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tion trials in humans. We also need more knowledge of the concentrations of chemopreventive agents and their metabolites that prevent cancer in REFERENCES 1. IARC (1997) Non-Steroidal Anti-Inflammatory Drugs (IARC Handbooks of Cancer Prevention, Vol. 1), Lyon, IARCPress. 2. IARC (1998) Carotenoids (IARC Handbooks of Cancer Prevention, Vol. 2), Lyon, IARCPress. 3. IARC (1998) Vitamin A (IARC Handbooks of Cancer Prevention, Vol. 3), Lyon, IARCPress. 4. IARC (1999) Retinoids (IARC Handbooks of Cancer Prevention, Vol. 4), Lyon, IARCPress. 5. IARC (2001) Sunscreens (IARC Handbooks of Cancer Prevention, Vol. 5 ), Lyon, IARCPress. 6. IARC (2002) Weight Control and Physical Activity (IARC Handbooks of Cancer Prevention, Vol. 6), Lyon, IARCPress. 7. Taketo MM (1998) Cyclooxygenase-2 inhibitors in tumorigenesis (Part I). J Natl Cancer Inst, 90: 1529-1536. 8. DiGiovanni J (1992) Multistage carcinogenesis in mouse skin. Pharmacol Ther, 54: 63-128. 9. Thun MJ, Henley SJ, Patrono C (2002) Nonsteroidal anti-inflammatory drugs as anticancer agents: mechanistic, pharmacologic, and clinical issues. J Natl Cancer Inst, 94: 252-266. 10. Gupta RA, DuBois RN (2001) Colorectal cancer prevention and treatment by inhibition of cyclooxygenase-2. Nature Reviews Cancer, 1: 11-21. 11. Shureiqi I, Lippman SM (2001) Lipoxygenase modulation to reverse carcinogenesis. Cancer Res, 61: 6307- 6312. 12. IARC (1996) Some Pharmaceutical Drugs (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 66), Lyon, IARCPress. 13. Hansen LA, Sigman CC, Andreola F, Ross SA, Kelloff GJ, De Luca LM (2000) Retinoids in chemoprevention and differentiation therapy. Carcinogenesis, 21: 1271-1279. rodents and how such concentrations relate to those achievable in target human tissues. Finally, the selected intervention agents should be tested in 14. Howe GR, Benito E, Castelleto R, Cornee J, Estève J, Gallagher RP, Iscovich JM, Deng-ao J, Kaaks R, Kune GA (1992) Dietary intake of fiber and decreased risk of cancers of the colon and rectum: evidence from the combined analysis of 13 case-control studies. J Natl Cancer Inst, 84: 1887-1896. 15. Fuchs CS, Giovannucci EL, Colditz GA, Hunter DJ, Stampfer MJ, Rosner B, Speizer FE, Willett WC (1999) Dietary fiber and the risk of colorectal cancer and adenoma in women. N Engl J Med, 340: 169-176. 16. Vainio H, Morgan G, Kleihues P (1997) An international evaluation of the cancer-preventive potential of nonsteroidal anti-inflammatory drugs. Cancer Epidemiol Biomarkers Prev, 6: 749-753. 17. Vainio H, Rautalahti M (1998) An international evaluation of the cancer preventive potential of carotenoids. Cancer Epidemiol Biomarkers Prev, 7: 725-728. 18. Hennekens CH, Buring JE, Manson JE, Stampfer M, Rosner B, Cook NR, Belanger C, LaMotte F, Gaziano JM, Ridker PM, Willett W, Peto R (1996) Lack of effect of longterm supplementation with beta carotene on the incidence of malignant neoplasms and cardiovascular disease. N Engl J Med, 334: 1145-1149. 19. Heinonen OP, Albanes D, Virtamo J, Taylor PR, Huttunen JK, Hartman AM, Haapakoski J, Malila N, Rautalahti M, Ripatti S, Maenpaa H, Teerenhovi L, Koss L, Virolainen M, Edwards BK (1998) Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial. J Natl Cancer Inst, 90: 440-446. 20. 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. pilot clinical studies before embarking on large-scale randomized efficacy trials. WEBSITES The NCI’s Rapid Access to Preventive Intervention Development (RAPID) Program: http://www.cancer.gov/prevention/rapid/#1 Medscape Drug Info (for information on aspirin, β-carotene, celecoxib, tamoxifen, vitamin A): http://www.medscape.com/druginfo Chemoprevention 155
