Invasive breast carcinoma - IARC

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A Fig. 2.04 A Serous borderline tumour with microinvasion. There is a transition from the typical small serous cells to cells with more abundant eosinophilic cytoplasm associated with disruption of the epithelial/stromal interface; the latter cell population invades the underlying stroma as isolated cells and small cell clusters in the lower part of the field. B Small clusters of cells and single cells within the stroma indicating microinvasion (arrow) in the lower central part of the field are demonstrated by cytokeratin immunohistochemistry. B Association with endometrial cancer Several studies provide evidence of associations between ovarian and other cancers, particularly endometrial {715, 1029}. The relative risk of developing endometrial cancer is about 1.5 among mothers and sisters of ovarian cancer cases, although in both studies the risk fell just short of statistical significance. Serous tumours Definition Ovarian tumours characterized in their better-differentiated forms by cell types resembling those of the fallopian tube. ICD-O codes Serous adenocarcinoma 8441/3 Serous borderline tumour 8442/1 Benign serous tumours Serous papillary cystadenoma 8460/0 Serous cystadenoma 8441/0 Serous surface papilloma 8461/0 Serous adenofibroma, cystadenofibroma 9014/0 Serous adenocarcinoma Definition An invasive ovarian epithelial neoplasm composed of cells ranging in appearance from those resembling fallopian tube epithelium in well diff e re n t i a t e d tumours to anaplastic epithelial cells with severe nuclear atypia in poorly differentiated tumours. Macroscopy The tumours range from not being macroscopically detectable to over 20- cm in diameter and are bilateral in twothirds of all cases, but only in one-third of stage I cases. Well differentiated tumours are solid and cystic with soft papillae within the cystic spaces or on the surface. The papillae tend to be softer and more confluent than in cases of borderline tumours. Rare tumours are confined to the ovarian surface. Poorly differentiated tumours are solid, friable, multinodular masses with necrosis and haemorrhage. Histopathology The architecture of the tumour varies from glandular to papillary to solid. The glands are typically slit-like or irregular. The papillae are usually irre g u l a r l y branching and highly cellular. In poorly d i ff e rentiated tumours solid areas are usually extensive and composed of poorly differentiated cells in sheets with small papillary clusters separated by myxoid or hyaline stroma. Psammoma bodies may be present in varying numbers. The stroma may be scanty or desmoplastic. Serous carcinomas may contain a variety of other cell types as a minor component (less than 10%) that may cause diagnostic problems but do not influence the outcome. Serous psammocarcinoma is a rare variant of serous carcinoma characterized by massive psammoma body formation and low grade cytological features. The epithelium is arranged in small nests with no areas of solid epithelial proliferation, and at least 75% of the epithelial nests are associated with psammoma body formation {1001}. Immunoprofile Serous carcinomas are always cytokeratin 7 positive and cytokeratin 20 negative. They are also positive for epithelial membrane antigen, CAM5.2, AE1/AE3, B72.3 and Leu M1 and for CA125 in 85% of the cases, but negative for calretinin and other mesothelial markers. Grading Various grading systems have been proposed for serous carcinomas. The utilization of a three-tiered grading system is recommended since the tumour grade has important prognostic and therapeutic implications {2687}. Somatic genetics The prevailing view of the pathogenesis of serous adenocarcinoma is that it arises directly from the ovarian surf a c e epithelium, invaginations or epithelial inclusions and progresses rapidly {205}. At present, serous carcinoma is regarded as a relatively homogeneous group of tumours from the standpoint of pathogenesis. Thus, although these neoplasms are graded as well, moderately and poorly diff e rentiated, they are thought to represent a spectrum of differentiation reflecting progression from a low grade to a high grade malignancy. W h e reas in colorectal carcinoma a Surface epithelial-stromal tumours 119
