world cancer report - iarc

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increases the level by transiently reducing the activity of the kinase. However, mutations in either the APC gene or in the part of the β-catenin (CTNNB1) gene which codes for the part of the molecule which REFERENCES 1. Fearon ER, Vogelstein B (1990) A genetic model for colorectal tumorigenesis. Cell, 61: 759-767. 2. Kinzler KW, Vogelstein B (1997) Cancer-susceptibility genes. Gatekeepers and caretakers. Nature, 386: 761, 763. 3. Heldin CH (1996) Protein tyrosine kinase receptors. Cancer Surv , 27: 7-24. 4. Krutovskikh V, Yamasaki H (1997) The role of gap junctional intercellular communication (GJIC) disorders in experimental and human carcinogenesis. Histol Histopathol, 12: 761-768. 5. Hirohashi S (1998) Inactivation of the E-cadherin-mediated cell adhesion system in human cancers. Am J Pathol, 153: 333-339. 6. Birchmeier EJ, Behrens J (1994) Cadherin expression in carcinoma: Role in the formation of cell junctions and prevention of invasiveness. Biochim Biophys Acta, 1198: 11-26. 112 Mechanisms of tumour development accepts the phosphate allow the levels of β-catenin to rise; when this happens the TCF/LEF-controlled genes are permanently activated. The fact that mutations of the CTNNB1, AXIN1, AXIN2 and APC genes 7. Bruzzone R, White TW, Paul DL (1996) Connections with connexins: the molecular basis of direct intercellular signaling. Eur J Biochem, 238: 1-27. 8. Loewenstein WR, Kanno Y (1966) Intercellular communication and the control of tissue growth: lack of communication between cancer cells. Nature, 209: 1248-1249. 9. Trosko JE, Chang CC, Madhukar BV, Klaunig JE (1990) Chemical, oncogene and growth factor inhibition gap junctional intercellular communication: an integrative hypothesis of carcinogenesis. Pathobiology, 58: 265-278. 10. Yamasaki H, Omori Y, Zaidan-Dagli ML, Mironov N, Mesnil M, Krutovskikh V (1999) Genetic and epigenetic changes of intercellular communication genes during multistage carcinogenesis. Cancer Detect Prev, 23: 273-279. 11. Stoker MG (1967) Transfer of growth inhibition between normal and virus-transformed cells: occur in many cancers, including those of the colon, breast and endometrium, shows the importance of this pathway and emphasizes the connection between cellcell contact and signal transduction. autoradiographic studies using marked cells. J Cell Sci, 2: 293-304. 12. Yamasaki H, Katoh F (1988) Novel method for selective killing of transformed rodent cells through intercellular communication, with possible therapeutic applications. Cancer Res, 48: 3203-3207. 13. Mesnil M, Yamasaki H (2000) Bystander effect in herpes simplex virus-thymidine kinase/ganciclovir cancer gene therapy: role of gap-junctional intercellular communication. Cancer Res, 60: 3989-3999. 14. Behrens J, Jerchow BA, Wurtele M, Grimm J, Asbrand C, Wirtz R, Kuhl M, Wedlich D, Birchmeier W (1998) Functional interaction of an axin homolog, conductin, with beta-catenin, APC, and GSK3beta. Science, 280: 596-599.
APOPTOSIS SUMMARY > The term apoptosis refers to a type of cell death that occurs both physiologically and in response to external stimuli, including X-rays and anticancer drugs. > Apoptotic cell death is characterized by distinctive morphological changes different from those occurring during necrosis, which follows ischaemic injury or toxic damage. > Apoptosis is regulated by several distinct signalling pathways. Dysregulation of apoptosis may result in disordered cell growth and thereby contribute to carcinogenesis. > Selective induction of apoptosis in tumour cells is among current strategies for the development of novel cancer therapies. Apoptosis is a mode of cell death that facilitates such fundamental processes as development (for example, by removal of unwanted tissue during embryogenesis) and the immune response (for example, by elimination of self-reactive T cells). This type of cell death is distinguished from necrosis both morphologically (Fig. 3.33) and functionally. Specifically, apoptosis involves single cells rather than areas of tissue and does not provoke inflammation. Tissue homeostasis is dependent on controlled elimination of unwanted cells, often in the context of a continuum in which specialization and maturation is ultimately succeeded by cell death in what may be regarded as the final phase of differentiation. Apart from elimination in a physiological context, cells that have been lethally exposed to cytotoxic drugs or radiation may be subject to apoptosis. The process of apoptosis can be described by reference to distinct phases, termed “regulation”, “effector” and “engulfing” respectively [1]. The regulatory phase includes all the signalling pathways that culminate in commitment to cell death. Some of these pathways regulate only cell death, but many of them have overlapping roles in the control of cell proliferation, differentiation, responses to stress and homeostasis. Critical to apoptosis signalling are the “initiator” caspases (including caspase-8, caspase-9 and caspase-10) whose role is to activate the more abundant “effector” caspases (including caspase-3 and caspase-7) which, in turn, brings about the morphological change indicative of apoptosis. Finally, the engulfing process involves the recognition of cellular “remains” and their elimination by the engulfing activity of surrounding cells. Identification of genes mediating apoptosis in human cells has been critically Organelle disruption and breakdown, cell swelling NECROSIS Membrane blebbing, residual ‘ghost’ cell APOPTOSIS dependent on definition of the ced genes in the nematode Caenorhabditis elegans, members of this gene family being variously homologous to human BCL2 (which suppresses apoptosis), APAF-1 (which mediates caspase activation) and the caspases themselves (proteases which mediate cell death). The centrality of apoptosis to cancer biology is indicated by excess tumorigenesis in BCL2-transgenic and p53-deficient mice. An appreciation of apoptosis provides a basis for the further development of novel and conventional cancer therapy The role of cell death in tumour growth Apoptosis, or lack of it, may be critical to tumorigenesis [2]. BCL2, a gene mediating resistance to apoptotic stimuli, was discovered at the t(14:18) chromosomal Condensation and fragmentation of chromatin Fig. 3.33 Apoptosis and necrosis are distinguished by characteristic morphological changes. Shrinking/ rounding up, fragmentation of cell and nucleus Engulfing by neighbouring cell as ‘apoptoticbody’ Apoptosis 113
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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
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 66 and 67: Fig. 2.64 Cancer following immunosu
Page 68 and 69: Syndrome Gene Location Cancer site/
Page 70 and 71: viduals, confirmation of a gene def
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
Page 97 and 98: ates a molecular bridge between p53
Page 99 and 100: potential cancer genes altered thro
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: Connexin genes and tumour suppressi
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 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
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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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