Invasive breast carcinoma - IARC

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Prognosis and predictive factors The clinical course of uterine carcinosarcoma is generally aggressive with a poor overall prognosis, considerably worse than that of a poorly diff e re n t i a t e d endometrial carcinoma. The pattern of spread is generally similar to that of high grade endometrial carcinoma, and deep myometrial invasion and extrauterine spread are often observed at the time of presentation. The clinical staging is the same as that for endometrial carcinoma. Some studies have found no independent prognostic factors other than tumour stage, whereas others have found that the characteristics of the epithelial component such as high grade carcinoma, including serous or clear cell components, are associated with a worse prognosis {2692}. Previously, it was thought that the presence of heterologous mesenchymal components indicated a worse outcome; however, recent larger studies have suggested that the histological features of the mesenchymal component bear no relationship to the overall prognosis {2692}. The biological behaviour of uterine carcinosarcomas is more akin to high grade endometrial carcinomas than to uterine sarcomas {282,2692}. Carcinosarcomas primarily spread via lymphatics, whereas pure uterine sarcomas commonly spread h a e m a t o g e n o u s l y. Detailed studies of uterine carcinosarcoma have shown that metastatic foci and foci within lymphatic or vascular spaces are commonly carcinomatous with pure sarcomatous elements being rare {282,2692,2767}. Although the tumour stage is the most important prognostic factor, recurrences may be encountered even in those rare cases lacking myometrial infiltration. However, tumours confined to an otherwise benign polyp appear to have a somewhat better outcome {188,1382}. Adenosarcoma Definition Adenosarcoma is a biphasic neoplasm containing a benign epithelial component and a sarcomatous mesenchymal component. Epidemiology Adenosarcoma occurs in women of all ages, ranging from 15-90 years with a median age at diagnosis of 58. Adenosarcomas have been reported in women undergoing tamoxifen therapy for breast cancer {509} and occasionally after prior pelvic radiation {515}. There is no association of adenosarcoma with obesity or hypertension. Clinical features Typical symptoms of patients with a d e n o s a rcoma are abnormal vaginal bleeding, an enlarged uterus and tissue p rotruding from the external os. The tumour may not be correctly diagnosed as adenosarcoma until re-excision of a recurrent polypoid lesion {515}. Macroscopy Adenosarcomas typically grow as exophytic polypoid masses that extend into the uterine cavity. Rarely, they may arise in the myometrium, presumably fro m adenomyosis. Although the tumour is usually a single polypoid mass, it sometimes may present as multiple papillary masses. On sectioning, the surface is tan b rown with foci of haemorrhage and necrosis. Small cysts are frequently present. Most adenosarcomas do not invade the myometrium. Histopathology Under low magnification a leaf-like pattern closely resembling phyllodes tumour of the breast is observed. Isolated glands, often dilated and compressed into thin slits, are dispersed throughout the mesenchymal component. Characte- ristically, t h e re is stromal condensation surro u n d i n g the glands and clefts. It is in these are a s w h e re the greatest degree of stro m a l atypia and mitotic activity is present. By definition the epithelium is benign and may show focal metaplastic changes. The mesenchymal component of an a d e n o s a rcoma is generally a low grade homologous stromal sarcoma containing v a rying amounts of fibrous tissue and smooth muscle. Mesenchymal mitotic figu res, usually stated to be more than one per 10 high power fields, are re q u i red in the hypercellular cuffs. Cytological atypia is typically only mild, but is occasionally moderate. Sex cord-like components resembling those in endometrial stro m a l s a rcomas are found in less than 10% of a d e n o s a rcomas. Heterologous components consisting of striated muscle (most commonly), cartilage, fat and other components are present in approximately 10- 15% of tumours The diagnosis of sarc o- matous overgrowth is made if the pure A Fig. 4.44 Adenosarcoma. A The tumour is composed of tubular and convoluted, cleft-like glands of endometrioid type surrounded by a cuff of cellular mesenchyme. B A polypoid structure compresses a glandular lumen producing a leaf-like pattern similar to that of a mammary phyllodes tumour. The epithelial component is cytologically bland, and the mesenchymal component is cellular and fibromatous without significant nuclear atypia but contained abundant mitoses. B Mixed epithelial and mesenchymal tumours 247
