world cancer report - iarc

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Infection with S. haematobium is associated with the development of squamous cell carcinoma and in endemic areas, such as Egypt, this type constitutes 90% of bladder tumours [7]. A number of genes which regulate enzymes involved in the metabolism of bladder carcinogens have been identified and it has been hypothesized that subjects carrying specific genotypes could be at an increased risk of bladder cancer [8]. For example, a dominant mutation in the NAT2 gene causes slow metabolism of aromatic amines, favouring their transformation into active carcinogens; slow metabolizers may be at a 40% increased risk of bladder cancer. Similarly, individuals who are null for the GSTM1 gene, which encodes an enzyme involved in the detoxification of polycyclic aromatic hydrocarbons, have been reported to be at increased risk of bladder cancer. There is no evidence for high-penetrance gene mutations that carry an elevated risk of bladder cancer. The oncogene HRAS is mutated at codon 12 in about 40% of bladder tumours. Overexpression of the epidermal growth factor receptor is associated with invasive disease. The gene encoding c-erbB2 (ERBB2) is amplified in a small proportion of bladder tumours. Cytogenetic and molecular techniques have implicated aberration/partial loss of chromosome 9 as a common feature in Cyclin D1 amplification Chromosome 9 LOH TRANSFORMED UROTHELIAL CELL p53 gene inactivation bladder cancer, and the cyclin-dependent kinase inhibitors p16 INK4A and p15 are also implicated in this context. Altered expression of the phosphorylated form of the retinoblastoma protein is common, and most often encountered in invasive tumours. Nuclear overexpression of p53 protein, essentially attributable to mutation of the gene, is common and is associated with disease progression (Fig. 5.86) [9]. Management Most patients with carcinoma in situ progress to muscle invasion within 10 years, but can achieve good responses to intravesical therapy - the administration of a therapeutic agent directly into the bladder, thereby exposing the mucosa to high drug concentrations [10]. The most commonly used agent in intravesical therapy for superficial transitional cell carcinomas, to prevent recurrence, and possibly decrease progression and improve survival, is bacille Calmette-Guérin (BCG), an attenuated strain of the Mycobacterium bovis bacterium which causes tuberculosis. Cytotoxic drugs such as thiotepa, doxorubicin, mitomycin C and/or ethoglucid may be used for superficial tumours to prevent recurrence. The currently preferred treatment for patients with invasive bladder cancer is radical cystectomy. This involves excision VEGF upregulation Cyclin D activation PAPILLARY TRANSITIONAL CELL CARCINOMA “superficial” CARCINOMA in situ (pre-invasive transitional cell carcinoma) p53, RB gene inactivation PDECGF expression Fig. 5.87 Five-year relative survival rates after diagnosis of bladder cancer. of the bladder, prostate and seminal vesicles in males or the bladder, ovaries, uterus, urethra and part of the vagina in females. Urinary diversion, and some restoration of bladder function, may be achieved through a range of reconstruction options that continue to be refined and improved. Adjuvant chemotherapy (e.g with cisplatin, methotrexate and vinblastine, or the latter combination plus doxorubicin) may be employed. Several new agents have been identified [11]. RECURRENT TRANSITIONAL CELL CARCINOMA INVASIVE TRANSITIONAL CELL CARCINOMA Fig. 5.86 Genetic alterations associated with the development of bladder cancer. LOH = loss of heterozygosity, VEGF = vascular endothelial growth factor, PDECGF = platelet derived endothelial cell growth factor. 230 Human cancers by organ site
