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Fig. 4.20 HBV vaccination of infants in the Gambia. in preventing chronic liver disease and hepatocellular carcinoma at the individual level. Taiwan, which has high HBV carriage rates and a high hepatocellular carcinoma incidence, was one of the first countries to introduce routine vaccination in 1984. A nationwide statistically significant reduction in childhood hepatocellular carcinoma has already been observed in Taiwan among the vaccinated cohort of children aged 6-14 compared to the cohort of chil- REFERENCES 1. Edmunds WJ, Medley GF, Nokes DJ, Hall AJ, Whittle HC (1993) The influence of age on the development of the hepatitis B carrier state. Proc R Soc Lond B Biol Sci, 253: 197- 201. 2. Hall AJ, Smith PG (1999) Prevention of hepatocellular cancer: one of the most cost-effective ways to reduce adult mortality? Br J Cancer, 81: 1097-1098. 3. Coursaget P, Muñoz N (1999) Vaccination against infectious agents associated with human cancer. In: Newton R, Beral V, Weiss RA eds, Infection and Human Cancer, Vol. 33, New York, Cold Spring Harbor Laboratory Press, 355-381. Fig. 4.21 Risk of becoming a chronic carrier of HBV based on age at infection. Risk is highest in very young children. [1] dren born before implementation of the vaccination programme [6]. Over 80 countries have now integrated hepatitis B vaccine into their routine immunization programme, with varying levels of coverage (Fig. 4.16). Hepatitis B vaccine may now be available to around half the world’s children. However, children from countries with the highest risk of HBV infection are frequently the same countries with limited resources or infrastruc- 4. Viviani S, Jack A, Hall AJ, Maine N, Mendy M, Montesano R, Whittle HC (1999) Hepatitis B vaccination in infancy in The Gambia: protection against carriage at 9 years of age. Vaccine, 17: 2946-2950. 5. Montesano R, Hainaut P, Wild CP (1997) Hepatocellular carcinoma: from gene to public health. J Natl Cancer Inst, 89: 1844-1851. 6. Chang MH, Chen CJ, Lai MS, Hsu HM, Wu TC, Kong MS, Liang DC, Shau WY, Chen DS (1997) Universal hepatitis B vaccination in Taiwan and the incidence of hepatocellular carcinoma in children. Taiwan Childhood Hepatoma Study Group. N Engl J Med, 336: 1855-1859. ture to provide the vaccination. Despite the decline in vaccine cost, limited health budgets in poorer countries make ability to purchase vaccine a primary obstacle to global immunization. WHO and other donor and non-profit agencies have focused on developing a vaccine support strategy to aid those needy countries with an adequate vaccination infrastructure to purchase and provide hepatitis B vaccine to the world’s children. WEBSITES WHO fact sheets on vaccination against HBV and HCV: http://www.who.int/health-topics/hepatitis.htm CDC National Center for Infectious Diseases: http://www.cdc.gov/ncidod/diseases/hepatitis/b/ index.htm Hepatitis B vaccination 147
HUMAN PAPILLOMAVIRUS VACCINATION SUMMARY >Infection with human papillomaviruses is common and causes some benign lesions as well as cervical and other cancers. > Vaccines based on human papillomaviruses may be prophylactic, therapeutic or a combination of both, and are potentially a safe and effective means of preventing or controlling disease. > Technical difficulties associated with the development of such vaccines are considerable, but several phase I, II and III trials are under way. From a public health perspective, there is an overwhelming case to justify the development of human papillomavirus (HPV) vaccines. At least 50% of sexually active adults have had a genital HPV infection. Socalled “low-risk” HPV types cause benign lesions or genital warts, while others, called “high-risk” or “oncogenic” types, are the principal cause of cervical cancer and are also associated with other cancers of the anogenital region, and possibly with cancers of the upper aerodigestive tract and of the skin (Chronic infections, p56; Cancers of the female reproductive tract, p215). Since both genital warts and cervical cancer rates are rising in young women in some populations, the burden of HPV-associated disease is likely to increase in coming decades. HPV-associated lesions can regress spontaneously due to cell-mediated immunity. This is indicated by an increased risk of HPV infection and of HPV-associated lesions in immunosuppressed patients, and the observation that neutralizing antibodies can block HPV infection in vivo and in vitro [1]. On the other hand, the occurrence of chronic HPV infections and reinfections suggests that in some individuals natural immunity is not effective in controlling HPV 148 Prevention and screening infection. Although the exact mechanisms of immune evasion are not fully understood, the development of effective vaccines for papillomaviruses in various animal models [2-4] has stimulated the development of similar vaccines for humans. Three main types of HPV vaccine are being developed: prophylactic vaccines, therapeutic vaccines and combined or chimeric vaccines which have both effects. Prophylactic vaccines Vaccines based on the induction of neutralizing antibodies against the HPV structural proteins L1 and L2 are termed “prophylactic”. The generation of virus-like particles (VLPs), which are morphologically indistinguishable from authentic virions, apart from lacking the viral genome [5], has greatly accelerated the development of these vaccines (Table 4.9). VLPs for HPV 6, 11, 16, 18, 31, 33, 39, 45 and 58 have been produced in various laboratories. At least five HPV VLP-based vaccines have been developed and have gone through pre-clinical evaluation. Phase I-II clinical trials to assess safety, immunogenicity, dose, schedule, route of administration and adjuvants for these vaccines are being planned or have been initiated. The US National Cancer Institute (NCI) vaccine has been shown, in a phase I study of 58 women and 14 men, to be able to induce serum antibody titres that are approximately 40-fold higher than that observed during natural infection [6]. However, certain basic issues need to be solved before the mass use of these vaccines can commence [7,8]. Such issues include the HPV types to be included (HPV 16 accounts for 50% and HPV 18, 31 and 45 for a further 30% of cervical cancers), the route of administration, the target population (ideally infants) and the cost (Table 4.10). The ideal HPV vaccine will have to be polyvalent (i.e. contain the VLPs of the HPV types most commonly associated with cancer in a given population, Fig. 4.22), inexpensive, and able to confer a long-lasting protection for infants of both sexes. Although HPV-associated genital tumours are much more frequent in women than men, men act as vectors of the virus. While the problems already outlined are being solved, phase III trials to assess the efficacy of available VLP-based vaccines to prevent HPV infection and cervical intraepithelial neoplasia are being planned. For example, the NCI vaccine will be used in a phase III trial in Costa Rica in the context of a large cohort study on the natural history of HPV in Guanacaste province. Therapeutic and combined vaccines Vaccines based on the induction of cellular immunity directed against cells expressing viral proteins are termed “therapeutic” and are intended to induce Fig. 4.22 The most common HPV types found in cervical carcinoma biopsies, by country. M = multiple infections with HPV 16 and/or 18.
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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
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
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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: Fig. 4.17 Chronic active HBV-associ
Page 145 and 146: Vaccine Site of trial Number of pat
Page 147 and 148: prolonged use. Similar drugs, that
Page 149 and 150: aspirin and other non-steroidal ant
Page 151 and 152: SCREENING FOR BREAST CANCER SUMMARY
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
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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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