Invasive breast carcinoma - IARC

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even with additional sectioning, it is recommended that invasion should not be diagnosed {3119}. The following criteria apply to the measurement of vulvar squamous cell carcinoma: (1) Thickness: measurement from the surface, or the granular layer if keratinized, to the deepest point of invasion. (2) Depth of invasion: measurement from the epithelial-stromal junction of the adjacent most superficial dermal papillae to the deepest point of invasion. The preferred measurement is the depth of invasion, as defined above. A Fig. 7.03 Verrucous carcinoma. A The characteristic exophytic and endophytic growth pattern is evident in the sectioned surface of the tumour on the right side of the field. B The tumour is composed of well differentiated squamous epithelium with an undulating surface, minimal cytological atypia and a pushing border. B Somatic genetics Cytogenetic data exist on 11 squamous cell carcinomas of the vulva {2897,3156}. The most common karyotypic changes are loss of 3p, 8p, 22q, Xp, 10q and 18q and gain of 3q and 11q21. There is an inverse correlation between histological differentiation and karyotypic complexity. F u rt h e rm o re, a comparative genomic hybridization study of 10 cases revealed losses of 4p, 3p, and 5q and gains of 3q and 8p {1338}. Loss of 10q and 18q seems to be particularly associated with a poor prognosis in squamous cell carcinoma {2897,3156}. On the other hand, the only cytogenetically analysed squamous cell carcinoma in situ of the vulva (VIN 3) had a rearrangement of 11p as the sole anomaly {2818}. TP53 mutation or HPV can independently lead to cell cycle disruption relevant to vulvar squamous cell carc i n o g e n e s i s . Besides mutational inactivation, T P 5 3 can be inactivated through binding of HPV protein E6. PTEN is another gene that is frequently mutated in carcinomas of the vulva {1234}. Both TP53 and PTEN mutations have also been detected in VIN, indicating that they are early events in vulvar carcinogenesis {1234,1866}. High frequencies of allelic imbalance have been detected at 1q, 2q, 3p, 5q, 8p, 8q, 10p, 10q, 11p, 11q, 15q, 17p, 18q, 21q and 22q, most of these irrespective of HPV status {2256}. This finding suggests that despite a diff e re n t pathogenesis both HPV-positive and HPV-negative vulvar squamous cell carcinomas share several genetic changes during their progression. Prognosis and predictive factors Risk factors for re c u r rence include advanced stage, tumour diameter >2.5 cm, m u l t i f o c a l i t , y capillary-like space involvement, associated VIN 2 or VIN 3 and involved margins of resection {1235,2004}. The extent of lymph node involvement and mode of treatment may also influence survival {721}. Patients whose tumours have a "spray" or finger-like pattern of invasion have a poorer survival than those with a "pushing" pattern {1235}. For patients with stage 1A carcinoma, the therapy is usually local excision with at least a 1-cm margin of normal tissue {3, 1428}. Inguinofemoral lymph node dissection is usually unnecessary {247,373,374,1105, 1428}. The risk of re c u r rence in stage 1A cases is very low, with 5 and 10-year re c u r- re n c e - f ree tumour specific survivals of 100% and 94.7%, respectively {1732}. Late re c u r rence or "re o c c u r rence" of a second squamous carcinoma in another site within the vulva is rare but can occur, and theref o re long-term follow-up is warranted. For tumours greater than stage 1A partial or total deep vulvectomy with ipsilateral or bilateral inguino-femoral lymph node resection may be required. If superficial lymph nodes contain tumour, radiotherapy to the deep pelvic nodes or chemoradiation may be necessary {360,373, 1749,2783}. Basal cell carcinoma Definition An infiltrating tumour composed predominantly of cells resembling the basal cells of the epidermis. Clinical features This tumour presents as a slow gro w- ing, locally invasive, but rarely metastasizing lesion in the vulva {218,833,1872, 2 2 6 0 } . Fig. 7.04 Basal cell carcinoma. Aggregates of uniform basaloid cells with peripherial palisading arise from the basal layer of the overlying squamous epithelium and infiltrate the stroma. 318 Tumours of the vulva
A B Fig. 7.05 Vulvar intraepithelial neoplasia (VIN). A VIN 1. Hyperkeratosis is prominent. Nuclear crowding is confined to the lower third of the epithelium. B VIN 3, warty type (severe displasia). Beneath a hyperkeratotic surface the epithelial cells are crowded and show minimal maturation. C VIN 3 (carcinoma in situ, basaloid type). Nearly the entire epithelium is composed of closely packed basaloid cells. C Histopathology The tumour is composed of aggregates of uniform basal cells with peripheral palisading. Squamous cell diff e re n t i a t i o n may occur at the centre of the tumour nests. Tumours containing gland-like structures are referred to as "adenoid basal cell carcinoma" {1850}. Those containing infiltrating malignant-appearing squamous cells may be diagnosed as metatypical basal cell carcinoma or basosquamous carcinoma. Immunohistochemical findings reflect these histological subtypes {183}. Basal cell carcinoma has been reported in association with vulvar Paget disease {1084}. Histogenesis This tumour is derived from the basal cells of the epidermis or hair follicles. Prognosis and predictive factors Basal cell carcinoma