world cancer report - iarc

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Cancers positively Sex Standardized mortality per 100,000/year Relative Absolute excess risk Attributable associated with smoking risk per 100,000/year proportion (%)* Life-long non-smoker Current cigarette smoker Lung cancer M 24 537 22.4 513 87 F 18 21 3 11.9 195 77 Cancer of the upper M 1 27 24.5 26 89 respiratory sites F 2 10 5.6 8 58 Cancer of the bladder and M 18 53 2.9 35 36 other urinary organs F 8 21 2.6 13 32 Pancreatic cancer M 18 38 2.1 20 25 F 16 37 2.3 21 29 Oesophageal cancer M 9 68 7.6 59 66 F 4 41 10.3 37 74 Kidney cancer M 8 23 3 15 37 F 6 8 1.4 2 11 American Cancer Study. Men and women aged 35 yrs and more. *Attributable proportion is the proportion of all deaths from the specified disease which are attributable to cancer, assuming that 30% of the population are current smokers and that all the excess risk in smokers is due to smoking. Table 2.3 Smoking increases the risk of many human cancers. Fig. 2.7 The five highest and the five lowest recorded lung cancer incidence rates in males and females. Interaction with other hazards Alcohol consumption, exposure to asbestos and exposure to ionizing radiation interact with smoking in determining risk of some cancers [13]. For alcohol drinking and smoking, risks for cancer of the larynx, oesophagus and oral cavity increase multiplicatively in relation to the respective risks generated by either expo- 26 The causes of cancer sure in the absence of the other. For individuals exposed to both asbestos and tobacco smoke (for example, insulation workers who smoke), risk of lung cancer is also increased multiplicatively, although smoking does not affect risk of mesothelioma (a tumour type specifically caused by asbestos). Quitting smoking can considerably lower the risk for lung cancer among people who were exposed to asbestos in the past. Mechanisms of carcinogenesis As tobacco is the most important human carcinogen, elucidation of mechanisms which result in cancer among humans exposed to tobacco smoke provides an important means for assessing some pre-
ventive options, and may be relevant to the prevention of other environmentallyinduced cancer. Mainstream smoke (the material inhaled by smokers) is an aerosol including approximately 4,000 specific chemicals and containing 10 10 particles per ml. The particulate matter (tar) is made up of some 3,500 compounds, the most abundant being nicotine (0.1-2.0 mg per cigarette) and also including most of the polycyclic aromatic hydrocarbons occurring in the smoke [14]. Another class of carcinogens represented in tobacco smoke is N-nitroso compounds, particularly including the nitroso derivatives of nicotine and nornicotine [15]. Chemicals such as aromatic amines, benzene and heavy metals, independently established as carcinogenic for humans, are present in tobacco smoke (Table 2.2). Use of smokeless tobacco results in exposure to tobaccorelated nitroso compounds, but not to polycyclic aromatic hydrocarbons, which are products of combustion. Cancer causation by tobacco smoke is not attributable to any one chemical component, or any one class of chemicals present, but to an overall effect of the complex mixture of chemicals in smoke. Mechanistic inferences which can be made from epidemiological studies, together with relevant experimental data, indicate a scenario compatible with “multistage carcinogenesis” as understood at the cellular and molecular level (Multistage carcinogenesis, p84) [16]. Epidemiological studies indicate that for cancers of the lung, bladder and head and neck (data for other cancers are inadequate for such evaluation), the various carcinogens in tobacco smoke exert an effect on both early and late steps in the process of carcinogenesis. Evidence for early effects comes from the higher risk associated with early age at starting smoking and with increasing time since beginning smoking, while the continued elevated risk, albeit at decreasing levels over time, following quitting smoking is a strong argument for late effects. Most chemical carcinogens in tobacco smoke require metabolic activation in order to exert a carcinogenic effect [17]. Fig. 2.8 Estimated prevalence of smoking among adults by region, in the early 1990s. Fig. 2.9 A model describing stages of the tobacco epidemic based on data from developed countries. Note the time lag between increase in consumption and the manifestation of lung cancer The requisite enzymes are present in lung and other “target” organs. Individual risk may be affected by the activity and levels of enzymes such as glutathione-S-transferase, cytochrome P450 and N-acetyl transferases. In the course of metabolism, reactive forms of polycyclic aromatic hydrocarbons, nitrosamines and aromatic amines are generated and become covalently bound to DNA in relevant tissues. Such DNA adducts, and the products of their repair, have been detected in tissues, bodily fluids and urine from smokers and from persons exposed to environmental tobacco smoke. The molecular genetics of tobacco smokeinduced lung and other cancers are being progressively elucidated. An increasing number of genes are implicated as being relevant to a carcinogenic outcome [18]. The degree of current understanding is exemplified by studies of the pattern of mutation in the p53 gene. When comparison is made of particular mutation frequencies in lung cancers from smokers and non-smokers, differences are evident. Using relevant experimental systems, mutations evident in smokers are attributable, at least in part, to the miscoding caused by the binding of some polycyclic aromatic hydrocarbons to DNA [19]. Tobacco 27
Page 2 and 3: WORLD HEALTH ORGANIZATION WHO OMS I
Page 4 and 5: WORLD CANCER REPORT Editors Bernard
Page 6 and 7: CONTENTS Foreword 9 1 The global bu
Page 8 and 9: The global burden of cancer Cancer
Page 10 and 11: Fig. 1.2 Incidence and mortality of
Page 12 and 13: Central and Southern Europe differ
Page 14 and 15: Incidence of cancer in South Centra
Page 16 and 17: from documentation of disease to a
Page 18 and 19: TOBACCO SUMMARY >In addition to lun
Page 20 and 21: Fig. 2.3 Smoking by children is inc
Page 24 and 25: PHARMACOLOGICAL APPROACHES TO SMOKI
Page 26 and 27: level the dose—response relations
Page 28 and 29: lipoprotein-associated cholesterol,
Page 30 and 31: Agent Cancer site/cancer Main indus
Page 32 and 33: Industry, occupation Cancer site/ca