Fig. 2.05 Serous borderline tumour. The sectioned surface shows a solid and cystic neoplasm with numerous papillary excrescences. tumour pro g ression model in which sequential accumulation of molecular genetic alterations leading to morphologically recognizable stages is well established {1468}, a similar model for ovarian s e rous carcinoma has not been proposed because well defined precursor lesions have not been identified. It has been reported that even the earliest histological serous carcinomas are already high grade and morphologically resemble their advanced stage counterparts {205}. The histological similarities are paralleled by recent molecular genetic findings demonstrating TP53 mutations in very small stage I serous carcinomas and in the adjacent "dysplastic" surface epithelium {2275}. Most studies have shown that approximately 60% of advanced stage ovarian serous carcinomas have mutant TP53 {230,3095}. Thus, although the molecular genetic findings in these early carcinomas are preliminary, they suggest that serous carcinoma in its very earliest stage of development resembles advanced stage serous carcinoma at the molecular level. This would support the view that there are no morphologically recognized interm e d i a t e steps in the progression of the conventional type of ovarian serous carcinoma. S e rous borderline tumours (SBTs), noninvasive and invasive micro p a p i l l a ry types, frequently display K R A S m u t a t i o n s but rarely mutant T P 5 3. Increased allelic imbalance of chromosome 5q is associated with the pro g ression from typical SBT to micro p a p i l l a ry SBT and incre a s e d allelic imbalance of chromosome 1p with the pro g ression from micro p a p i l l a ry SBT to invasive serous carcinoma {2706}. In contrast, K R A S mutations are very rare in conventional serous carcinoma, but T P 5 3 mutations occur in approximately 60%. Recently, mutations were also identified in the BRAF gene, a downstream mediator of KRAS. BRAF and KRAS mutations appear to be mutually exclusive. These mutations were only detected in low grade ovarian serous carcinomas {2707}. Thus, there appears to be more than one pathway of tumorigenesis for serous carcinoma. In one pathway, conventional serous carcinoma, a high grade neoplasm, develops "de novo" from the surface epithelium of the ovary, grows rapidly and is highly aggressive {205}. These tumours, even at their earliest stage, display TP53 mutations but not KRAS mutations. In the other pathway a SBT progresses in a "stepwise" fashion t h rough a non-invasive micro p a p i l l a ry stage before becoming invasive {2706} or through microinvasion in a backg round of typical SBT. The indolent m i c ro p a p i l l a ry tumours frequently display KRAS mutations, but TP53 mutations are only rarely detected. Genetic susceptibility The neoplasms that develop in women with germline B R C A 1 mutations are mostly serous carcinomas of the ovary, fallopian tube and peritoneum. Prognosis and predictive factors The overall 5-year survival is appro x i m a t e- ly 40%; however, many of those alive at 5 years are alive with disease. Up to 85% of cases present with widespread metastatic disease. Survival at 5 years in this gro u p is 10-20%. Patients with disease confined Table 2.01 Histological criteria for the diagnosis of serous borderline tumours. - Epithelial hyperplasia in the form of stratification, tufting, cribriform and micropapillary arrangements - Atypia (usually mild to moderate) - Detached cell clusters - Variable and usually minimal mitotic activity - Absence of destructive stromal invasion to the ovary or pelvis have a 5-year survival of 80%. Patients with serous psamm o c a rcinoma have a protracted clinical course and a relatively favourable pro g- nosis; their clinical behaviour more closely resembles that of SBT than serous carcinoma of the usual type. Serous borderline tumour with microinvasion Definition An ovarian serous tumour of low malignant potential exhibiting early stromal invasion characterized by the presence in the stroma of individual or clusters of neoplastic cells cytologically similar to those of the associated non-invasive tumour. One or more foci may be present; none should exceed 10 mm 2 . Synonyms Serous tumour of low malignant potential with microinvasion, serous tumour of borderline malignancy with microinvasion. Epidemiology P resent in about 10-15% of SBTs , microinvasion occurs in women ranging in age from 17-83 years with a median age of 34.5 years {203,2867}. Clinical features Most symptomatic women present with a pelvic mass or pain. About 28% of the 39 women in the 2 major series were pre g- nant at the time of presentation {203,2867}. Macroscopy The macroscopic features are similar to those of SBT without microinvasion. Tumour spread and staging At presentation about 60% of the neoplasms are stage IA, 13% stage 1B, 5% stage IC, 8% stage IIC, 10% stage III (mostly IIIC) and 2.5% stage IV (liver metastases). Histopathology The hallmark of serous borderline tumours with microinvasion is the presence within the tumour stroma of single cells and cell clusters with generally abundant eosinophilic cytoplasm morphologically identical to those of the adjacent non-invasive tum o u r. The microinvasive foci form microp a p i l l a ry, solid or rarely cribriform arrangements without or with only minimal stro m a l or cellular reaction. These cells are often 120 Tumours of the ovary and peritoneum
