world cancer report - iarc

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Fig. 2.64 Cancer following immunosuppression as a result of infection. The annual incidence of Kaposi sarcoma and non-Hodgkin lymphoma in San Francisco, USA, 1973-1998. Incidence increased dramatically between 1982 and 1990 as a result of the AIDS/HIV epidemic. Recent declines are partly attributable to the introduction of HAART therapy, although long-term risks remain unclear (Box: Tumours associated with AIDS/HIV, p60). C. Clarke (2001) AIDS, 15: 1913-1914 REFERENCES 1. Kinlen LJ (1996) Immunologic factors, including AIDS. In: Schottenfeld D, Fraumeni, JF eds, Cancer Epidemiology and Prevention, New York, Oxford University Press, 532- 545. 2. Neubert R, Neubert D (1999) Immune system. In: Marquardt H, Schafer SG, McClellan RO, Welsch F eds, Toxicology, San Diego, Academic Press, 371-436. 3. Hart PH, Grimbaldeston MA, Finlay-Jones JJ (2001) Sunlight, immunosuppression and skin cancer: role of histamine and mast cells. Clin Exp Pharmacol Physiol, 28: 1-8. 4. Penn I (2000) Cancers in renal transplant recipients. Adv Ren Replace Ther, 7: 147-156. 5. Mosier DE (1999) Epstein-Barr virus and lymphoproliferative disease. Curr Opin Hematol, 6: 25-29. 70 The causes of cancer 6. IARC (1997) Epstein-Barr Virus and Kaposi's Sarcoma Herpesvirus / Human Herpesvirus 8 (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 70), Lyon, IARCPress. 7. Wilson RE, Hager EB, Hampers CL, Corson JM, Merrill JP, Murray JE (1968) Immunologic rejection of human cancer transplanted with a renal allograft. N Engl J Med, 278: 479-483. 8. IARC (1996) Human Immunodeficiency Viruses and Human T-Cell Lymphotropic Viruses (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Vol. 67), Lyon, IARCPress. Immunosuppression caused by infectious agents Immunosuppression as a consequence of infection is especially severe in individuals infected with human immunodeficiency virus (HIV), the cause of acquired immune deficiency syndrome (AIDS). Certain cancers are characteristic of AIDS and in fact are AIDS-defining conditions in HIV-infected individuals [8]. These include non- Hodgkin lymphoma, especially of the brain, associated with EBV co-infection, and Kaposi sarcoma, which is associated with co-infection with another oncogenic herpesvirus, human herpesvirus 8 (Box: Tumours associated with HIV/AIDS, p60). The incidence of such tumours is increasing, partly as a result of the AIDS epidemic (Fig. 2.64). Both EBV and HIV-1, the principal cause of AIDS, are classified as Group 1 - carcinogenic to humans - in the IARC Monographs. WEBSITES International Association of Physicians in AIDS Care: http://www.iapac.org/ The Transplantation Society: http://www.transplantation-soc.org/ The United Network for Organ Sharing: http://www.unos.org/
GENETIC SUSCEPTIBILITY SUMMARY > Inherited cancer syndromes, usually involving germline mutations in tumour suppressor or DNA repair genes, may account for up to 4% of all cancers. > Inherited mutations of the BRCA1 gene account for a small proportion of all breast cancers, but affected family members have a greater than 70% lifetime risk of developing breast or ovarian cancer. > Identification of a germline mutation allows for preventive measures, clinical management and counselling. > Environmental factors may modify the cancer risk of individuals affected by inherited cancer syndromes. > Altered cancer susceptibility may be mediated by genetic variations in genes which, while not causing cancer, affect metabolism of carcinogens such as tobacco smoke. The genetic basis of cancer may be understood at two levels. Firstly, malignant cells differ from normal cells as a consequence of the altered structure and/or expression of oncogenes and tumour suppressor genes, which are found in all cancers. In this case, “the genetic basis of cancer” refers to acquired genetic differences (somatic) between normal and malignant cells due to mutation in the one individual. Secondly, the same phrase, “the genetic basis of cancer” may be used to refer to an increased risk of cancer that may be inherited from generation to generation. This section is concerned with the latter phenomenon. In many instances, the genes concerned have been identified, and have also sometimes been found to play a role in sporadic cancers as well. 1 mut 1 Marker A 1 mut Marker B 1 INHERITED 1 wt 1 2 wt 2 2 wt 2 2 wt 2 2 mut Fig. 2.65 Knudson’s hypothesis, explaining the development of an inherited cancer caused by the inactivation of a suppressor gene. Tumours of the eye (retinoblastoma) in individuals who have inherited a mutation in one allele of the retinoblastoma