world cancer report - iarc

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REFERENCES 1. Jorgensen J, Imrie CW (1998) Pancreatic cancer. In: Morris D, Kearsley J., Williams C. eds, Cancer: a comprehensive clinical guide, Harwood Academic Publishers. 2. Andren-Sandberg A, Hoem D, Backman PL (1999) Other risk factors for pancreatic cancer: hormonal aspects. Ann Oncol, 10 Suppl 4: 131-135. 3. Gold EB, Goldin SB (1998) Epidemiology of and risk factors for pancreatic cancer. Surg Oncol Clin N Am, 7: 67- 91. 4. Barkin JS, Goldstein JA (1999) Diagnostic approach to pancreatic cancer. Gastroenterol Clin North Am, 28: 709- 22, xi. 5. DiMagno EP (1999) Pancreatic cancer: clinical presentation, pitfalls and early clues. Ann Oncol, 10 Suppl 4: 140- 142. 6. Hilgers W, Kern SE (1999) Molecular genetic basis of pancreatic adenocarcinoma. Genes Chromosomes Cancer, 26: 1-12. 7. Hruban RH, Petersen GM, Goggins M, Tersmette AC, Offerhaus GJ, Falatko F, Yeo CJ, Kern SE (1999) Familial pancreatic cancer. Ann Oncol, 10 Suppl 4: 69-73. 8. Whitcomb DC (1999) The spectrum of complications of hereditary pancreatitis. Is this a model for future gene therapy? Gastroenterol Clin North Am, 28: 525-541. 252 Human cancers by organ site 9. Lowenfels AB, Maisonneuve P (1999) Pancreatic cancer: development of a unifying etiologic concept. Ann N Y Acad Sci, 880: 191-200. 10. Sakorafas GH, Tsiotou AG, Tsiotos GG (2000) Molecular biology of pancreatic cancer; oncogenes, tumour suppressor genes, growth factors, and their receptors from a clinical perspective. Cancer Treat Rev, 26: 29- 52. 11. Schutte M (1999) DPC4/SMAD4 gene alterations in human cancer, and their functional implications. Ann Oncol, 10 Suppl 4: 56-59. 12. Klöppel G, Hruban RH, Longnecker MP, Adler G, Kern SE, Partanen TJ (2000) Ductal adenocarcinoma of the pancreas. In: Hamilton SR, Aaltonen LA eds, World Health Organization Classification of Tumours. Pathology and Genetics of Tumours of the Digestive System, Lyon, IARCPress, 221-230. 13. Birk D, Beger HG, Fortnagel G, Hermanek P (1997) International documentation system for pancreatic cancer (IDS). The future in pancreatic cancer evaluation. Digestion, 58: 578-579. WEBSITES NCI Pancreatic Cancer Homepage: http://www.cancer.gov/cancer_information/cancer_type /pancreatic/ The Johns Hopkins Medical Institution, Pancreatic Cancer Homepage: http://www.path.jhu.edu/pancreas/
MELANOMA SUMMARY > Approximately 133,000 new cases of malignant melanoma are diagnosed worldwide each year. > The risk of developing this highly malignant skin tumour varies markedly according to racial background (skin pigmentation) and geography (sunlightderived ultraviolet irradiation); highest incidence rates occur in white populations in Australia. > In Nordic countries, a steep increase in melanoma incidence has been attributed to excessive sun exposure during vacations in Southern countries. > Prognosis for patients with early-stage < 0.5 < 1.3 < 2.6 < 4.7 < 34.9 melanoma is very good, while metastatic melanoma is largely resistant to cur- Age-standardized incidence/100,000 population rent therapies. Fig. 5.127 The global burden of melanoma of the skin in women. Incidence rates are high in North America, Europe, Australia and New Zealand. Definition Melanoma is a malignant proliferation of melanocytes, the pigment-forming cells of the skin, which is the site of most (>95%) disease. Epidemiology There are about 133,000 new cases of melanoma worldwide each year, of which almost 80% are in North America, Europe, Australia and New Zealand. Incidence is similar in men and in women. Malignant melanoma of the skin occurs predominantly in white-skinned populations (“Caucasians”) living in countries where there is high intensity ultraviolet radiation but this malignancy afflicts to some degree all ethnic groups (Fig. 5.127). Assessed in relation to skin colour, melanoma incidence falls dramatically as skin pigmentation increases and the disease is very rare in dark skinned people. The highest incidence of melanoma occurs in Australia where the population is predominantly white, there is an average of six hours of bright sunlight every day of the year and there is an essentially outdoors lifestyle. The lifetime risk of developing melanoma in Australia is 4-5% in men and 3-4% in women. Dark-skinned people have a low risk of melanoma. In Africa and South America, the sole of the foot, where the skin is not pigmented, is the most frequent site affected in the context of a low incidence. Asian peoples have a low risk of melanoma despite their paler skins; naevi in Asian people, though common, are predominantly of the acral-lentiginous type which have low malignant potential. Marked increases in incidence and mortality are being observed in both sexes in many countries (e.g. Fig. 5.128), even where rates were formerly low, such as Japan. In the Nordic countries, for example, this averages some 30% every five years. Mortality rates are slightly higher in men than in women, with Australia and New Zealand registering rates of 4.8 and 5.3 for men, and 2.5 and 3.2 for women, respectively [1]. Etiology It is estimated that 80% of melanoma is caused by ultraviolet damage [2] to sensitive skin, i.e. skin that burns easily, fair or reddish skin, multiple freckles, skin that does not tan and develops naevi in response to early sunlight exposure. Prevention of melanoma is based on limitation of exposure to ultraviolet radiation, particularly in the first 20 years of life (Reduction of exposure to UV radiation, p141). Ultraviolet radiation is particularly hazardous when it involves sporadic intense exposure and sunburn. Most damage caused by sunlight occurs in childhood and adolescence, making this the most important target group for prevention programmes. Established but rare risk factors include congenital naevi, immunosuppression and excessive use of solaria. While melanoma may occur anywhere on the skin, the majority of melanoma in men is Melanoma 253
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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
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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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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 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
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: Hereditary condition Mode of inheri
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
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
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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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