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TNM CLASSIFICATION OF MALIGNANT TUMOURS The TNM system for the classification of malignant tumours (http://tnm.uicc.org/) is a form of clinical shorthand used to describe the anatomic extent (staging) of a cancer in terms of: T - the primary tumour N - regional lymph nodes M - distant metastases These components are given a number that reflects the absence or presence and extent of the disease. For example, a tumour of the colon that is classified as T2N1M0 would have extended into the colon’s muscular wall, spread to 1 to 3 regional lymph nodes but without evidence of distant metastasis. Evaluation by the TNM system can therefore help in the planning of treatment by the oncologist and in monitoring the efficacy of this treatment, as well as giving some indication of prognosis. Moreover, the use of a standardized system facilitates the dissemination of information in the clinical community. The TNM system was developed by Pierre Denoix (President of the UICC, 1973-1978) between 1943 and 1952 (Sobin LH, TNM – principles, history and relation to other prognostic factors. Cancer, 91:1589-92, 2001). In 1968, a series of brochures published by UICC describing the classification of cancers at 23 body sites were combined to produce the Livre de Poche, which has been subject to regular re-edition, enlargement and revision over subsequent years. In order to prevent unwanted variations in the classification by its users, in 1982 it was agreed that a adhere to reticular fibres in the subcapsular sinus. These fibres contain laminin, fibronectin and collagen IV, and different integrins expressed by different tumour cells may be responsible for adhesion to these structures and to the lymphatic endothelial cells [11]. Sarcomas tend to metastasize to lungs because the venous drainage returns 124 Mechanisms of tumour development T = primary tumour TX Primary tumour cannot be assessed T0 No evidence of primary tumour Tis Carcinoma in situ T1 Tumour invades submucosa T2 Tumour invades muscularis propria T3 Tumour invades through muscularis propria into subserosa or into nonperitonealized pericolic or perirectal tissues T4 Tumour directly invades other organs or structures and/or perforates visceral peritoneum N = regional lymph nodes NX Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis N1 Metastasis in 1 to 3 regional lymph nodes N2 Metastasis in 4 or more regional lymph nodes M = distant metastasis MX Distant metastasis cannot be assessed M0 No distant metastasis M1 Distant metastasis Table 3.8 TNM classification of cancer of the colon and rectum. single international TNM classification should be formulated. This is achieved via meetings of experts that update existing classifications, as well as develop new ones. The present TNM edition (Eds. Sobin LH and Wittekind Ch, TNM Classification of Malignant Tumours, 6th Edition, Wiley, 2002) contains guidelines for classification and staging that correspond exactly with those of the 6th edition of the AJCC Cancer Staging Manual (2002). TNM, now the most widely used system to classify tumour spread, is published in 12 languages and is accompanied by an illustrated TNM Atlas (Eds. Hermanek P et al., 4th Edition, Springer-Verlag, 1997), a TNM Mobile Edition (Wiley, 2002) and a TNM supplement (Eds. Wittekind Ch et al., TNM Supplement 2001. A Commentary on there; colon carcinoma cells enter the portal circulation which delivers cells to the liver, and so on (Fig. 3.45). However, a non-random element in metastatic patterns has long been recognized (Table 3.6). Stephen Paget developed the “seed and soil” hypothesis in 1889, based on his observations from autopsies of over 700 women with breast cancer. He proposed Uniform Use, 2nd Edition, Wiley 2001) with rules and explanations. The challenge for the future is the incorporation into TNM of information from new diagnostic and imaging technologies (such as endoscopic ultrasound, magnetic resonance imaging, sentinel node biopsy, immunohistochemistry and polymerase chain reaction). There is an expanding array of known and potential prognostic factors (Eds. Gospodarowicz M et al., Prognostic Factors in Cancer, Wiley, 2001) with which TNM could be integrated to form a comprehensive prognostic system. Such integration could potentially be exploited to enhance the prediction of prognosis, and individualize cancer patient treatment. that specific cancer cells (the seed) had an affinity for certain organs (the soil). In experimental systems there are many examples showing that primary tumours are heterogeneous, and that cloned cells can vary in their ability to metastasize to different sites. Some of the patterns relate to the ability of malignant cells to adhere to the endothelial cells in target
organs, and to respond to local growth factors once they have extravasated. It used to be thought that escape from the primary tumour and survival in the circulation were the major rate-limiting steps for successful metastasis. However, while there is a good deal of attrition at these REFERENCES 1. Yoshida BA, Sokoloff MM, Welch DR, Rinker-Schaeffer CW (2000) Metastasis-suppressor genes: a review and perspective on an emerging field. J Natl Cancer Inst, 92: 1717- 1730. 2. Simone NL, Paweletz CP, Charboneau L, Petricoin EF, Liotta LA (2000) Laser capture microdissection: Beyond functional genomics to proteomics. Mol Diagn, 5: 301-307. 3. Fidler IJ (2000) Angiogenesis and cancer metastasis. Cancer J Sci Am, 6 Suppl 2: S134-S141. 4. Eccles SA (2000) Cell biology of lymphatic metastasis. The potential role of c-erbB oncogene signalling. Recent Results Cancer Res, 157: 41-54. 5. Fidler IJ (1999) Critical determinants of cancer metastasis: rationale for therapy. Cancer Chemother Pharmacol, 43 Suppl: S3-10. 6. Stracke ML, Liotta LA (1992) Multi-step cascade of tumor cell metastasis. In Vivo, 6: 309-316. stages, both in experimental models and in man, many tumour cells reach distant sites but may remain dormant, either due to lack of appropriate growth factors, or their failure to induce neoangiogenesis. Indeed, using sensitive assays such as immunocytochemistry and polymerase 7. Berman AE, Kozlova NI (2000) Integrins: structure and functions. Membr Cell Biol, 13: 207-244. 8. Ridley A (2000) Molecular switches in metastasis. Nature, 406: 466-467. 9. McCawley LJ, Matrisian LM (2000) Matrix metalloproteinases: multifunctional contributors to tumor progression. Mol Med Today, 6: 149-156. 10. Bergers G, Brekken R, McMahon G, Vu TH, Itoh T, Tamaki K, Tanzawa K, Thorpe P, Itohara S, Werb Z, Hanahan D (2000) Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis. Nat Cell Biol, 2: 737- 744. 11. Brodt P (1991) Adhesion mechanisms in lymphatic metastasis. Cancer Metastasis Rev, 10: 23-32. chain reaction (PCR), individual tumour cells (or specific genetic markers) can be found in blood, nodes, bone marrow, body fluids etc, but the significance of “positive” results, and whether they can be used to predict subsequent overt metastases is not yet established. WEBSITE The Metastasis Research Society (UK): http://www.metastasis.icr.ac.uk Invasion and metastasis 125
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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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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 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
Page 117 and 118: laminin, entactin and also heparan
Page 119: Target Example of agent Comments Ad
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
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
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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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