SCREENING FOR BREAST CANCER SUMMARY > The epidemic increase in breast cancer incidence has led to the introduction of population-based mammography screening. > The analysis of large randomized trials has shown that in women aged 50 to 69 years, mammography screening can reduce mortality from breast cancer by 25-30%. For women in the age group 40- 49 years the screening efficacy is significantly less. > The benefits of mammography in regional or national screening programmes is lower. Under optimal conditions with a high compliance rate, a mortality reduction of 20% appears achievable. > There is only indirect evidence that screening by clinical breast examination will reduce the number of breast cancer deaths. Cancer of the breast is the most common cancer in women worldwide and in many regions, including Europe and Australia, it is still the most common cause of death from cancer in women. Until recently, there has been little change in mortality rates in spite of the steady improvement in prognosis observed in recent years. Breast cancer is characterized by early systemic dissemination. As a result, awareness of symptoms, and subsequent diagnosis, often occur when disease is advanced and metastatic. Mammography (an X-ray examination of the breasts) can detect preclinical cancer, that is, detect the tumour before it is palpable, or before it causes symptoms. Tumours detected and treated at an early stage, can be expected to be associated with a better survival rate than those detected symptomatically. Early diagnosis may permit breast-conserving surgery (stage I disease), reduce the need for adjuvant thera- 156 Prevention and screening py or decrease complications related to intensive treatment and recurrence [1]. Population-based mammographic screening programmes were introduced in this context. The impact of screening Since the 1970s, the incidence of breast cancer has continued to increase. Only in 4 out of 70 populations assessed worldwide was there an average change between 1975 and 1990 of less than 0.5% per year [2,3]. Steep increases of the order of 3-5% per year have occurred in some Asian countries (e.g. Japan, Singapore), in Asian migrants to the USA (Japanese, Chinese and Filipino) and Southern Europe (Spain) (Fig. 4.31). In some developed countries (e.g. England and Wales, Finland, Denmark, The Netherlands, USA), a clear change in the speed of increase can be linked to the introduction of mass screening that occurred at different times in different countries, e.g. in the early 1980s in the USA, 1987-88 in England and Wales, early 1990s in The Netherlands. Some increase is attributable to reduced fertility and changing dietary habits. However, mam- Fig. 4.31 Populations exhibiting the largest increases in the incidence of breast cancer between 1975 and 1990. Fig. 4.30 Mammography, an X-ray examination of the breasts, is used to screen for breast cancer. ©GE Medical Systems mography is the main determinant of these relatively recent increases as indicated by trends in the incidence of in situ cancers [4,5]. Mortality has not consistently paralleled incidence trends everywhere. In fact, in some developed countries rates have been rather stable, even with incidence on the increase. No clear overall decline in mortality had been observed in any place before the late 1980s, when a smooth downturn occurred in Europe, North America and Australia. Such changes before the era of mammography can be attributed to a progression towards early diagnosis that took place in the 1970s, particularly in young generations. More recently, in the early 1990s, a drastic fall in mortality was seen in the UK and North America [6,7]. However, the fall occurred too soon after the widespread availability of mammography to be a consequence of it; rather, the success of adjuvant therapy based on chemotherapy and tamoxifen is the likely major cause of this trend. Protocols for screening As currently practised, population-based screening for breast cancer is based on mammographic examination, at prescribed intervals, of all women within a
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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
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Central and Southern Europe differ
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Incidence of cancer in South Centra
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from documentation of disease to a
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TOBACCO SUMMARY >In addition to lun
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Fig. 2.3 Smoking by children is inc
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Cancers positively Sex Standardized
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PHARMACOLOGICAL APPROACHES TO SMOKI
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level the dose—response relations
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lipoprotein-associated cholesterol,
