Invasive breast carcinoma - IARC

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A Fig. 1.50 Carcinosarcoma. A Two aggregates of carcinoma are separated by abundant sarcoma. B Immunostaining shows absence of reactivity with Kermix in the mesenchymal component, while the epithelial cells are positive. B The squamous and adenosquamous carcinoma should be distinguished from pleomorphic carcinomas that may have either pattern admixed with a large number of bizarre tumour giant cells; this distinction is important as pleomorphic carcinomas are far more aggressive than either squamous or adenosquamous carcinoma. Adenocarcinomas with chondroid differentiation should be distinguished from pleomorphic adenomas. Pleomorphic adenomas invariably have a myoepithelial cell component (that may be dominant in some tumours) growing around spaces lined by benign epithelial cells. Myoepithelial cells are not evident in adenocarcinomas with chondroid differentiation. Prognosis and predictive factors of metaplastic carcinomas Given the tumour size of >3-4 cm in many cases, metastases to axillary nodes are relatively uncommon; approximately 10-15% of pure squamous cell carcinomas have axillary node metastases {503,1928}. About 19-25% of those with chondro-osseous elements have a x i l l a ry node metastases {752,1273, 2259}, and 21% have distant metastases {752}. Axillary node metastases were more common (56%) among tumours with spindle and squamous metaplasia in Huvos’s study {239}, however. When metaplastic carcinomas metastasize to the axillary nodes or beyond, they retain and often manifest their metaplastic potential. In studies combining carcinomas with chondroid and osseous metaplasia, the five year survival has ranged from 28-68% {474,1273,3060}; those with spindle or squamous differentiation have a 63% 5-year survival {1273}. Advanced stage and lymph node involvement is associated with a more aggre s s i v e course as anticipated. Among squamous cell carcinomas, the acantholytic variant may exhibit a more aggressive behaviour {807}. The carc i n o s a rcomas are very aggre s- sive tumours. Some metastasize as mixed epithelial and mesenchymal tumours, while only the epithelial or the s a rcomatous component may metastasize in others. T h e re is not much information available on the efficacy of current therapies in the management of metaplastic carc i- n o m a s . Lipid-rich carcinoma Definition A breast carcinoma in which approximately 90% of neoplastic cells contain abundant cytoplasmic neutral lipids. ICD-O code 8314/3 Synonym Lipid secreting carcinoma. Epidemiology Using conventional morphological features only (i.e. foamy to vacuolated clear cells), incidences of
Lobular neoplasia F.A. Tavassoli R.R. Millis W. Boecker S.R. Lakhani Definition Characterized by a proliferation of generally small and often loosely cohesive cells, the term lobular neoplasia (LN) refers to the entire spectrum of atypical epithelial proliferations originating in the terminal duct-lobular unit (TDLU), with or without pagetoid involvement of terminal ducts. In a minority of women after longterm follow-up, LN constitutes a risk factor and a nonobligatory precursor for the subsequent development of invasive carcinoma in either breast, of either ductal or lobular type. ICD-O code Lobular carcinoma in situ (LCIS) 8520/2 Synonyms and historical annotation The designations atypical lobular hyperplasia (ALH) and lobular carcinoma in situ (LCIS) have been widely used for variable degrees of the lesion. Two series published in 1978 {1100, 2438} concluded that the features generally used to subdivide the lobular changes into LCIS and ALH were not of prognostic significance. To avoid o v e rt reatment, Haagensen suggested the designation lobular neoplasia (LN) for these lesions {1100}. To emphasize their non-invasive nature, the term lobular intraepithelial neoplasia (LIN) has been proposed. Based on morphological criteria and clinical outcome, LIN has been categorized into three grades {338}. Epidemiology The frequency of LN ranges from less than 1% {3106,3107} to 3.8 % {1099} of all breast carcinomas. It is found in 0.5- 4% of otherwise benign breast biopsies {2150}. Women with LN range in age from 15 {32} to over 90 years old {2876}, but most are premenopausal. Clinical features The lesion is multicentric in as many as 85% of patients {2446,2876} and bilateral in 30% {1096} to 67% {2001} of women who had been treated by bilateral mastectomy. No mammographic abnormalities are recognized {2128,2273}, except in the occasional variant of LN characterized by calcification developing within central necrosis {2534}. Macroscopy LN is not associated with any grossly recognizable features. Histopathology The lesion is located within the terminal duct-lobular unit {3091} with pagetoid involvement of the terminal ducts evident in as many as 75% of cases {86,1096}. On low power examination, while lobular architecture is maintained, the acini of one or more lobules are expanded to v a rying degrees by a monomorphic proliferation of loosely cohesive, usually small cells, with uniform round nuclei, indistinct nucleoli, uniform chro m a t i n and rather indistinct cell margins with sparse cytoplasm. Necrosis and calcification are uncommon and mitoses are infrequent. Intracytoplasmic lumens are often p resent but are not specific to LN {89}. In some lesions, however, the pro l i f e r a t i n g cells are larger and more pleomorphic or of signet ring type. Apocrine metaplasia occurs but the existence of endocrine variant of LN {801} is disputed. Two types of LN have been recognized {1100}: Type A with the more usual morphology described above and Type B composed of larger, more atypical cells with less uniform chromatin and conspicuous nucleoli. The two cell types may be mixed. When composed of pleomorphic cells, the term pleomorphic LN has been used. The neoplastic cells either replace or displace the native epithelial cells in the TDLU. The myoepithelial cells may remain in their original basal location or they may be dislodged and admixed with the neoplastic cells. The basement membrane is generally intact although this is not always visible in all sections. Pagetoid involvement of adjacent ducts between intact overlying flattened epithelium and underlying basement membrane is frequent and can result in several different patterns including a ‘clover leaf’ or ‘necklace’ appearance {1099}. Solid obliteration of acini may occur, sometimes with massive distension and central necrosis. LN may involve a variety of lesions including sclerosing adenosis, radial scars, papillary lesions, fibroadenomas and collagenous spherulosis. Immunoprofile LN is positive for estrogen receptor (ER) in 60-90% of cases and in a slightly lower p e rcentage for pro g e s t e rone re c e p t o r (PR) {62,369,1010,2159,2483}. The classical variety of LN is more likely to be positive than the pleomorphic variant {223,2683}. Unlike high grade DCIS, h o w e v e r, classic LN rarely expre s s e s ERBB2 or TP53 protein {62,2327a,2483, 2746}. Positivity is more likely with the pleomorphic variant {1859,2683}. Intra- A Fig. 1.74 Early lobular neoplasia. A The few neoplastic lobular cells are hardly apparent on a quick examination of the TDLU. B Double immunostaining with E-cadherin (brown) and CK34BE12 (purple) unmasks the few neoplastic cells (purple) proliferating in this lobule. These early lesions are often missed on H&E stained sections. B 60 Tumours of the breast
