world cancer report - iarc

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COLORECTAL CANCER SUMMARY > Cancers of the colon and rectum are rare in developing countries, but are the second most frequent malignancy in affluent societies; over 940,000 cases occur annually worldwide. > A major etiological factor is lifestyle involving a diet rich in fat, refined carbohydrates and animal protein, combined with low physical activity. >Studies suggest that risk can be reduced by decreasing meat consumption and increasing intake of vegetables and fruit. >Sequential genetic alterations mediate development of colon cancer, the earliest such change being mutation of the APC gene. >Familial clustering has usually a genetic basis. Typical syndromes include familial adenomatosis polyposis (FAP) and hereditary non-polyposis colon cancer (HNPCC). > Colonoscopy is the most reliable means for early detection. Progressively improved treatment has resulted in a five-year survival rate of about 50%. Definition The majority of cancers occurring in the colon and rectum are adenocarcinomas, which account for more than 90% of all large bowel tumours. Epidemiology Colorectal cancer ranks second in terms of both incidence and mortality in more developed countries. Nearly 945,000 new colorectal cancer cases are diagnosed worldwide each year and colorectal cancer is responsible for some 492,000 deaths. There is significant geographical variation in age-standardized incidence as well as in cumulative 0-74 year incidence, 198 Human cancers by organ site Fig. 5.29 Global incidence of colorectal cancer in women. Incidence rates are highest in North America, Western Europe and Australia/New Zealand. high rates occurring in countries of Europe, North America, in Australia and, more recently, in Japan (Fig. 5.29, Table 5.4). Migrant groups rapidly reach the higher level of risk of the adopted country, indicating that environmental factors play an important role in etiology. In North America, the trend towards increased incidence is now reversed [1] and a possible beneficial influence of dietary change and/or endoscopic polypectomy has been suggested. In Western Europe, this recent downward trend has not yet been observed. Most cases occur after the age of 60, except in individuals who carry a genetic predisposition. Etiology Colorectal cancer most commonly occurs sporadically and is inherited in only 5% of cases. Diet is by far the most important exogenous factor so far identified in the etiology of colorectal cancer [2]. It has been estimated that 70% of colorectal cancers could be prevented by nutritional intervention; various promot- < 3.8 < 7.7 < 12 < 21.2 Age-standardized incidence/100,000 population < 43.4 ing and protective factors have been identified in cohort and case-control studies [3]. There is convincing evidence that a diet high in calories and rich in animal fats, most often as red meat, and Cumulative incidence (%) Country Male Female Black, USA 5.60 4.22 White, USA 4.98 3.38 Denmark 4.48 3.53 Netherlands 4.25 3.25 Osaka, Japan 4.03 2.28 Qidong China 1.13 0.29 Khon Kaen,Thailand 1.06 0.64 Table 5.4 Cumulative incidence of colorectal cancer. The sum of incidence rates for all ages 0-74 provides a measure of the risk of developing colorectal cancer over a life span, in the absence of any other cause of death.
Fig. 5.30 A diet rich in fresh fruit and vegetables is associated with a lower risk of colorectal cancer. LKB1 DPC 4 PTEN ? NORMAL EPITHELIUM p53 PEUTZ-JEGHER SYNDROME JUVENILE POLYPOSIS SYNDROME HEREDITARY MIXED POLYPOSIS SYNDROME COWDEN SYNDROME 1p poor in vegetables and fibre is associated with an increased risk of colorectal cancer. Alcohol intake and smoking (for polyps only) have also been suggested to increase risk. Conversely, a low fat, high vegetable and possibly high fibre diet has a protective effect. Persons with an increased intake of vitamin D and calcium have a reduced risk of colon cancer [4]. Physical activity is also protective. The chronic use of non-steroidal anti-inflammatory drugs (NSAIDs) and aspirin is associated with a significant risk reduction in certain groups [5] (Chemoprevention, p151). It has also been suggested that use of hormone replacement therapy in postmenopausal women may decrease the risk of colon cancer. Conditions that predispose to the development of colorectal cancer include inflammatory bowel disease and Crohn disease [4]. Patients who have had previous malignant disease are also at a greater risk of developing a second colorectal tumour. EARLY INTERMEDIATE SMAD 4 LATE APC CTNNB1 ADENOMA KRAS ADENOMA SMAD 2 DCC ADENOMA p53 Aneuploidy METAPLASTIC POLYP FLAT ADENOMA Hypomethylation BCL 2 C MYC ? LOW GRADE DYSPLASIA EARLY MHAP/ SERRATED ADENOMA ? progression Familial PMS2 PMS1 MLH1 MSH2 GTBP δ polymerase HIGH GRADE DYSPLASIA INTERMEDIATE ADENOMA FLAT CANCER LATE RER+ ADENOMA LATE ADENOMA Detection Bleeding is a common symptom of advanced cancer. Diarrhoea suggests a right-sided tumour and constipation or occlusion suggests a left-sided tumour. However, premalignant lesions (adenomatous polyps) and cancer limited to the mucosa and submucosa are asymptomatic as a rule. Thus screening is now proposed for healthy people, with a view to cancer prevention (Screening for colorectal cancer, p163). Appropriate populations for screening may be those at an average risk who are above the age of 50, or individuals selected by a risk factor questionnaire (which may also be used to search for other cases in the family of the person examined). Should the questionnaire findings be positive, the risk is increased 2.5 fold for that individual. The questionnaire is included in the assessment of patients with sporadic colorectal cancer. It also aims to detect genetic syndromes, transmitted in a dominant autosomal fashion, which are much less frequent than sporadic cancer. SPORADIC CANCER ULCERATIVE COLITIS- ASSOCIATED COLORECTAL CARCINOMA SPORADIC CANCER RER+ CANCER Fig. 5.31 Putative genetic pathways in colorectal cancer. It is thought that the majority of tumours develop according to the original Vogelstein model (bold arrows). See Multistage carcinogenesis, p 84. MHAP=Mixed hyperplastic adenomatous polyps. Sporadic Hypermethylation TGFBR2 IGFIIR BAX E2F4 p15 p16 Bub1 cyclin D1 7q 17q 14q 22q 8p tPa CEA nm23 MMP E-cadherin CD44 Colorectal cancer 199
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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
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 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: depends on staging. Small intramuco
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 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
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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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