sarcomatous component, usually of high grade, occupies 25% or more of the total tumour volume. Immunoprofile As might be expected, the epithelial component reacts with a broad spectrum of antibodies to cytokeratins. The mesenchymal component usually re a c t s focally with antibodies to CD10. Variable degrees of staining for smooth muscle markers, desmin and caldesmon, can also be observed. Differential diagnosis The differential diagnosis includes adenofibroma and in children sarcoma botryoides (embryonal rhabdomyosarcoma). Prognosis and predictive factors A d e n o s a rcoma is considered a low grade neoplasm but recurs in approximately 25-40% of cases, typically in the pelvis or vagina, and distant metastasis has been reported in 5% of cases {515}. The metastases almost always are composed of a sarcomatous element only, but rarely epithelium has been reported. Factors in the primary tumour that are p redictive of a poor outcome are extrauterine spread, deep myometrial invasion into the outer half of the myometrium and sarcomatous overgrowth. Vascular invasion is usually not identified but, if present, is a poor risk factor. Rhabdomyosarcomatous differentiation was an adverse prognostic factor in one series {1388}. There appears to be no correlation between the pro g n o s i s and the level of mitotic activity. Longt e rm follow-up is necessary because re c u r rences may manifest after many years. Most tumour deaths occur more than five years after the diagnosis. Carcinofibroma Definition A neoplasm composed of an admixture of a malignant epithelial element and a benign mesenchymal component. Epidemiology These are extremely uncommon neoplasms with few cases reported in the literature {1286,2228,2916}. Histopathology In one case the epithelial component was clear cell in type {2228}. The mesenchymal component is usually fibro u s , although occasional cases with a hetero l- ogous mesenchymal component have been described and have been designated as carcinomesenchymoma {459}. Prognosis and predictive factors The behaviour is not well established since so few cases have been reported but would be expected to depend on the stage, depth of myometrial invasion and histological subtype of the epithelial component. Adenofibroma Definition A biphasic uterine neoplasm composed of benign epithelial and mesenchymal components. Epidemiology Uterine adenofibroma is an uncommon neoplasm, much less frequent than adenosarcoma, which occurs most often in postmenopausal patients but also in younger women. {3245}. Occasional cases have been associated with tamoxifen therapy {1258}. Macroscopy Adenofibromas usually present as polypoid lesions, commonly have a fibrous consistency on sectioning, and sometimes contain dilated cystic spaces. Histopathology Adenofibromas have a papillary or clublike growth pattern. They are composed of benign epithelial and mesenchymal components, the epithelial component forming a lining on the underlying mesenchymal core. Cleft-like spaces are often present. The epithelial component may be endometrioid or ciliated in type but often is non-descript cuboidal or columnar. Rarely, there are foci of squamous metaplasia. The mesenchyme is usually of a non-specific fibro b l a s t i c type, although rarely it may contain endometrial stromal or smooth muscle components. Stromal atypia, mitotic activity and periglandular cuffing are absent or inconspicuous. Rare l y, adipose tissue or skeletal muscle components are present, and such lesions have been designated lipoadenofibroma or adenomyofibroma {1239,2711}. Differential diagnosis If there is a stromal mitotic count of >1 mitosis per 10 high power fields, marked stromal hypercellularity with periglandular cuffing and/or more than mild stromal atypia, a diagnosis of low grade adenosarcoma should be made. Prognosis and predictive factors A d e n o f i b romas are benign lesions, although they may recur following "polypectomy" {2625}. Occasional Fig. 4.45 Atypical polypoid adenomyoma. This polypoid lesion shows a biphasic epithelial and stromal proliferation. The glandular component consists of endometrioid glands with a variable degree of complexity, whereas the mesenchymal component is myofibromatous and cytologically bland. 248 Tumours of the uterine corpus
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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
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Differential diagnosis There may be
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quality metaphase spreads from an i
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Fig. 1.67 Lobular carcinoma of brea
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detectable distant metastasis displ
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detected at a late stage as small t
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Extent of ductal carcinoma in situ
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Benign epithelial proliferations G.