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Previous volumes in this series Kle
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World Health Organization Classific
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Published by IARC Press, Internatio
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CHAPTER 1 Tumours of the Breast Can
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TNM classification of carcinomas of
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Invasive breast carcinoma I.O. Elli
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Rapid growth and greater adult heig
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tives, administrative and clerical
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Grade 1 - well differentiated: 3-5
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ent and this is occasionally extens
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Most melanotic tumours of the breas
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A Fig. 1.22 A Classic invasive lobu
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yet others at 90% {97,2147}. For pr
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Fig. 1.27 Medullary carcinoma. The
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myoepithelial cells in fibro a d e
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A Fig. 1.33 Neuroendocrine carcinom
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Macroscopy Fisher et al. reported t
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Fig. 1.39 Apocrine carcinoma. Note
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cells contain intracytoplasmic lume
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A Fig. 1.50 Carcinosarcoma. A Two a
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A B C Fig. 1.75 Lobular neoplasia.
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Intraductal proliferative lesions F
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A B absence of either microcalcific
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Fig. 1.83 Atypical ductal hyperplas
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A B Fig. 1.88 Large excision biopsy
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unusual variants as well. Using thi
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esemble those identified in invasiv
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A B Fig. 1.97 Microinvasive carcino
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A Papilloma may be subject to morph
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A B C Fig. 1.103 Papillary intraduc
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colour measuring from 0.5 to 12 cm.
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Immunoprofile The cases studied by
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Glycogen-rich, clear cell carcinoma
Page 70 and 71: Differential diagnosis There may be
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Page 74 and 75: Fig. 1.67 Lobular carcinoma of brea
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Page 78 and 79: detected at a late stage as small t
Page 80 and 81: Extent of ductal carcinoma in situ
Page 82 and 83: Benign epithelial proliferations G.
Page 84 and 85: Fig. 1.112 Microglandular adenosis.
Page 86 and 87: A Apocrine adenoma ICD-O code 8401/
Page 88 and 89: A B Fig. 1.128 Adenomyoepithelioma,
Page 90 and 91: Mesenchymal tumours M. Drijkoningen
Page 92 and 93: 1113,1275}. There is a complex patt
Page 94 and 95: A B Fig. 1.137 A Lipoma. Intraparen
Page 96 and 97: Fig. 1.141 Angiosarcoma after breas
Page 98 and 99: A Fig. 1.144 Mammary osteosarcoma.
Page 100 and 101: Fibroepithelial tumours J.P. Belloc
Page 102 and 103: aged women (average age of presenta
Page 104 and 105: lished data suggests a 21% rate of
Page 106 and 107: A Fig. 1.157 Syringomatous adenoma
Page 108 and 109: Malignant lymphoma and metastatic t
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Page 112 and 113: male population both in the USA and
Page 114 and 115: CHAPTER 2 Tumours of the Ovary and
Page 116 and 117: Polyembryoma 9072/3 Non-gestational
Page 118 and 119: Surface epithelial-stromal tumours
Page 122 and 123: A Fig. 2.06 Serous borderline tumou
Page 124 and 125: A Fig. 2.10 Invasive peritoneal imp
Page 126 and 127: Fig. 2.15 Mucinous carcinoma with i
Page 128 and 129: Fig. 2.20 Mucinous endocervical-lik
Page 130 and 131: A Fig. 2.28 Mucinous cystic tumour
Page 132 and 133: early secretory endometrium {2605}.
