world cancer report - iarc

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Fig. 2.30 Correlation between regional incidence of hepatocellular carcinoma, dietary exposure to aflatoxin B 1, and prevalence of G>T mutations at codon 249 of the p53 tumour suppressor gene. Polychlorinated dibenzo-para-dioxins (which include 2,3,7,8-tetrachlorodibenzopara-dioxin, TCDD) are ubiquitous pollutants in soil sediments and air (Environmental pollution, p39). Human exposure occurs through eating meat and related foods. The burden of cancer attributable to such exposure is unknown [9]. Chemicals generated during food preparation Some chemicals formed during food preparation may present a carcinogenic hazard. The toxicity of these chemicals generally warrants the adoption of means to minimize their formation, particularly during industrialized food preparation. It has not been possible to attribute cancer causation in humans to hazards of this type specifically. A possible pragmatic approach to the prioritization of chemical carcinogens occurring as food contaminants has been proposed. The highest priority category is chemical carcinogens that are believed to act by a genotoxic mechanism [10]. 46 The causes of cancer p53 Heterocyclic amines Certain heterocyclic amines are formed by pyrolysis of two amino acids, creatine and creatinine, during cooking of meat and fish at high temperature. Heterocyclic amines are carcinogenic in various organs of mice, rats and non-human primates, although their carcinogenic potential in humans has not yet been established [11]. Metabolism of heterocyclic amines can vary between individuals due to various genetic polymorphisms. Polycyclic aromatic hydrocarbons Polycyclic aromatic hydrocarbons can be generated in meat when it is fried, roasted or cooked over an open flame, and many members of this chemical class are carcinogenic. These compounds can also be formed during the curing and processing of raw foods prior to cooking. A number of polycyclic aromatic hydrocarbons, such as benzo[a]pyrene and benzanthracene, are present in smoke from the burning of fuels, tobacco and weeds. Fig. 2.31 Nitrosamines are present in smoked fish consumed in many parts of the world, including the Gambia. N-Nitroso compounds N-Nitroso compounds are a wide class of chemicals, many of which (particularly N-nitrosamines) are potent carcinogens in several species of experimental animals, and probably in humans [12]. Nitrosamines may be formed by chemical reactions in foods containing added nitrates and nitrites, such as salt-preserved fish and meat, and in foods processed by smoking or direct fire drying. The use of fertilizers may influence the level of nitrites in food, which may be a factor in determining generation of nitrosamines during food preparation and storage. Some industrial procedures, including brewing of beer, have been modified to reduce nitrosamine formation. Studies on volunteers consuming supplements of nitrate, or large portions of red meat, indicate that N-nitroso compounds can also be produced endogenously in the stomach and colon. Endogenous formation of nitrosamines is inhibited by several natural antioxidants, such as vitamins C and E, present in fruit and vegetables. Metals The hazard presented by dietary metals, whether regarded as essential nutrients or contaminants, is difficult to assess [13].
REFERENCES 1. Wild CP, Hall AJ (2000) Primary prevention of hepatocellular carcinoma in developing countries. Mutat Res, 462: 381-393. 2. Smela ME, Currier SS, Bailey EA, Essigmann JM (2001) The chemistry and biology of aflatoxin B(1): from mutational spectrometry to carcinogenesis. Carcinogenesis, 22: 535-545. 3. Montesano R, Hainaut P, Wild CP (1997) Hepatocellular carcinoma: from gene to public health. J Natl Cancer Inst, 89: 1844-1851. 4. IARC (1993) Some Naturally Occurring Substances: Food Items and Constituents, Heterocyclic Aromatic Amines and Mycotoxins (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 56), Lyon, IARCPress . 5. Castegnaro M, Plestina R, Dirheimer G, Chernozemsky IN, Bartsch H, eds (1991) Mycotoxins, Endemic Nephropathy and Urinary Tract Tumours (IARC Scientific Publications, No. 115), Lyon, IARCPress. 6. Prakash AS, Pereira TN, Reilly PE, Seawright AA (1999) Pyrrolizidine alkaloids in human diet. Mutat Res, 443: 53- 67. 7. Shahin M, Smith BL, Prakash AS (1999) Bracken carcinogens in the human diet. Mutat Res, 443: 69-79. 8. Department of Health (1999) Organochlorine insecticides and breast cancer. In: 1999 Annual Report of the Committees on Toxicity, Mutagenicity, Carcinogenicity of Chemicals in Food, Consumer Products and the Environment, London, Department of Health (UK), 67-75. 9. van Leeuwen FX, Feeley M, Schrenk D, Larsen JC, Farland W, Younes M (2000) Dioxins: WHO's tolerable daily intake (TDI) revisited. Chemosphere, 40: 1095-1101. 10. McDonald AL, Fielder RJ, Diggle GE, Tennant DR, Fisher CE (1996) Carcinogens in food: priorities for regulatory action. Hum Exp Toxicol, 15: 739-746. 11. Layton DW, Bogen KT, Knize MG, Hatch FT, Johnson VM, Felton JS (1995) Cancer risk of heterocyclic amines in cooked foods: an analysis and implications for research. Carcinogenesis, 16: 39-52. 12. O'Neill IK, Chen J, Bartsch H, Dipple A, Shuker DEG, Kadlubar FF, Segerbäck D, Bartsch H, eds (1991) Relevance to Human Cancer of N-Nitroso Compounds, Tobacco Smoke and Mycotoxins (IARC Scientific Publications, No. 105), Lyon, IARCPress. 13. Rojas E, Herrera LA, Poirier LA, Ostrosky-Wegman P (1999) Are metals dietary carcinogens? Mutat Res, 443: 157-181. WEBSITE WHO Food Safety Programme: http://www.who.int/fsf/index.htm Food contaminants 47
