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The Epidemiological Revolution and Prevention of Non-Communicable Chronic Diseases

This article discusses the epidemiological revolution of the 20th century and the importance of prevention in non-communicable chronic diseases. It explores the mortality rates and prevalence of various diseases in Italy, as well as the mechanisms of cardiotoxicity in anticancer drugs and potential protective agents. The text also touches on the carcinogenesis process, prevention strategies, and the role of dietary and pharmacological agents in interfering with cigarette smoke carcinogenesis.

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The Epidemiological Revolution and Prevention of Non-Communicable Chronic Diseases

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  1. GE ATHE NUEN NAE SE UM CASTELBRANDO8 – VITTORIO VENETO 100 LA PREVENZIONE DELLE MALATTIE CRONICHE NON TRASMISSIBILI - INTRODUZIONE Silvio De Flora Dipartimento di Scienze della Salute Università degli Studi di Genova Coordinatore GdLSItI «Prevenzione Tumori / Screening Oncologici»

  2. CARD CAN CER ACC DIG INF THE EPIDEMIOLOGICAL REVOLUTION OF THE 20th CENTURY S. De Flora, A. Quaglia, C. Bennicelli & M. Vercelli, FASEB J. 19, 892–897, 2005 ITALY, 1901–2000 (RAW MORTALITY DATA) 1407 500 400 300 Deaths per 100,000 200 100 RESP 0 1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000

  3. CER THE EPIDEMIOLOGICAL REVOLUTION OF THE 20th CENTURY S. De Flora, A. Quaglia, C. Bennicelli & M. Vercelli, FASEB J. 19, 892–897, 2005 ITALY, 1901–2000 (AGE-STANDARDIZED MORTALITY DATA) M –72.4% 1436 CEREBROVASCULAR DISEASES –74.4% F 500 M –51.9% CARDIOVASCULAR DISEASES –67.9% F 400 –18.3% M CANCER F –12.9% 300 Deaths per 100,000 CARD 200 CAN 100 ACC RESP INF DIG 0 1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000

  4. IL CANCRO IN ITALIA N. di casi (AIRTUM, 2016) 365.000 (190.000 M, 176.000 F) 52.000 50.000 41.000 35.000 27.000 13.500 13.000 N. di morti (ISTAT, 2013) 176.000 (99.000 M, 77.000 F) 19.000 12.000 33.000 7.000 5.600 11.000 10.000 Sede del cancro Tutte le sedi Colon-retto Mammella Polmone Prostata Vescica Pancreas Stomaco Prevalenza (2015) 2.200.000 (2006) 3.000.000 (2015) (4,7% M, 5,3% F) 427.000 693.000 88.000 399.000 254.000 Dal 2008 al 2013 diminuzione nei maschi (-1,5% annuo) e nelle femmine (-0,7% annuo) Dal 2008 al 2016 diminuzione annuale del 2,5% nei maschi, piccolo aumento nelle femmine (da 169.000 nuovi casi nel 2015 a 176.000 nel 2016)

  5. Anticancer drugs Mechanisms of cardiotoxicity Protective agents Mitochondrial dysfunction Apoptosis of cardiomyocytes ROS generation DNA damage Endothelial cell damage Antibody directed cellular cytotoxicity ATP block Cell signaling, survival block Fibrosis Hypertension Sinus bradicardia Atrium-ventricular block Ventricular tachycardia Arrhythmias Thromboembolism ACE inhibitors Beta–blockers Statins Dexrazoxane L–Carnitine Coenzyme Q10 N–Acetyl–L–Cysteine Glutathione Erdosteine Selenium Zinc Melatonin Flavonoids and polyphenols Platelet antiaggregants Anthracyclines and anthraquinolones Capecitabine, Cytarabine, 5–Fluorouracil Paclitaxel, Vinca alkaloids Cyclophosphamide TK Inhibitors (Trastuzumab, Imatinib, Bevacizumab, Sorafenib, Sunitinib, etc) COX–2 inhibitors Estrogen receptor modulators Irradiation to the thorax • Albini, G. Pennesi, R. Cammarota, F. Donatelli, S. De Flora, D.M. Noonan, • Cardiotoxicityofanticancerdrugs: The needforcardio-oncology and • cardio-oncologicalprevention,J. NatlCancerInst., 102, 14-25, 2010

  6. STOP GROWTH OF THE NEOPLASTIC MASS Exposure dose CARCINOGENESIS PROCESS C H E M O P R E V E N T I O N Pharmacological dose Cell divisions No. of cells Weight (g) Cellular dose TOXICOKINETIKS AND METABOLISM 0 -9 10 10 0 Target dose 1 -8 10 10 DNA DAMAGE AND REPAIR 5 Molecular dose 2 -7 10 10 PRIMARY INITIATION PREVENTION (days - weeks) -6 3 10 10 10 H.P. 4 -5 10 10 PROMOTION 15 (years - decades) 5 -4 10 10 -3 6 10 20 10 7 -2 10 10 25 8 -1 10 10 BENIGN TUMOR SECONDARY PROGRESSION 9 0 10 10 30 (~ 1 year) PREVENTION CANCER 10 1 10 10 THERAPY - REHABILITATION 35 11 2 INVASION 10 10 METASTASIS TERTIARY PREVENTION 3 12 10 10 40 NEOPLASTIC MASS • Celebrazioni 83 anni dell'Istituto Superiore di SanitàRoma. 19-21 aprile 2017 S. De Flora et al., Mutat. Res. 480-481, 9-22, 2001

  7. DIETARY AND PHARMACOLOGICAL AGENTS THAT HAVE BEEN TESTED FOR THE ABILITY TO INTERFERE IN CIGARETTE SMOKE CARCINOGENESIS (S. De Flora et al., Trends Pharmacol. Sci. 37, 120-142, 2016) Anticancer drugs Bexarotene Lapatinib Vorinostat Anti- inflammatory drugs Antidiabeticdrugs Budesonide Aspirin Celecoxib Licofelone Naproxen Metformin Pioglitazone Natural agents Phenethyl Isothiocyanate Myo-inositol N-Acetylcysteine Ascorbic acid Blackberry Strawberry

  8. STOP GROWTH OF THE NEOPLASTIC MASS Exposure dose CARCINOGENESIS PROCESS C H E M O P R E V E N T I O N Pharmacological dose Cell divisions No. of cells Weight (g) Cellular dose TOXICOKINETIKS AND METABOLISM 0 -9 10 10 0 Target dose 1 -8 10 10 DNA DAMAGE AND REPAIR 5 Molecular dose 2 -7 10 10 PRIMARY INITIATION PREVENTION (days - weeks) -6 3 10 10 10 H.P. 4 -5 10 10 PROMOTION 15 (years - decades) 5 -4 10 10 -3 6 10 20 10 7 -2 10 10 25 8 -1 10 10 BENIGN TUMOR SECONDARY PROGRESSION 9 0 10 10 30 (~ 1 year) PREVENTION CANCER 10 1 10 10 THERAPY - REHABILITATION 35 11 2 INVASION 10 10 METASTASIS TERTIARY PREVENTION 3 12 10 10 40 NEOPLASTIC MASS Celebrazioni 83 anni dell'Istituto Superiore di SanitàRoma. 19-21 aprile 2017 S. De Flora et al., Mutat. Res. 480-481, 9-22, 2001

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