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Fig. 1.112 Microglandular adenosis.
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A Apocrine adenoma ICD-O code 8401/
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A B Fig. 1.128 Adenomyoepithelioma,
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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
Page 198 and 199: Peritoneal tumours S.C. Mok J.O. Sc
Page 200 and 201: A B Fig. 2.140 Cystic adenomatoid m
Page 202 and 203: whelmingly poor {1038,1547,2310}. H
Page 204 and 205: CHAPTER 3 Tumours of the Fallopian
Page 206 and 207: TNM and FIGO classification of carc
Page 208 and 209: Endometrioid adenocarcinoma Endomet
Page 210 and 211: Two examples of adenofibroma of bor
Page 212 and 213: A Fig. 3.11 Adenomatoid tumour. A T
Page 214 and 215: Clinical features Patients range in
Page 216 and 217: Fig. 3.16 Uterus-like mass. The cys
Page 218 and 219: CHAPTER 4 Tumours of the Uterine Co
Page 220 and 221: TNM and FIGO classification of non-
Page 222 and 223: Epithelial tumours and related lesi
Page 224 and 225: endometrioid adenocarcinoma fro m a
Page 226 and 227: fers from the prototypical type I e
Page 228 and 229: the ovary and bladder. Unlike prima
Page 230 and 231: schema {1535,2602}. Although this c
Page 232 and 233: Table 4.03 Altered gene function in
Page 234 and 235: Mesenchymal tumours and related les
Page 236 and 237: areas are limited to less than 30%
Page 238 and 239: A B C Fig. 4.30 Leiomyosarcoma. A T
Page 240 and 241: e used sparingly and is reserved fo
Page 242 and 243: A B Fig. 4.38 Leiomyoma with perino
Page 244 and 245: cytological atypia, tumour cell nec
Page 246 and 247: Mixed epithelial and mesenchymal tu
Page 250 and 251: tumours may superficially invade th
Page 252 and 253: A Fig. 4.46 A Gestational choriocar
Page 254 and 255: A Fig. 4.49 A Classic complete hyda
Page 256 and 257: Sex cord-like, neuroectodermal and
Page 258 and 259: Secondary tumours of the uterine co
Page 260 and 261: WHO histological classification of
Page 262 and 263: Epithelial tumours M. Wells J.M. Ne
Page 264 and 265: Fig. 5.04 Mechanisms of human papil
Page 266 and 267: Fig. 5.08 Keratinizing squamous cel
Page 268 and 269: in their Asian population {2957}. I
Page 270 and 271: have a strong association with high
Page 272 and 273: e red by squamous epithelium {380}.
Page 274 and 275: endometrioid adenocarcinoma of the
Page 276 and 277: metrial epithelium. In some cases t
Page 278 and 279: with distinct cell borders and a gr
Page 280 and 281: Mesenchymal tumours M.L. Carcangiu
Page 282 and 283: {781}, liposarcoma {2840,3016}, ost
Page 284 and 285: Mixed epithelial and mesenchymal tu
Page 286 and 287: Fig. 5.44 Wilms tumour. The tumour
Page 288 and 289: A Fig. 5.47 Implant of endometrial
Page 290 and 291: CHAPTER 6 Tumours of the Vagina Alt
Page 292 and 293: Epithelial tumours E.S. Andersen A.
Page 294 and 295: Aetiology The fact that both VAIN a
Page 296 and 297: 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,
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
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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