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 22 and 23: Cancers positively Sex Standardized
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 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
Page 72 and 73: REPRODUCTIVE FACTORS AND HORMONES S
Page 74 and 75: PHYTO-ESTROGENS AND CANCER PEVENTIO
Page 76 and 77: Indicator Number of oral contracept
Page 79 and 80: Mechanisms of tumour development Th
Page 81 and 82: The stages in tumorigenesis have be
Page 83 and 84: PRECURSOR LESIONS IN CHEMOPREVENTIO
Page 85 and 86: CARCINOGEN ACTIVATION AND DNA REPAI
Page 87 and 88: adducts, a few weeks or months for
Page 89 and 90: I Reactive oxygen species Methylati
Page 91 and 92: 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
Page 155 and 156:
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
Page 161 and 162:
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
Page 199 and 200:
Fig. 5.39 A woman in the Gambia pre
Page 201 and 202:
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
Page 217 and 218:
OESOPHAGEAL CANCER SUMMARY >Cancer
Page 219 and 220:
Fig. 5.76 A radiographic view of an
Page 221 and 222:
with a stent; laser recannulation,
Page 223 and 224:
Fig. 5.82 Risk of bladder cancer am
Page 225 and 226:
Partial cystectomy is appropriate f
Page 227 and 228:
poorly known since hypopharyngeal c
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Fig. 5.92 Oral leukoplakia with mil
Page 231 and 232:
LYMPHOMA SUMMARY > Malignant lympho
Page 233 and 234:
T Fig. 5.101 Nuclear magnetic reson
Page 235 and 236:
Fig. 5.106 Five-year relative survi
Page 237 and 238:
Fig. 5.109 The immediate aftermath
Page 239 and 240:
A B Fig. 5.113 Acute myeloid leukae
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Fig. 5.118 Five-year relative survi
Page 243 and 244:
Fig. 5.120 Age-specific incidence a
Page 245 and 246:
Hereditary condition Mode of inheri
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MELANOMA SUMMARY > Approximately 13
Page 249 and 250:
Fig. 5.131 Primary melanoma with a
Page 251 and 252:
THYROID CANCER SUMMARY > Cancer of
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Papillary carcinoma RET/PTC TRK BRA
Page 255 and 256:
KIDNEY CANCER SUMMARY > Cancer of t
Page 257 and 258:
Stage Clear cell carcinoma Papillar
Page 259 and 260:
TUMOURS OF THE NERVOUS SYSTEM SUMMA
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ing the optic tract, brain stem and
Page 263 and 264:
mut = mutant p53 wt = wildtype p53
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SURGICAL ONCOLOGY SUMMARY > Surgica
Page 267 and 268:
Year Radical mastectomy (%) Modifie
Page 269 and 270:
TELEMEDICINE The prospects for tele
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Equipment Energy 50% depth dose App
Page 273 and 274:
CANCER EDUCATION IN MEDICAL COURSES
Page 275 and 276:
Fig. 6.10 Crystals of cisplatin: mo
Page 277 and 278:
Responsiveness Cancer (in decreasin
Page 279 and 280:
Most of the world’s most common c
Page 281 and 282:
treatment of cancer. The problems l
Page 283 and 284:
duction. It is clear that tumour ce
Page 285 and 286:
REHABILITATION SUMMARY > Rehabilita
Page 287 and 288:
cer and its associated disability.
Page 289 and 290:
REFERENCES 1. Garden FH, Gillis TA
Page 291 and 292:
Cancer pain relief varies and in so
Page 293 and 294:
EMERGING ISSUES IN PALLIATIVE CARE
Page 295 and 296:
Cancer control The negative impact
Page 297 and 298:
priority to cancer control activiti
Page 299 and 300:
Prevention of cancer Every country
Page 301 and 302:
- Assessing the magnitude of the ca
Page 303 and 304:
high-risk women. Further details on
Page 305 and 306:
ecords departments are either rudim
Page 307 and 308:
THE INTERNATIONAL AGENCY FOR RESEAR
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in the capitals/urban areas of four
Page 311 and 312:
in the overall cancer strategy. WHO
Page 313 and 314:
68% 1955 1975 1995 2025 32% 40% by
Page 315 and 316:
Fig. 7.15 A grandfather at work in
Page 317 and 318:
Fig. 7.17 Main causes of death in d
Page 319 and 320:
Contributors and Reviewers Sources
Page 321 and 322:
Dr Vera Luiz da Costa e Silva Tobac
Page 323 and 324:
Georgia Moore Centers for Disease C
Page 325 and 326:
REVIEWERS Dr Sandra E. Brooks 405 W
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2.53 T. Norat and E. Riboli, IARC 2
Page 329 and 330:
Gastroenterology, 118(2 Suppl 1): S
Page 331 and 332:
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
Page 337 and 338:
Fibroblast growth factor (FGF), 117
Page 339 and 340:
Microarray, 240 Micronutrients, 65,
Page 341 and 342:
S Saccharin, 64, 85 Salicin, 153 Sa
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