Page 34 and 35: to occupational exposures in develo
Page 36 and 37: Air pollutant WHO Air Quality Guide
Page 38 and 39: der cancer of the order of 50% is p
Page 40 and 41: AFLATOXIN B 1 HEPATITIS VIRUS (chro
Page 42 and 43: Fig. 2.30 Correlation between regio
Page 44 and 45: MEDICINAL DRUGS SUMMARY > Certain d
Page 46 and 47: Drug or drug combination Cancer IAR
Page 48 and 49: Agent or substance Cancer site/canc
Page 50 and 51: sources of electromagnetic fields [
Page 52 and 53: CHRONIC INFECTIONS SUMMARY > Infect
Page 54 and 55: Infection Subclinical Mutagenic fac
Page 56 and 57: TUMOURS ASSOCIATED WITH HIV/AIDS Ap
Page 58 and 59: DIET AND NUTRITION SUMMARY > Up to
Page 60 and 61: Fig. 2.54 The age-adjusted mortalit
Page 62 and 63: OVERWEIGHT, OBESITY AND PHYSICAL AC
Page 64 and 65: IMMUNOSUPPRESSION SUMMARY >Persiste
Page 66 and 67: Fig. 2.64 Cancer following immunosu
Page 68 and 69: Syndrome Gene Location Cancer site/
Page 70 and 71: viduals, confirmation of a gene def
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REPRODUCTIVE FACTORS AND HORMONES S
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PHYTO-ESTROGENS AND CANCER PEVENTIO
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Indicator Number of oral contracept
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Mechanisms of tumour development Th
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The stages in tumorigenesis have be
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PRECURSOR LESIONS IN CHEMOPREVENTIO
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CARCINOGEN ACTIVATION AND DNA REPAI
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adducts, a few weeks or months for
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I Reactive oxygen species Methylati
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which remove the mismatched bases,
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Common human oncogenes Many common
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product of the RB1 gene (pRb) and a
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ates a molecular bridge between p53
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potential cancer genes altered thro
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One of the earliest genes to be ide
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Regulation of the cell cycle and co
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CELL-CELL COMMUNICATION SUMMARY > C
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Connexin genes and tumour suppressi
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APOPTOSIS SUMMARY > The term apopto
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Caspase-8 Caspase-3 c-FLIP Procaspa
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ways. Several options are under inv
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INVASION AND METASTASIS SUMMARY > T
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laminin, entactin and also heparan
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Target Example of agent Comments Ad
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organs, and to respond to local gro
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TOBACCO CONTROL SUMMARY > Tobacco-i
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Region Deaths due to % of total dea
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ipated, is primarily attributable t
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smoke. This may be achieved in part
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there is no evidence for the effica
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industries, processes and occupatio
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stoves arises in rural areas of dev
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Climbing plants on trellis at end r
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HEPATITIS B VACCINATION SUMMARY > P
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Fig. 4.17 Chronic active HBV-associ
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HUMAN PAPILLOMAVIRUS VACCINATION SU
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Vaccine Site of trial Number of pat
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prolonged use. Similar drugs, that
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aspirin and other non-steroidal ant
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SCREENING FOR BREAST CANCER SUMMARY
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Fig. 4.35 Cumulative mortality from
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SCREENING FOR PROSTATE CANCER SUMMA
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Fig. 4.39 Poster designed for an an
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is around 10% for cancer (out of ev
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45 with one positive rehydrated FOB
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eing based on (i) time trends in th
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Fig. 4.48 Women at a clinic in Indi
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SCREENING FOR ORAL CANCER SUMMARY >
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India will provide useful informati
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cer incidence following cure of inf
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100 50 25 10 5 2.5 1 Japan Males Fe
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Human cancers by organ site Maligna
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tobacco smoking: age at start, aver
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diagnosis is usually confirmed by h
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is frequent and survival rates are
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Fig. 5.14 Physician reading digital
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Markers of prognosis in breast canc
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cer in the contralateral breast (Ch
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100 50 25 10 5 2.5 1 Japan Chile Po
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depends on staging. Small intramuco
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Fig. 5.30 A diet rich in fresh frui
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ane protein involved in cell adhesi