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Agent Cancer site/cancer Main indus
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Industry, occupation Cancer site/ca
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to occupational exposures in develo
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Air pollutant WHO Air Quality Guide
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der cancer of the order of 50% is p
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AFLATOXIN B 1 HEPATITIS VIRUS (chro
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Fig. 2.30 Correlation between regio
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MEDICINAL DRUGS SUMMARY > Certain d
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Drug or drug combination Cancer IAR
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Agent or substance Cancer site/canc
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sources of electromagnetic fields [
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CHRONIC INFECTIONS SUMMARY > Infect
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Infection Subclinical Mutagenic fac
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TUMOURS ASSOCIATED WITH HIV/AIDS Ap
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DIET AND NUTRITION SUMMARY > Up to
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Fig. 2.54 The age-adjusted mortalit
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OVERWEIGHT, OBESITY AND PHYSICAL AC
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IMMUNOSUPPRESSION SUMMARY >Persiste
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Fig. 2.64 Cancer following immunosu
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Syndrome Gene Location Cancer site/
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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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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
Page 113 and 114: ways. Several options are under inv
Page 115 and 116: INVASION AND METASTASIS SUMMARY > T
Page 117 and 118: laminin, entactin and also heparan
Page 119 and 120: Target Example of agent Comments Ad
Page 121 and 122: organs, and to respond to local gro
Page 123 and 124: TOBACCO CONTROL SUMMARY > Tobacco-i
Page 125 and 126: Region Deaths due to % of total dea
Page 127 and 128: ipated, is primarily attributable t
Page 129 and 130: smoke. This may be achieved in part
Page 131 and 132: there is no evidence for the effica
Page 133 and 134: industries, processes and occupatio
Page 135 and 136: stoves arises in rural areas of dev
Page 137 and 138: Climbing plants on trellis at end r
Page 139 and 140: HEPATITIS B VACCINATION SUMMARY > P
Page 141 and 142: Fig. 4.17 Chronic active HBV-associ
Page 143 and 144: HUMAN PAPILLOMAVIRUS VACCINATION SU
Page 145 and 146: Vaccine Site of trial Number of pat
Page 147 and 148: prolonged use. Similar drugs, that
Page 149: aspirin and other non-steroidal ant
Page 153 and 154: Fig. 4.35 Cumulative mortality from
Page 155 and 156: SCREENING FOR PROSTATE CANCER SUMMA
Page 157 and 158: Fig. 4.39 Poster designed for an an
Page 159 and 160: is around 10% for cancer (out of ev
Page 161 and 162: 45 with one positive rehydrated FOB
Page 163 and 164: eing based on (i) time trends in th
Page 165 and 166: Fig. 4.48 Women at a clinic in Indi
Page 167 and 168: SCREENING FOR ORAL CANCER SUMMARY >
Page 169 and 170: India will provide useful informati
Page 171 and 172: cer incidence following cure of inf
Page 173 and 174: 100 50 25 10 5 2.5 1 Japan Males Fe
Page 175 and 176: Human cancers by organ site Maligna
Page 177 and 178: tobacco smoking: age at start, aver
Page 179 and 180: diagnosis is usually confirmed by h
Page 181 and 182: is frequent and survival rates are
Page 183 and 184: Fig. 5.14 Physician reading digital
Page 185 and 186: Markers of prognosis in breast canc
Page 187 and 188: cer in the contralateral breast (Ch
Page 189 and 190: 100 50 25 10 5 2.5 1 Japan Chile Po
Page 191 and 192: depends on staging. Small intramuco
Page 193 and 194: Fig. 5.30 A diet rich in fresh frui
Page 195 and 196: ane protein involved in cell adhesi
Page 197 and 198: LIVER CANCER SUMMARY > About 560,00
Page 199 and 200: 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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