world cancer report - iarc

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OVERWEIGHT, OBESITY AND PHYSICAL ACTIVITY The body mass is most usefully measured as the body mass index (BMI), calculated by dividing the body weight in kilograms by the height in metres squared. The normal range is 18.5 to 25; overweight corresponds to BMI > 25 and obesity to a value greater than 30. In many developed countries, as much as half of the adult population may be overweight and more than 25% obese. Epidemiological studies have shown with varying degrees of consistency that excess body mass is associated with an increased cancer risk. The strongest and most consistent association with body mass has so far been seen for endometrial cancer, the risk of which is increased two- to six-fold in obese compared to lean women, both before and after menopause. A possible biological explanation for this association is that adipose tissue is rich in aromatase, which converts androstenedione to estrone, thus increasing estrogenic stimulation of the endometrial mucosa. Several studies have investigated markers of fat distribution such as waist-to-hip ratio or subscapular-to-tight-skinfold ratio Caloric intake and other dietary-related factors The results of animal experiments in which dietary restriction decreases the risk of cancer at some sites are not readily extrapolated to humans. While caloric intake can be employed as a single parameter of diet, caloric intake considered in isolation is an inadequate basis upon which to address a broad spectrum of studies concerning cancer risk. These studies indicate inter-relationships between caloric intake, body mass and physical activity. Thus it is argued that high energy intake per se is not a risk factor for cancer, but positive energy balance (energy balance being the difference 66 The causes of cancer in relation to endometrial cancer risk, with inconsistent results. Some studies found increased risk for markers of abdominal or android obesity (high waist-to-hip ratio or subscapular-to-tight-skinfold ratio) after adjustment for body mass index, while others did not. The relationship between body mass index and breast cancer is even more complex. The majority of case-control and prospective studies found that high body mass index increased breast cancer risk in postmenopausal women, while it may slightly reduce risk in premenopausal women. A possible explanation for this apparent paradox is that overweight before menopause could be related to anovulatory cycles and fewer ovulatory cycles (as determined by pregnancy and lactation) are generally associated with lower breast cancer risk. After menopause, obesity may act as for endometrial cancer by enhancing the peripheral (as opposed to gonadal and adrenal) production of estrogens. There is growing evidence that metabolic factors related to diet, nutritional status, anthropometry and physical activity have an influence on the development and clinical manifestation of various forms of can- between caloric intake and caloric expenditure) leading to obesity is a cancer risk factor [17]. Data have accumulated suggesting that some metabolic factors related to nutritional status, such as obesity and physical activity, may also play a role by increasing the risk of certain cancers (Box: Overweight, obesity and physical activity, above). Recently, several prospective studies have lent strong support to the hypothesis formulated decades ago regarding the prominent role of endogenous hormone levels in determining risk of cancer of the breast. It is also proposed that the insulin-resistance syndrome may underlie the relationship between obesity and hormone- Fig. 2.59 Regular physical exercise appears to be correlated with decreased risk of cancer. cer (Weight Control and Physical Activity, IARC Handbooks of Cancer Prevention, Vol. 6, 2001). Epidemiological studies suggest certain different dietary patterns may be specifically related to higher risk of particular types of cancer. The Western diet and lifestyle are generally associated with high incidence of cancers of the colorectum, breast, prostate and endometrium, but with low incidence of cancers of the stomach, oesophagus, liver and cervix uteri (see Reproductive factors and hormones, p76). dependent cancers. Variations in the pattern of estrogens, androgens, insulin-like growth factor and their binding proteins are probably determined by both environmental and lifestyle factors, as well as by inherited genetic characteristics, as suggested by recent studies on polymorphisms of genes encoding for enzymes regulating steroid hormone metabolism and hormone receptors (Reproductive factors and hormones, p76) Accordingly, the relationship between diet and cancer is proving to be more complex than was previously thought. Research based on a combination of laboratory investigations on human subjects and sound epidemiological projects of a