Page 134 and 135: IV, 6% {2233}. Patients with grade
Page 136 and 137: A Fig. 2.37 A This polypoid intracy
Page 138 and 139: Fig. 2.40 Endometrioid cyst with at
Page 140 and 141: 1 tumours are extremely rare. Almos
Page 142 and 143: Fig. 2.50 Borderline Brenner tumour
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Page 148 and 149: is yellow to tan with a variable ad
Page 150 and 151: Genetic susceptibility JGCTs may pr
Page 152 and 153: Clinical features F i b romas may b
Page 154 and 155: distinguishes this tumour from the
Page 156 and 157: A Fig. 2.77 A Retiform Sertoli-Leyd
Page 158 and 159: Mean ages of 21 and 38 years and me
Page 160 and 161: Tumours unassociated with PJS form
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Page 164 and 165: Germ cell tumours F. Nogales A. Tal
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Table 2.06 Grading of ovarian immat
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A B Fig. 2.102 A Mature cystic tera
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Diagnostic procedures Elevated urin
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associated with mature teratomas sh
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atives intimately admixed. The germ
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Fig. 2.113 Mixed germ cell-sex cord
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A Fig. 2.116 A Adenomatous hyperpla
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Fig. 2.117 Small cell carcinoma, hy
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Clinical features Adenoid cystic-li
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Histopathology This epithelial tumo
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sis. Corpus luteum of pregnancy has
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Lymphomas and leukaemias L.M. Roth
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Secondary tumours of the ovary J. P
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Occasionally, the colonic adenocarc
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Peritoneal tumours S.C. Mok J.O. Sc
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A B Fig. 2.140 Cystic adenomatoid m
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whelmingly poor {1038,1547,2310}. H
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CHAPTER 3 Tumours of the Fallopian
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TNM and FIGO classification of carc
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Endometrioid adenocarcinoma Endomet
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Two examples of adenofibroma of bor
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A Fig. 3.11 Adenomatoid tumour. A T
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Clinical features Patients range in
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Fig. 3.16 Uterus-like mass. The cys
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CHAPTER 4 Tumours of the Uterine Co
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TNM and FIGO classification of non-
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Epithelial tumours and related lesi
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endometrioid adenocarcinoma fro m a
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fers from the prototypical type I e
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the ovary and bladder. Unlike prima
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schema {1535,2602}. Although this c
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Table 4.03 Altered gene function in
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Mesenchymal tumours and related les
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areas are limited to less than 30%
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A B C Fig. 4.30 Leiomyosarcoma. A T
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e used sparingly and is reserved fo
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A B Fig. 4.38 Leiomyoma with perino
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cytological atypia, tumour cell nec
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Mixed epithelial and mesenchymal tu
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Prognosis and predictive factors Th
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tumours may superficially invade th
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A Fig. 4.46 A Gestational choriocar
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A Fig. 4.49 A Classic complete hyda
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Sex cord-like, neuroectodermal and
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Secondary tumours of the uterine co
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WHO histological classification of
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Epithelial tumours M. Wells J.M. Ne
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Fig. 5.04 Mechanisms of human papil
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Fig. 5.08 Keratinizing squamous cel
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in their Asian population {2957}. I
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have a strong association with high
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e red by squamous epithelium {380}.