of the vulva is usually treated by local excision; however, groin metastases have been reported {1017}. Vulvar intraepithelial neoplasia Definition An intraepithelial lesion of the vulvar squamous epithelium characterized by d i s o rd e red maturation and nuclear abnormalities, i.e. loss of polarity, pleomorphism, coarse chromatin, irregularities of the nuclear membrane and mitotic figures, including atypical forms. Synonym Dysplasia/carcinoma in situ. Epidemiology The incidence of VIN, unlike that of vulvar carcinoma, has been increasing over the past 20 years, especially in women of reproductive age, with the highest frequency reported in women 20-35 years old {538,1312,2804}. Aetiology VIN is predominately of the warty or basaloid types, and both are associated with HPV, most commonly type 16 {1106, 1197,1663,2936}. Women with HPV-related vulvar disease have an increased risk of associated cervical intraepithelial neoplasia (CIN) {2766}. Women infected with human immunodeficiency virus (HIV) have a high frequency of HPV infection of the lower genital tract and associated CIN and/or VIN {2766}. Clinical features Women with VIN may present with vulvar pruritus or irritation or may observe the lesions and seek medical assistance {919}. VIN is typically a macular or papular lesion or lesions, which in approximately one-half of the cases are white or aceto-white. Approximately one-quarter of VIN lesions are pigmented. VIN is multifocal in approximately two-thirds of the cases. The remaining patients usually present as a solitary lesion, a more common finding in older women {431}. Large confluent lesions are uncommon {919, 3123}. Tumour spread and staging Up to one-fifth of the women presenting with VIN are found to have an associated squamous cell carcinoma {431,1197, 1272}. In most cases these squamous cell carcinomas are superficially invasive. Histopathology The epithelial cells are typically crowded, and acanthosis may be present. A prominent granular layer may be associated with parakeratosis, hyperkeratosis or both. Involvement of skin appendages is seen in over one-third of the cases, which in hairy skin may be as deep as 2.7 mm. Skin appendage involvement should not be misinterpreted as invasion {219,2636}. There may be associated HPV changes. The term "bowenoid papulosis" should not be used as a histological diagnosis (see below). The grading of HPV-related VIN is similar to that used in the cervix. The simplex type of VIN (carcinoma in situ, simplex Fig. 7.06 Vulvar intraepithelial neoplasia, differentiated (simplex) type. The atypia is confined to the basal and parabasal layers. The squamous cells have nuclear abnormalities with prominent eosinophilic abortive pearl formations in the deeper portions of the epithelium. The presence of paradoxical maturation abutting on the epithelial-stromal junction is suggestive of impending invasion. Epithelial tumours 319
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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
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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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Page 272 and 273: e red by squamous epithelium {380}.
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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
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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
Page 298 and 299: er of mitoses varies but is usually
Page 300 and 301: ICD-O codes Adenosquamous carcinoma
Page 302 and 303: A C Fig. 6.17 Sarcoma botryoides. A
Page 304 and 305: 1-11 cm. They may arise anywhere in
Page 306 and 307: elsewhere in the female genital tra
Page 308 and 309: A Fig. 6.24 Yolk sac tumour. A The
Page 310 and 311: g rowing in sheets. Some may have s
Page 312 and 313: WHO histological classification of
Page 314 and 315: Epithelial tumours E.J. Wilkinson M
Page 318 and 319: type) is a highly diff e rentiated
Page 320 and 321: Clinical features Bartholin gland c
Page 322 and 323: glandular elements surrounded by fi
Page 324 and 325: Mesenchymal tumours R.L. Kempson M.
Page 326 and 327: Table 7.03 Differential diagnosis o
Page 328 and 329: Prognosis and predictive factors A
Page 330 and 331: Table 7.04 Clark levels of cutaneou
Page 332 and 333: A Fig. 7.23 Vulvar peripheral primi
Page 334 and 335: Familial aggregation of cancers of
Page 336 and 337: BRCA1 syndrome Definition Inherited
Page 338 and 339: dispose individuals to the developm
Page 340 and 341: Fig. 8.05 To assess whether wild-ty
Page 342 and 343: Fig. 8.07 Factors that modify risk
Page 344 and 345: BRCA2 syndrome R. Eeles S. Piver S.
Page 346 and 347: tubal or ovarian carcinomas. Howeve
Page 348 and 349: in typical nuclear foci that may re
Page 350 and 351: Breast tumours Frequency Breast can
Page 352 and 353: Fig. 8.14 Codon distribution of som
Page 354 and 355: Breast tumours Age distribution and
Page 356 and 357: Hereditary non-polyposis colon canc
Page 358 and 359: essary in the evaluation of the pat
Page 360 and 361: Age distribution and penetrance Mos
Page 362 and 363: Contributors Dr Vera M. ABELER** De
Page 364 and 365: 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
Page 428 and 429:
MPNST, see Malignant peripheral ner
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Small cell / oat cell carcinoma, 32
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