Page 2: Previous volumes in this series Kle
Page 6 and 7: World Health Organization Classific
Page 8 and 9: Published by IARC Press, Internatio
Page 10 and 11: CHAPTER 1 Tumours of the Breast Can
Page 12 and 13: TNM classification of carcinomas of
Page 14 and 15: Invasive breast carcinoma I.O. Elli
Page 16 and 17: Rapid growth and greater adult heig
Page 18 and 19: tives, administrative and clerical
Page 20 and 21: Grade 1 - well differentiated: 3-5
Page 22 and 23: ent and this is occasionally extens
Page 24 and 25: Most melanotic tumours of the breas
Page 26 and 27: A Fig. 1.22 A Classic invasive lobu
Page 28 and 29: yet others at 90% {97,2147}. For pr
Page 30 and 31: Fig. 1.27 Medullary carcinoma. The
Page 32 and 33: myoepithelial cells in fibro a d e
Page 34 and 35: A Fig. 1.33 Neuroendocrine carcinom
Page 36 and 37: Macroscopy Fisher et al. reported t
Page 38 and 39: Fig. 1.39 Apocrine carcinoma. Note
Page 40 and 41: cells contain intracytoplasmic lume
Page 44 and 45: A B C Fig. 1.75 Lobular neoplasia.
Page 46 and 47: Intraductal proliferative lesions F
Page 48 and 49: A B absence of either microcalcific
Page 50 and 51: Fig. 1.83 Atypical ductal hyperplas
Page 52 and 53: A B Fig. 1.88 Large excision biopsy
Page 54 and 55: unusual variants as well. Using thi
Page 56 and 57: esemble those identified in invasiv
Page 58 and 59: A B Fig. 1.97 Microinvasive carcino
Page 60 and 61: A Papilloma may be subject to morph
Page 62 and 63: A B C Fig. 1.103 Papillary intraduc
Page 64 and 65: colour measuring from 0.5 to 12 cm.
Page 66 and 67: Immunoprofile The cases studied by
Page 68 and 69: Glycogen-rich, clear cell carcinoma
Page 70 and 71: Differential diagnosis There may be
Page 72 and 73: quality metaphase spreads from an i
Page 74 and 75: Fig. 1.67 Lobular carcinoma of brea
Page 76 and 77: detectable distant metastasis displ
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
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1113,1275}. There is a complex patt
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A B Fig. 1.137 A Lipoma. Intraparen
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Fig. 1.141 Angiosarcoma after breas
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A Fig. 1.144 Mammary osteosarcoma.
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Fibroepithelial tumours J.P. Belloc
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aged women (average age of presenta
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lished data suggests a 21% rate of
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A Fig. 1.157 Syringomatous adenoma
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Malignant lymphoma and metastatic t
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used. Inflammatory conditions in th
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male population both in the USA and
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CHAPTER 2 Tumours of the Ovary and
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Polyembryoma 9072/3 Non-gestational
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Surface epithelial-stromal tumours
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A Fig. 2.04 A Serous borderline tum
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A Fig. 2.06 Serous borderline tumou
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A Fig. 2.10 Invasive peritoneal imp
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Fig. 2.15 Mucinous carcinoma with i
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Fig. 2.20 Mucinous endocervical-lik
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A Fig. 2.28 Mucinous cystic tumour
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early secretory endometrium {2605}.
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IV, 6% {2233}. Patients with grade
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A Fig. 2.37 A This polypoid intracy
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Fig. 2.40 Endometrioid cyst with at
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1 tumours are extremely rare. Almos
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Fig. 2.50 Borderline Brenner tumour
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express thrombomodulin and have bee
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serous and transitional cell carcin
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is yellow to tan with a variable ad
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Genetic susceptibility JGCTs may pr
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Clinical features F i b romas may b
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distinguishes this tumour from the
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A Fig. 2.77 A Retiform Sertoli-Leyd
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Mean ages of 21 and 38 years and me
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Tumours unassociated with PJS form
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mal origin without crystals of Rein
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Germ cell tumours F. Nogales A. Tal
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cases, anisokaryosis has no prognos
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ation may coexist in the same neopl
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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
Page 366 and 367:
Dr Manuel TEIXEIRA Department of Ge
Page 368 and 369:
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,
Page 378 and 379:
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
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MPNST, see Malignant peripheral ner
Page 430:
Small cell / oat cell carcinoma, 32
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Invasive breast carcinoma - IARC

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