorable circumstances.”1 Many of the cancers related to inflammation are associated with specific viral, parasitic, or bacterial infections (eg, hepatitis C, papillomavirus, schistosomes, Helicobacter), others to chronic nonspecific infections (eg, chronic urinary catheters with recurrent infections, chronic cholecystitis, draining cutaneous ulcers from osteomyelitis), and still others to noninfectious chronic inflammatory processes, such as ulcerative colitis, reflux esophagitis, chronic pancreatitis, and atrophic gastritis.2 With this large body of data in mind, the historical, mostly anecdotal, reports that lung cancers occasionally arose in pulmonary scars (so-called scar carcinomas) were consonant with these observations in other organs. Detailed statistical estimates of the incidence and risk of these cancers, however, awaited more recent studies of larger groups, such as the 2007 British study of lung cancer incidence in patients with idiopathic pulmonary fibrosis.3 These patients showed a significant increase in lung cancer risk. In this issue of the Archives, Yu et al have performed a systematic study of the risk for lung cancer associated with pulmonary scarring, presumably related to prior or ongoing inflammation. They included more than 66 000 cancer-free participants, aged 55 to 74 years, who received baseline chest radiography as part of their participation in the PLCO Screening Trial. Subjects were followed up for up to 12 years. The data were adjusted for variables such as age, sex, race, and smoking. Over the course of the study, subjects with evidence of pulmonary scarring on their screening examination had a risk for lung cancer in the ipsilateral lung almost twice that of the subjects without scarring. What are the common threads linking the causes of inflammation-associated cancers? In addition to clinical observations, the inflammatory milieu has been proven experimentally to be conducive to cancer development. The primary effector cells of inflammation, phagocytes such as neutrophils and macrophages, produce a wide variety of toxic substances and metabolites that are proven carcinogens and can cause genetic damage and genetic instability in the adjacent “innocent bystander” tissues. Furthermore, the inflammatory microenvironment can contain high concentrations of mediators such as growth factors, cytokines, and chemokines, that can trigger proliferation, activate antiapoptotic signaling pathways, promote loss of adherence and invasion, and promote angiogenesis. Finally, can these cancers be prevented? While there is an increased risk of lung cancer in the presence of pulmonary scarring, the overall risk appears relatively low. In the study by Yu et al, 91 cancers arose in the ipsilateral scarred lungs of 5041 subjects with pulmonary scarring, and the incidence did not appear to be increasing over time. Chemoprevention trials in otherwise healthy people require effective agents that are extremely safe—so safe that they can be taken for long periods with negligible risk. There are no agents proven useful for this purpose in lung cancer. Studies of genetic susceptibility may in the future suggest why certain individuals with chronic inflammation get cancer and others do not.4 Recent studies on screening individuals at higher risk of lung cancer show the promise of reducing mortality.5 Perhaps individuals with pulmonary scarring may ultimately benefit from screening for cancer. Correspondence: Dr Weitzman, Division of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 (s-weitzman@northwestern.edu). References 1. Boerhaave H Cancer and inflammation. Shimkin MB Contrary to Nature. Washington, DC US Dept of Heath, Education and Welfare1977;79- 80Google Scholar 2. Shacter EWeitzman SA Chronic inflammation and cancer. Oncology (Williston Park) 2002;16 (2) 217- 229PubMedGoogle Scholar 3. Le Jeune IGribbin JWest JSmith CCullinan PHubbard R The incidence of cancer in patients with idiopathic pulmonary fibrosis and sarcoidosis in the UK. Respir Med 2007;101 (12) 2534- 2540PubMedGoogle ScholarCrossref 4. Hold GLEl-Omar EM Genetic aspects of inflammation and cancer. Biochem J 2008;410 (2) 225- 235PubMedGoogle ScholarCrossref 5. The International Early Lung Cancer Action Program Investigators, Survival of patients with stage I lung cancer detected on CT screening. N Engl J Med 2006;355 (17) 1763- 1771PubMedGoogle ScholarCrossref http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Archives of Internal Medicine American Medical Association

Lung Cancer Risk Following Detection of Pulmonary Scarring by Chest Radiography in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial—Invited Commentary

Archives of Internal Medicine , Volume 168 (21) – Nov 24, 2008

Lung Cancer Risk Following Detection of Pulmonary Scarring by Chest Radiography in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial—Invited Commentary

Abstract

An association between cancer and chronic inflammation has been recognized for centuries. Hermann Boerhaave of Leiden (1668-1738) wrote that inflammation might lead to “scirrhus” (scar formation), and that scirrhus “may change to cancer under unfavorable circumstances.”1 Many of the cancers related to inflammation are associated with specific viral, parasitic, or bacterial infections (eg, hepatitis C, papillomavirus, schistosomes, Helicobacter), others to chronic...
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References (5)