Partial cystectomy is appropriate for only a minor proportion of patients with invasive bladder cancer. Radical radiation therapy as sole treatment has been evaluated, and criteria contributing to a favourable outcome (tumour size, stage, morphology, REFERENCES 1. Ferlay J, Bray F, Parkin DM, Pisani P, eds (2001) Globocan 2000: Cancer Incidence and Mortality Worldwide (IARC Cancer Bases No. 5), Lyon, IARCPress. 2. Brennan P, Bogillot O, Cordier S, Greiser E, Schill W, Vineis P, Lopez-Abente G, Tzonou A, Chang-Claude J, Bolm- Audorff U, Jockel KH, Donato F, Serra C, Wahrendorf J, Hours M, T'Mannetje A, Kogevinas M, Boffetta P (2000) Cigarette smoking and bladder cancer in men: a pooled analysis of 11 case-control studies. Int J Cancer, 86: 289- 294. 3. Silverman DT, Morrison AS, Devesa SS (1996) Bladder cancer. In: Scottenfeld D, Fraumeni, FJ eds, Cancer Epidemiology and Prevention, Oxford, New York, Oxford University Press, 1156-1179. 4. Pisani P, Parkin DM, Muñoz N, Ferlay J (1997) Cancer and infection: estimates of the attributable fraction in 1990. Cancer Epidemiol Biomarkers Prev, 6: 387-400. 5. Saad A, Hanbury DC, McNicholas TA, Boustead GB, Woodman AC (2001) The early detection and diagnosis of bladder cancer: a critical review of the options. Eur Urol, 39: 619-633. 6. Lee R, Droller MJ (2000) The natural history of bladder cancer. Implications for therapy. Urol Clin North Am, 27: 1- 13, vii. etc.) have been determined. Tumour staging is based on the degree to which the tumour has invaded the bladder wall. In more developed countries, five-year relative survival is in the order of 65% (Fig. 5.87), and there has been a steady 7. Noss M, Klotz L (1998) Male urogenital cancer. In: Morris D, Kearsley J, Williams C eds, Cancer: a comprehensive clinical guide, Harwood Academic Publishers, 213- 222. 8. d'Errico A, Malats N, Vineis P, Boffetta P (1999) Review of studies of selected metabolic polymorphisms and cancer. In: Vineis P, Malats N, Lang M, d'Errico A, Caporaso N, Cuzick J, Boffetta P eds, Metabolic Polymorphisms and Susceptibility to Cancer (IARC Scientific Publication No. 148), Lyon, IARCPress, 323-393. 9. Brandau S, Bohle A (2001) Bladder cancer. I. Molecular and genetic basis of carcinogenesis. Eur Urol, 39: 491-497. 10. Metts MC, Metts JC, Milito SJ, Thomas CR, Jr. (2000) Bladder cancer: a review of diagnosis and management. J Natl Med Assoc, 92: 285-294. 11. Maluf FC, Bajorin DF (2001) Chemotherapy agents in transitional cell carcinoma: the old and the new. Semin Urol Oncol, 19: 2-8. improvement during the last decades. Survival is poorer in developing countries, with five-year relative survival rates of 30- 50%. WEBSITE NCI Bladder Cancer Homepage. http://www.cancer.gov/cancer_information/cancer_type/ bladder/ Bladder cancer 231
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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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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
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
Page 201 and 202: REFERENCES 1. Ferlay J, Bray F, Par
Page 203 and 204: Certain Possible Uncertain Age Andr
Page 205 and 206: Management The dramatic division be
Page 207 and 208: TUMOUR NORMAL Gastrula PGC 2n Impri
Page 209 and 210: CANCERS OF THE FEMALE REPRODUCTIVE
Page 211 and 212: Fig. 5.62 Five-year relative surviv
Page 213 and 214: Inheritance of high-penetrance gene
Page 215 and 216: 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: Fig. 5.82 Risk of bladder cancer am
Page 227 and 228: poorly known since hypopharyngeal c
Page 229 and 230: 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
Page 241 and 242: 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
Page 247 and 248: MELANOMA SUMMARY > Approximately 13
Page 249 and 250: Fig. 5.131 Primary melanoma with a
Page 251 and 252: THYROID CANCER SUMMARY > Cancer of
Page 253 and 254: 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
Page 261 and 262: ing the optic tract, brain stem and
Page 263 and 264: mut = mutant p53 wt = wildtype p53
Page 265 and 266: SURGICAL ONCOLOGY SUMMARY > Surgica
Page 267 and 268: Year Radical mastectomy (%) Modifie
Page 269 and 270: TELEMEDICINE The prospects for tele
Page 271 and 272: Equipment Energy 50% depth dose App
Page 273 and 274: 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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