gene on chromosome 13 (“mut” rather than the normal wildtype “wt”), almost always occur in both eyes, due to inherited susceptibility. When this tumour type occurs spontaneously in a single retinal cell (“sporadic”) by a somatic mutation, only one eye is affected. The mechanisms by which the tumour arises can be determined by analysing the genotypes produced from normal (“N”) and tumour (“T”) tissues. Interplay between genes and environmental factors The influence of lifestyle factors (especially smoking), occupational exposures, dietary habits and environmental exposures (such as air pollution, sun exposure or low levels of radiation) on the development of cancer is clear; such factors account for a specific fraction of cancers. Another large fraction of cancers is caused by viral and other infectious agents, this being particularly relevant to the developing world. Carcinogenic agents, as diverse as chemicals, radiation and viruses, act primarily by damaging DNA in individual cells. Such damage has broad ramifications when it involves disruption of genes which control cell proliferation, repair of further DNA damage, and ability of cells to infiltrate (invade) surrounding tissue 2 wt 2 Germline mutation 2 Somatic mutation wt PREDISPOSED CELL 1 1 2 wt 2 Loss 1 1 Loss/duplication mut mut Recombination Localized TUMOUR AUTORADIOGRAM N T N T 1 1 1 1 1 (Chapter 3). Because each of these changes is relatively rare, the chance that the necessary combination of such events occurs to allow a normal cell to progress into a fully malignant tumour is small. However, the risk to an individual over his or her lifetime can be as large as 10% for cancers of the breast or prostate (that is, in some instances, 10% of the population will suffer from one of these cancer types in their lifetime). Genetic alterations accumulate gradually either through random events and/or by the action of specific environmental carcinogens, and thus most cancers in the population occur in middleaged and elderly individuals. Some individual cancers can be attributed to particular environmental factors. In the absence of apparent causative factors, a cancer is described as “sporadic” or “spontaneous”. 1 mut 1 1 2 mut mut 1 2 mut mut 2 N N N A B T N T A B T N T A B T N T A B Genetic susceptibility 71
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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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Page 18 and 19: TOBACCO SUMMARY >In addition to lun
Page 20 and 21: Fig. 2.3 Smoking by children is inc
Page 22 and 23: Cancers positively Sex Standardized
Page 24 and 25: PHARMACOLOGICAL APPROACHES TO SMOKI
Page 26 and 27: level the dose—response relations
Page 28 and 29: lipoprotein-associated cholesterol,
Page 30 and 31: Agent Cancer site/cancer Main indus
Page 32 and 33: Industry, occupation Cancer site/ca
Page 34 and 35: to occupational exposures in develo
Page 36 and 37: Air pollutant WHO Air Quality Guide
Page 38 and 39: der cancer of the order of 50% is p
Page 40 and 41: AFLATOXIN B 1 HEPATITIS VIRUS (chro
Page 42 and 43: Fig. 2.30 Correlation between regio
Page 44 and 45: MEDICINAL DRUGS SUMMARY > Certain d
Page 46 and 47: Drug or drug combination Cancer IAR
Page 48 and 49: Agent or substance Cancer site/canc
Page 50 and 51: sources of electromagnetic fields [
Page 52 and 53: CHRONIC INFECTIONS SUMMARY > Infect
Page 54 and 55: Infection Subclinical Mutagenic fac
Page 56 and 57: TUMOURS ASSOCIATED WITH HIV/AIDS Ap
Page 58 and 59: DIET AND NUTRITION SUMMARY > Up to
Page 60 and 61: Fig. 2.54 The age-adjusted mortalit
Page 62 and 63: OVERWEIGHT, OBESITY AND PHYSICAL AC
Page 64 and 65: IMMUNOSUPPRESSION SUMMARY >Persiste
Page 68 and 69: Syndrome Gene Location Cancer site/
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Page 72 and 73: REPRODUCTIVE FACTORS AND HORMONES S
Page 74 and 75: PHYTO-ESTROGENS AND CANCER PEVENTIO
Page 76 and 77: Indicator Number of oral contracept
Page 79 and 80: Mechanisms of tumour development Th
Page 81 and 82: The stages in tumorigenesis have be
Page 83 and 84: PRECURSOR LESIONS IN CHEMOPREVENTIO
Page 85 and 86: CARCINOGEN ACTIVATION AND DNA REPAI
Page 87 and 88: adducts, a few weeks or months for
Page 89 and 90: 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
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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
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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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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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