Publisher
American Medical Association
Copyright
Copyright © 2008 American Medical Association. All Rights Reserved.
ISSN
0003-9926
eISSN
1538-3679
DOI
10.1001/archinte.168.21.2332
Publisher site
See Article on Publisher Site

Abstract

An association between cancer and chronic inflammation has been recognized for centuries. Hermann Boerhaave of Leiden (1668-1738) wrote that inflammation might lead to “scirrhus” (scar formation), and that scirrhus “may change to cancer under unfavorable circumstances.”1 Many of the cancers related to inflammation are associated with specific viral, parasitic, or bacterial infections (eg, hepatitis C, papillomavirus, schistosomes, Helicobacter), others to chronic nonspecific infections (eg, chronic urinary catheters with recurrent infections, chronic cholecystitis, draining cutaneous ulcers from osteomyelitis), and still others to noninfectious chronic inflammatory processes, such as ulcerative colitis, reflux esophagitis, chronic pancreatitis, and atrophic gastritis.2 With this large body of data in mind, the historical, mostly anecdotal, reports that lung cancers occasionally arose in pulmonary scars (so-called scar carcinomas) were consonant with these observations in other organs. Detailed statistical estimates of the incidence and risk of these cancers, however, awaited more recent studies of larger groups, such as the 2007 British study of lung cancer incidence in patients with idiopathic pulmonary fibrosis.3 These patients showed a significant increase in lung cancer risk. In this issue of the Archives, Yu et al have performed a systematic study of the risk for lung cancer associated with pulmonary scarring, presumably related to prior or ongoing inflammation. They included more than 66 000 cancer-free participants, aged 55 to 74 years, who received baseline chest radiography as part of their participation in the PLCO Screening Trial. Subjects were followed up for up to 12 years. The data were adjusted for variables such as age, sex, race, and smoking. Over the course of the study, subjects with evidence of pulmonary scarring on their screening examination had a risk for lung cancer in the ipsilateral lung almost twice that of the subjects without scarring. What are the common threads linking the causes of inflammation-associated cancers? In addition to clinical observations, the inflammatory milieu has been proven experimentally to be conducive to cancer development. The primary effector cells of inflammation, phagocytes such as neutrophils and macrophages, produce a wide variety of toxic substances and metabolites that are proven carcinogens and can cause genetic damage and genetic instability in the adjacent “innocent bystander” tissues. Furthermore, the inflammatory microenvironment can contain high concentrations of mediators such as growth factors, cytokines, and chemokines, that can trigger proliferation, activate antiapoptotic signaling pathways, promote loss of adherence and invasion, and promote angiogenesis. Finally, can these cancers be prevented? While there is an increased risk of lung cancer in the presence of pulmonary scarring, the overall risk appears relatively low. In the study by Yu et al, 91 cancers arose in the ipsilateral scarred lungs of 5041 subjects with pulmonary scarring, and the incidence did not appear to be increasing over time. Chemoprevention trials in otherwise healthy people require effective agents that are extremely safe—so safe that they can be taken for long periods with negligible risk. There are no agents proven useful for this purpose in lung cancer. Studies of genetic susceptibility may in the future suggest why certain individuals with chronic inflammation get cancer and others do not.4 Recent studies on screening individuals at higher risk of lung cancer show the promise of reducing mortality.5 Perhaps individuals with pulmonary scarring may ultimately benefit from screening for cancer. Correspondence: Dr Weitzman, Division of Hematology/Oncology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL 60611 (s-weitzman@northwestern.edu). References 1. Boerhaave H Cancer and inflammation. Shimkin MB Contrary to Nature. Washington, DC US Dept of Heath, Education and Welfare1977;79- 80Google Scholar 2. Shacter EWeitzman SA Chronic inflammation and cancer. Oncology (Williston Park) 2002;16 (2) 217- 229PubMedGoogle Scholar 3. Le Jeune IGribbin JWest JSmith CCullinan PHubbard R The incidence of cancer in patients with idiopathic pulmonary fibrosis and sarcoidosis in the UK. Respir Med 2007;101 (12) 2534- 2540PubMedGoogle ScholarCrossref 4. Hold GLEl-Omar EM Genetic aspects of inflammation and cancer. Biochem J 2008;410 (2) 225- 235PubMedGoogle ScholarCrossref 5. The International Early Lung Cancer Action Program Investigators, Survival of patients with stage I lung cancer detected on CT screening. N Engl J Med 2006;355 (17) 1763- 1771PubMedGoogle ScholarCrossref

Journal

Archives of Internal MedicineAmerican Medical Association

Published: Nov 24, 2008

Keywords: lung,cicatrix,chest x-ray,prostate,lung cancer

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