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COPD AND LUNG CANCER

LA PNEUMOLOGIA NEL TERZO MILLENNIO. Modena, 12 Dicembre 2003. COPD AND LUNG CANCER. Prof. Leonardo M. Fabbri Clinica di Malattie dell’Apparato Respiratorio Università di Modena e Reggio Emilia. HIGHER RISK OF LUNG CANCER IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE.

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COPD AND LUNG CANCER

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  1. LA PNEUMOLOGIA NEL TERZO MILLENNIO Modena, 12 Dicembre 2003 COPD AND LUNG CANCER Prof. Leonardo M. Fabbri Clinica di Malattie dell’Apparato Respiratorio Università di Modena e Reggio Emilia

  2. HIGHER RISK OF LUNG CANCER IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE • 113 “cases” (FEV1 <70%) and 113 “controls (FEV1 >85%) matched for age, sex, occupation and smoking • All persons observed from 1973 through 1984 for a diagnosis of lung cancer, death from lung cancer and death from any cause Skillrud DM et al, Ann Intern Med 1986; 105: 503-7

  3. HIGHER RISK OF LUNG CANCER IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE • 9/113 lung cancer diagnosis in “cases” group vs 2/113 in “controls“ (all lung cancers in smokers). • Cumulative probability curves for developing lung cancer were significantly different (p=0.024) for the two groups. • The estimated cumulative probability of developing lung cancer by 10 years was 8.8% for “cases” and 2.0% for “controls”: 4.4 times increase in risk. COPD constituted a risk factor for lung cancer after matching for sex, smoking, age and occupation Skillrud DM et al, Ann Intern Med 1986; 105: 503-7

  4. AIRWAYS OBSTRUCTION AND THE RISK FOR LUNG CANCER • Patients with moderate to severe obstruction and a sample of patients with no obstruction to moderate obstruction from two different trials (a total of 4395 subjects) • On follow-up, the risk of developing lung cancer was associated with age, smoking and ventilatory status Tockman MS et al, Ann Intern Med 1987; 106: 512-8

  5. LUNG CANCER AND PACK-YEARS SMOKED Tockman MS et al, Ann Intern Med 1987; 106: 512-8

  6. LUNG CANCER AND AGE Tockman MS et al, Ann Intern Med 1987; 106: 512-8

  7. LUNG CANCER AND AIRFLOW LIMITATION • Lung cancer mortality rates of 11/1000 person-years (impaired lung function) vs 3.5/1000 person-years (normal lung function). • More than a 3-fold risk for lung cancer in those with abnormal spirometric findings. The presence of airways obstruction explains much of the contribution of age and pack-years to the risk for lung cancer Tockman MS et al, Ann Intern Med 1987; 106: 512-8

  8. EFFECT OF SMOKING INTERVENTION AND THE USE OF AN INHALED ANTICHOLINERGIC BRONCHODILATOR ON THE RATE OF DECLINE OF FEV1: THE LUNG HEALTH STUDY 20 more lung cancer deaths than from cardiovascular disease or stroke and, in fact, lung cancer deaths exceeded all other deaths Anthonisen NR et al, JAMA 1994; 272: 1497-505

  9. A COMMON FAMILIAL COMPONENT IN LUNG CANCER AND CHRONIC OBSTRUCTIVE PULMONARY DISEASE The patterns of familial clustering of pulmonary dysfunction in relatives of lung cancer patients and those of COPD cases are clearly consistent Lung cancer and COPD share a common familial component other than smoking Cohen BH et al, Lancet 1977; Sept 10: 523-6

  10. Is COPD a genetic disorder? Only 15-20 % of smokers develops COPD Prevalence of COPD is different in different racial groups Increased prevalence of COPD in relatives of patients with COPD Lomas DA, Silverman EK. Respiratory Research 2001; 2: 20-26

  11. COPD, a multifactorial disease (?) COPD with 1 AT deficit Enviroment Genes Infections Congentital cardiomyopathy Schizofrenia Diabetes Teratogenic disorder Monogenic disorder Coronaropathy Trauma Kingston HM, Br Med J 1989;298:949-952

  12. Candidate genes in COPD • PROTEASEANTIPROTEASE IMBALANCE • 1 antitrypsin (PI MA 1 anti-protease) • 1-antichimotrypsin • Catepepsin G • 2 macroglobulin • OXIDATIVE STRESS • Extracellular superoxide dismutase • Glutathione – S – transferase • DETOXIFYING ENZYME • microsomal epoxide hydrolase • INFLAMMATION • TNF  • different cytokines (e.g. IL-8) • BRONCHIAL HYPERSECRETION • Cystic fibrosis transmembrane regulator (CFTR) Lomas DA, Silverman EK. Respiratory Research 2001; 2: 20-26

  13. THE GENETICS OF COPD • Many candidate genes • have been assessed, • but the data are often conflicting Lomas DA, Silverman EK. Respiratory Research 2001; 2: 20-26

  14. “The response of the body to a cancer is not a unique mechanism but has many parallels with inflammation and wound healing. … If genetic damage is the “match that lights the fire” of cancer, some types of inflammation may provide the “fuel that feeds the flames”. Chronic Obstructive Lung Disease, NF Voelkel & W MacNee Eds. 2002

  15. COMMON ELEMENTS IN THE PATHOGENESIS OF COPD AND LUNG CANCER • Genetic predisposition (p53, Rb, K-ras) • Peptides and endopeptidases (bombesin-like) • Inflammation and oxidants (cigarette smoking) • Dysregulation of growth factor expression Chronic Obstructive Lung Disease, NF Voelkel & W MacNee Eds. 2002

  16. “The response of the body to a cancer is not a unique mechanism but has many parallels with inflammation and wound healing. … If genetic damage is the “match that lights the fire” of cancer, some types of inflammation may provide the “fuel that feeds the flames”. Balkwill and Mantovani, Lancet 2001; 357: 539-45

  17. Balkwill and Mantovani, Lancet 2001; 357: 539-45

  18. ADVICE FOR CLINICIACNS ! • Always take a careful smoking history and look for airflow obstruction. • If patients are heavy smokers and have airflow limitation, standard posteroanterior and lateral chest roentgenographic films, sputum cytology, or both should be employed. Petty LT. Oncol Clin North Amer 1997; 11: 531-41

  19. LA PNEUMOLOGIA NEL TERZO MILLENNIO Modena, 12 Dicembre 2003 COPD AND LUNG CANCER Prof. Leonardo M. Fabbri Clinica di Malattie dell’Apparato Respiratorio Università di Modena e Reggio Emilia

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