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endometrioid adenocarcinoma of the
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metrial epithelium. In some cases t
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with distinct cell borders and a gr
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Mesenchymal tumours M.L. Carcangiu
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{781}, liposarcoma {2840,3016}, ost
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Mixed epithelial and mesenchymal tu
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Fig. 5.44 Wilms tumour. The tumour
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A Fig. 5.47 Implant of endometrial
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CHAPTER 6 Tumours of the Vagina Alt
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Epithelial tumours E.S. Andersen A.
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Aetiology The fact that both VAIN a
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Fig. 6.10 Fibroepithelial polyp.A m
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er of mitoses varies but is usually
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ICD-O codes Adenosquamous carcinoma
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A C Fig. 6.17 Sarcoma botryoides. A
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1-11 cm. They may arise anywhere in
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elsewhere in the female genital tra
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A Fig. 6.24 Yolk sac tumour. A The
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g rowing in sheets. Some may have s
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WHO histological classification of
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Epithelial tumours E.J. Wilkinson M
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even with additional sectioning, it
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type) is a highly diff e rentiated
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Clinical features Bartholin gland c
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glandular elements surrounded by fi
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Mesenchymal tumours R.L. Kempson M.
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Table 7.03 Differential diagnosis o
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Prognosis and predictive factors A
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Table 7.04 Clark levels of cutaneou
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A Fig. 7.23 Vulvar peripheral primi
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Familial aggregation of cancers of
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BRCA1 syndrome Definition Inherited
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dispose individuals to the developm
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Fig. 8.05 To assess whether wild-ty
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Fig. 8.07 Factors that modify risk
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BRCA2 syndrome R. Eeles S. Piver S.
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tubal or ovarian carcinomas. Howeve
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in typical nuclear foci that may re
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Breast tumours Frequency Breast can
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Fig. 8.14 Codon distribution of som
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Breast tumours Age distribution and
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Hereditary non-polyposis colon canc
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essary in the evaluation of the pat
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Age distribution and penetrance Mos
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Contributors Dr Vera M. ABELER** De
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Dr Carlo LA VECCHIA Laboratory of E
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Dr Manuel TEIXEIRA Department of Ge
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02.100 Dr. A. Ostor 02.101 Dr. F.A.
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52. Akhtar M, Robinson C, Ashraf Al
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180. Bapat K, Brustein S (1989). Ut
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307. Bolis GB, Maccio T (2000). Cle
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436. Chang J, Sharpe JC, A'Hern RP,
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562. Costa MJ, Ames PF, Walls J, Ro
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689. Di Domenico A, Stangl F, Benni
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820. Falck J, Petrini JH, Williams
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943. Gad A, Azzopardi JG (1975). Lo
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1067. Grimes MM (1992). Cystosarcom
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1197. Herod JJ, Shafi MI, Rollason
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1323. Jacques SM, Qureshi F, Ramire
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1449. Khalifa MA, Mannel RS, Harawa
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1564. Lagios MD (1977). Multicentri
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1687. Loman N, Johannsson O, Kristo
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1807. McCluggage G, McBride H, Maxw
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1937. Mukai M, Torikata C, Iri H (1
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2056. Norris HJ, Taylor HB (1967).
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2180. Park JS, Jones RW, McLean MR,
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2304. Puls LE, Hamous J, Morrow MS,
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2 4 3 4 . Rosen PP, Groshen S, Saig
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2559. Schlesinger C, Silverberg SG
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2686. Silverberg SG (1999). Protoco
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2806. Stutz JA, Evans AJ, Pinder S,
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2942. Tornos C, Silva EG, Ordonez N
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3061. Wargotz ES, Norris HJ (1990).
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3189. Yoshioka T, Tanaka T (2000).
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References 425
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Biphasic teratomas, 168 BLM, 341, 3
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G GADD45, 343, 353 GCDFP-15, 25, 33
Page 428 and 429:
MPNST, see Malignant peripheral ner
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Small cell / oat cell carcinoma, 32
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Invasive breast carcinoma - IARC

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