prospective nature is likely to shed new light on the link between nutritionally related factors and cancer [18]. In the REFERENCES 1. Doll R, Payne P, Waterhouse J, eds (1966) Cancer Incidence in Five Continents - A Technical Report, Berlin, Springer-Verlag. 2. Doll R, Muir C, Waterhouse J, eds (1970) Cancer Incidence in Five Continents, Berlin, Springer-Verlag. 3. WCRF/AICR (1997) Food, Nutrition and the Prevention of Cancer: a Global Perspective, World Cancer Research Fund/American Institute of Cancer Research. 4. Bueno-de-Mesquita HB, Ferrari P, Riboli E on behalf of EPIC (2002) Plant foods and the risk of colorectal cancer in Europe: preliminary findings. In Riboli E, Lambert R, Eds. Nutrition and Lifestyle: Opportunities for Cancer Prevention (IARC Scientific Publication No. 156), Lyon, IARCPress. 5. Palli D (2000) Epidemiology of gastric cancer: an evaluation of available evidence. J Gastroenterol, 35 Suppl 12: 84-89. 6. 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. 7. Norat T, Lukanova A, Ferrari P, Riboli E (2002) Meat consumption and colorectal cancer risk: dose response meta-analysis of epidemiological studies. Int J Cancer, 98: 241-256. 8. Reddy B, Engle A, Katsifis S, Simi B, Bartram HP, Perrino P, Mahan C (1989) Biochemical epidemiology of colon cancer: effect of types of dietary fiber on fecal mutagens, acid, and neutral sterols in healthy subjects. Cancer Res, 49: 4629-4635. 9. Layton DW, Bogen KT, Knize MG, Hatch FT, Johnson VM, Felton JS (1995) Cancer risk of heterocyclic amines in meantime, public health recommendations should focus on the benefits that can be expected from a diet rich in veg- cooked foods: an analysis and implications for research. Carcinogenesis, 16: 39-52. 10. Trichopoulou A, Lagiou P, Kuper H, Trichopoulos D (2000) Cancer and Mediterranean dietary traditions. Cancer Epidemiol Biomarkers Prev, 9: 869-873. 11. Ferguson LR (1999) Natural and man-made mutagens and carcinogens in the human diet. Mutat Res, 443: 1-10. 12. IARC (1999) Some Chemicals that Cause Tumours of the Kidney or Urinary Bladder in Rodents and Some Other Substances (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 73), Lyon, IARCPress. 13. Doll R, Peto R (1981) The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today. J Natl Cancer Inst, 66: 1191-1308. 14. Goodman GE (2000) Prevention of lung cancer. Crit Rev Oncol Hematol, 33: 187-197. 15. Choi SW, Mason JB (2000) Folate and carcinogenesis: an integrated scheme. J Nutr, 130: 129-132. 16. Clark LC, Dalkin B, Krongrad A, Combs GF, Jr., Turnbull BW, Slate EH, Witherington R, Herlong JH, Janosko E, Carpenter D, Borosso C, Falk S, Rounder J (1998) Decreased incidence of prostate cancer with selenium supplementation: results of a double-blind cancer prevention trial. Br J Urol, 81: 730-734. 17. Willett WC (2001) Diet and cancer: one view at the start of the millennium. Cancer Epidemiol Biomarkers Prev, 10: 3-8. 18. Riboli E, Kaaks R (2000) Invited commentary: the challenge of multi-center cohort studies in the search for diet and cancer links. Am J Epidemiol, 151: 371-374. etables and fruit, the maintenance of a healthy weight and a physically active lifestyle. WEBSITE NCI Division of Cancer Prevention: Diet, food, nutrition: http://www.cancer.gov/prevention/lifestyle.html#diet Diet and nutrition 67
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WORLD HEALTH ORGANIZATION WHO OMS I
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WORLD CANCER REPORT Editors Bernard
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CONTENTS Foreword 9 1 The global bu
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The global burden of cancer Cancer
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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 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 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,
Page 93 and 94: Common human oncogenes Many common
Page 95 and 96: product of the RB1 gene (pRb) and a
Page 97 and 98: ates a molecular bridge between p53
Page 99 and 100: potential cancer genes altered thro
Page 101 and 102: One of the earliest genes to be ide
Page 103 and 104: Regulation of the cell cycle and co
Page 105 and 106: CELL-CELL COMMUNICATION SUMMARY > C
Page 107 and 108: Connexin genes and tumour suppressi
Page 109 and 110: APOPTOSIS SUMMARY > The term apopto
Page 111 and 112: 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,
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S Saccharin, 64, 85 Salicin, 153 Sa
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