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Fig. 5.56 Five-year relative survival rates after diagnosis of testicular cancer. REFERENCES 1. Stanford JL, Damber JE, Fair WR, Sancho-Garnier H, Griffiths K, Gu FL, Kiemeney LA (2000) Epidemiology of prostate cancer. In: Murphy G, Khoury S, Partin A, Denis L eds, Prostate cancer, Health Publication Ltd, UK, 21-55 . 2. von Eschenbach AC (1996) The biologic dilemma of early carcinoma of the prostate. Cancer, 78: 326-329. 3. Griffiths K, Denis LJ, Turkes A (2001) Oestrogens, phyto-oestrogens and the pathogenesis of prostatic disease. London, Martin Dunitz Publishers. 4. Dunn IB, Kirk D (2000) Legal pitfalls in the diagnosis of prostate cancer. BJU Int, 86: 304-307. 5. Sakr WA (1999) Prostatic intraepithelial neoplasia: A marker for high-risk groups and a potential target for chemoprevention. Eur Urol, 35: 474-478. 6. Abate-Shen C, Shen MM (2000) Molecular genetics of prostate cancer. Genes Dev, 14: 2410-2434. 7. Ozen M, Hopwood VL, Johnston DA, Babaian RJ, Logothetis CJ, von Eschenbach AC, Pathak S (1999) Aneuploidy index in blood: a potential marker for early onset, androgen response, and metastasis in human prostate cancer. Urology, 53: 381-385. 8. Navone NM, Labate ME, Troncoso P, Pisters LL, Conti CJ, von Eschenbach AC, Logothetis CJ (1999) p53 mutations in prostate cancer bone metastases suggest that 214 Human cancers by organ site found to have positive nodes can consider two cycles of adjuvant chemotherapy (100% cure rate). Disseminated germ cell tumours Guidelines for treatment of disseminated germ cell tumours (both seminoma and nonseminoma) are driven by the International Germ Cell Consensus (IGCC) prognostic index. Patients with low-risk nonseminoma (56% of cases) or seminoma (90% of cases) should receive three cycles of bleomycin, etoposide and cisplatin (BEP). Cure rate is approximately 90-95%. Patients with intermediate-risk disease or high-risk disease should receive four cycles of BEP, with an expected cure rate of 75% or 50% of patients respectively. selected p53 mutants in the primary site define foci with metastatic potential. J Urol, 161: 304-308. 9. Ozen M, Hopwood VL, Balbay MD, Johnston DA, Babaian RJ, Logothetis CJ, von Eschenbach AC, Pathak S (2000) Correlation of non-random chromosomal aberrations in lymphocytes of prostate cancer patients with specific clinical parameters. Int J Oncol, 17: 113-117. 10. Lu-Yao GL, Yao SL (1997) Population-based study of long-term survival in patients with clinically localised prostate cancer. Lancet, 349: 906-910. 11. Incrocci L, Slob AK, Levendag PC (2002) Sexual (dys)function after radiotherapy for prostate cancer: a review. Int J Radiat Oncol Biol Phys, 52: 681-693. 12. Denis L, Murphy GP (2000) Cancer of the Prostate. In: Pollock RE ed., UICC Manual of Clinical Oncology, New York, Wiley-Liss, 563-574. 13. 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. 14. Oliver RT (2001) Testicular cancer. Curr Opin Oncol, 13: 191-198. 15. Chaganti RS, Houldsworth J (2000) Genetics and biology of adult human male germ cell tumors. Cancer Res, 60: 1475-1482. Patients with nonseminoma who have normalized serum tumour markers and residual radiographic abnormalities should be considered for post-chemotherapy resection of residual disease. Teratoma (a malignant tumour that contains a variety of embryo-derived tissues, such as bone, muscle, cartilage, nerve, tooth buds) and persistent cancer are common findings in this setting. In contrast, patients with seminoma and residual masses after chemotherapy should be simply observed, as teratoma and residual cancer are not common findings in this situation. Patients with recurrent disease after chemotherapy still have the potential for cure. Salvage chemotherapy with vinblastine, ifosamide and cisplatin cures approximately 25% of these patients. WEBSITES Information for GPs: Screening for Prostate Cancer: http://www.sesahs.nsw.gov.au/publichealth/Cancer Control/default.htm The Prostate Cancer Research Institute (USA): http://www.prostate-cancer.org/ NCI Prostate Cancer Homepage : http ://www.cancer.gov/prostate
CANCERS OF THE FEMALE REPRODUCTIVE TRACT SUMMARY > Cervical cancer is the second most common cancer of women worldwide with more than 470,000 new cases per year. Of about 230,000 deaths every year, more than 80% occur in developing countries. Five-year survival rates are up to 70%. > Sexually transmitted infection with human papillomavirus is fundamental to development of carcinoma of the cervix. > Population-based screening has greatly reduced mortality in developed countries > Endometrial cancer mainly affects postmenopausal women in developed countries; 188,000 new cases are diagnosed annually and obesity is a major risk factor. > About 190,000 cases of ovarian cancer occur each year, predominantly among postmenopausal women in developed countries; five-year survival rates are about 40%. CERVICAL CANCER Definition The majority of epithelial tumours of the cervix are squamous cell carcinomas (85%). Adenocarcinomas are less common. Most cervical carcinomas arise at the junction between the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix, a site of continuous metaplastic change, especially in utero, at puberty and during a first pregnancy. Epidemiology Cancer of the cervix is the second most common cancer among women worldwide, second only to breast cancer; about < 9.3 < 16.1 Fig. 5.57 The global burden of cervical cancer. Note the high incidence rates in Central and South America, Southern Africa and India. Today, more than 80% of all cervical cancers occur in developing countries. 470,000 new cases are diagnosed each year. 80% of cases of cervical cancer occur in developing countries where, in many regions, it is the most common cancer of women. The highest incidence rates are in South America and the Caribbean, sub- Saharan Africa, and South and South- Eastern Asia (Fig. 5.57). However, very low rates are observed in China, and in Western Asia. In developed countries, the incidence rates are generally low, with agestandardized rates of less than 15 per 100,000, with the exception of Eastern Europe, where incidence rates range from 18-35 per 100,000. The incidence of cancer of the cervix begins to rise at ages 20- 29, and then increases rapidly to reach a peak at around ages 45-49 in European populations, but often rather later in developing countries. Incidence and mortality have declined markedly in the last 40 years in Western Europe, USA, Canada, Australia and New Zealand, mainly in relation to extensive screening programmes based on exfolia- < 23.8 < 35.8 Age-standardized incidence/100,000 population < 93.9 tive cervical cytology, typically by means of the Pap smear (Screening for cervical cancer, p167). Nevertheless, in several countries, notably the UK, Australia, New Zealand, and in central Europe, there have been increases in risk in younger women, probably the result of changes in exposure to risk factors. These changes are most evident for adenocarcinomas, which share to some extent the etiological agents of squamous cell carcinomas, but for which cytological screening is ineffective in countering the increase in risk. In developing countries the situation is more mixed, with high rates persisting in some areas (Latin America, India, Africa), and declines elsewhere, most notably in China. Etiology Molecular epidemiological studies have shown that certain human papillomavirus types (HPV) are the central cause of cervical cancer and cervical intraepithelial neoplasia (CIN) [1, 2, 3]. It is now clear that the well-established risk factors associat- Cancers of the female reproductive tract 215
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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
Page 157 and 158: Fig. 4.39 Poster designed for an an
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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
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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 and 192: depends on staging. Small intramuco
Page 193 and 194: 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: TUMOUR NORMAL Gastrula PGC 2n Impri
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 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
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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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