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LIVER CANCER SUMMARY > About 560,00
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Fig. 5.39 A woman in the Gambia pre
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REFERENCES 1. Ferlay J, Bray F, Par
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Certain Possible Uncertain Age Andr
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Management The dramatic division be
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TUMOUR NORMAL Gastrula PGC 2n Impri
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CANCERS OF THE FEMALE REPRODUCTIVE
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Fig. 5.62 Five-year relative surviv
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Inheritance of high-penetrance gene
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invasive malignant. Malignant germ
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OESOPHAGEAL CANCER SUMMARY >Cancer
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Fig. 5.76 A radiographic view of an
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with a stent; laser recannulation,
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Fig. 5.82 Risk of bladder cancer am
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Partial cystectomy is appropriate f
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poorly known since hypopharyngeal c
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Fig. 5.92 Oral leukoplakia with mil
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LYMPHOMA SUMMARY > Malignant lympho
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T Fig. 5.101 Nuclear magnetic reson
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Fig. 5.106 Five-year relative survi
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Fig. 5.109 The immediate aftermath
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A B Fig. 5.113 Acute myeloid leukae
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Fig. 5.118 Five-year relative survi
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Fig. 5.120 Age-specific incidence a
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Hereditary condition Mode of inheri
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MELANOMA SUMMARY > Approximately 13
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Fig. 5.131 Primary melanoma with a
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THYROID CANCER SUMMARY > Cancer of
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Papillary carcinoma RET/PTC TRK BRA
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KIDNEY CANCER SUMMARY > Cancer of t
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Stage Clear cell carcinoma Papillar
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TUMOURS OF THE NERVOUS SYSTEM SUMMA
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ing the optic tract, brain stem and
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mut = mutant p53 wt = wildtype p53
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SURGICAL ONCOLOGY SUMMARY > Surgica
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Year Radical mastectomy (%) Modifie
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TELEMEDICINE The prospects for tele
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Equipment Energy 50% depth dose App
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CANCER EDUCATION IN MEDICAL COURSES
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Fig. 6.10 Crystals of cisplatin: mo
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Responsiveness Cancer (in decreasin
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Most of the world’s most common c
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treatment of cancer. The problems l
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duction. It is clear that tumour ce
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REHABILITATION SUMMARY > Rehabilita
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cer and its associated disability.
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REFERENCES 1. Garden FH, Gillis TA
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Cancer pain relief varies and in so
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EMERGING ISSUES IN PALLIATIVE CARE
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Cancer control The negative impact
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priority to cancer control activiti
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Prevention of cancer Every country
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- Assessing the magnitude of the ca
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high-risk women. Further details on
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ecords departments are either rudim
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THE INTERNATIONAL AGENCY FOR RESEAR
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in the capitals/urban areas of four
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in the overall cancer strategy. WHO
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68% 1955 1975 1995 2025 32% 40% by
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Fig. 7.15 A grandfather at work in
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Fig. 7.17 Main causes of death in d
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Contributors and Reviewers Sources
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Dr Vera Luiz da Costa e Silva Tobac
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Georgia Moore Centers for Disease C
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REVIEWERS Dr Sandra E. Brooks 405 W
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2.53 T. Norat and E. Riboli, IARC 2
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Gastroenterology, 118(2 Suppl 1): S
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5.106 & 5.107 IARC/SEER/Osaka Cance
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4.17 R. Lambert, IARC/Adapted from
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Brain cancer, see nervous system tu
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Fibroblast growth factor (FGF), 117
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Microarray, 240 Micronutrients, 65,
Page 341 and 342:
S Saccharin, 64, 85 Salicin, 153 Sa
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