Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

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acinar pattern. The alveolar and acinar structures may dilate, producing microcystic and macrocystic patterns. Infrequently, clear cell renal cell carcinoma has a distinct tubular pattern and rarely a pseudopapillary architecture is focally present. The cytoplasm is commonly filled with lipids and glycogen, which are dissolved in routine histologic processing, creating a clear cytoplasm surrounded by a distinct cell membrane. Many tumours contain minority populations of cells with eosinophilic cytoplasm; this is particularly common in high grade tumours and adjacent to areas with necrosis or haemorrhage. In well preserved preparations, the nuclei tend to be round and uniform with finely granular, evenly distributed chromatin. Depending upon the grade, nucleoli may be inconspicuous, small, or large and prominent. Very large nuclei lacking nucleoli or bizarre nuclei may occasionally occur. A host of unusual histologic findings are described in clear cell renal cell carcinoma. Sarcomatoid change occurs in 5% of tumours and is associated with worse prognosis. Some tumours have central areas of fibromyxoid stroma, areas of calcification or ossification {991}. Most clear cell RCCs have little associated inflammatory response; infrequently, an intense lymphocytic or neutrophilic infiltrate is present. Immunoprofile Clear cell RCCs frequently react with antibodies to brush border antigens, low molecular weight cytokeratins, CK8, CK18, CK19, AE1, Cam 5.2 and vimentin {1675,2086,2818,2880}. High molecular weight cytokeratins, including CK14 {464}, and 34βE12 are rarely detected. The majority of clear cell RCCs react positively for renal cell carcinoma marker {1675}, CD10 {140} and epithelial membrane antigen {776}. MUCΙ and MUC3 are consistently expressed {1479}. Grading Nuclear grade, after stage, is the most important prognostic feature of clear cell renal cell carcinoma {441,764, 815,949,2433,2473,2940}. The prognostic value of nuclear grade has been validated in numerous studies over the past 8 decades. Both 4-tiered and 3- tiered grading systems are in widespread use. The 4-tiered nuclear grading system {815} is as follows: Using the 10x objective, grade 1 cells have small hyperchromatic nuclei (resembling mature lymphocytes) with no visible nucleoli and little detail in the chromatin. Grade 2 cells have finely granular "open" chromatin but inconspicuous nucleoli at this magnification. For nuclear grade 3, the nucleoli must be easily unequivocally recognizable with the 10x objective. Nuclear grade 4 is characterized by nuclear pleomorphism, hyperchromasia and single to multiple macronucleoli. Grade is assigned based on the highest grade present. Scattered cells may be discounted but if several cells within a single high power focus have high grade characteristics, then the tumour should be graded accordingly. Genetic susceptibility Clear cell renal cell carcinoma constitutes a typical manifestation of von Hippel-Lindau disease (VHL) but may also occur in other familial renal cell cancer syndromes. Somatic genetics Although most clear cell RCCs are not related to von Hippel Lindau disease, 3p deletions have been described in the vast majority of sporadic clear cell renal cell carcinoma by conventional cytogenetic, FISH, LOH and CGH analyses {1372,1754,1760,1786,2109,2614,2690, 2691,2723,2925}. At least 3 separate regions on chromosome 3p have been implicated by LOH studies as relevant for sporadic renal cell carcinoma: one coincident with the von Hippel-Lindau (VHL) disease gene locus at 3p25-26 {1445,2400}, one at 3p21-22 {2689} and one at 3p13-14 {2721}, which includes the chromosomal translocation point in familial human renal cell carcinoma. These data suggest involvement of multiple loci on chromosome 3 in renal cancer development {474,2686}. Mutations of the VHL gene have been described in 34-56% of sporadic clear cell RCC {307,792,897,2342,2400,2810}. DNA methylation was observed in 19% of clear cell renal cell carcinomas {1082}. Therefore, somatic inactivation of the VHL gene may occur by allelic deletion, mutation, or epigenetic silencing in 70% or more {897,1082,1445,2342}. These data suggest that the VHL gene is the most likely candidate for a tumour suppressor gene in sporadic clear cell RCC. A B Fig. 1.18 A VHL, renal carcinoma. Note clear cells and cysts. B Clear cell renal cell carcinoma. Typical alveolar arrangement of cells. 24 Tumours of the kidney
Fig. 1.20 Clear cell renal cell carcinoma. Survival curves by grade for patients with clear cell renal cell carcinoma. From C.M. Lohse et al. {1532}. Fig. 1.19 Clear cell RCC. Note deletion of 3p as the only karyotype change. However, recent data give evidence for other putative tumour suppressor genes at 3p, e.g. RASSF1A at 3p21 {1789} and NRC-1 at 3p12 {1562}. Chromosome 3p deletions have been observed in very small clear cell tumours of the kidney and are regarded as the initial event in clear cell cancer development {2107,2109,2925}. Inactivation of the VHL gene has consequences for VHL protein function. The VHL protein negatively regulates hypoxia-inducible factor, which activates genes involved in cell proliferation, neo-vascularization, and extracellular matrix formation {642,1310,1828}. Fig. 1.22 Clear cell RCC. VHL deletion, there are two signals in red (chromosome 3), and one signal in green (VHL gene). FISH expression. Clonal accumulation of additional genetic alterations at many chromosomal locations then occurs in renal cancer progression and metastasis {247,339,958, 1218,1754,2109,2179,2344,2345}. High level gene amplifications are rare in clear cell renal cell carcinoma {1754}. Individual chromosomal gains and losses have been analyzed for an association with patient prognosis. Chromosome 9p loss seems to be a sign of poor prognosis {1754,2341}. Losses of chromosome 14q were correlated with poorer patient outcome, high histologic grade and high pathologic stage {226,1080, 2344,2849}. LOH on chromosome 10q around the PTEN/MAC locus have been frequently detected and were related to poor prognosis {2722}. Expression levels of many genes have been studied in clear cell RCC. The role of p53 expression in renal cell carcinoma is controversial. A few studies suggest that p53 overexpression is associated with poor prognosis and with sarcomatoid transformation {1932,1939,2164, 2659}. High expression levels of bFGF, VEGF, IL-8, MMP-2, MMP-9, vimentin, MHC class II and E-cadherin may be important for development and/or progression {320,1472,1892,2391,2437}. Expression of epidermal growth factor receptor (EGFR) is frequent in renal cell carcinoma and has been proposed as prognostic parameter {1755}. Whereas Fig. 1.21 Clear cell carcinoma. Survival of patients depends on the presence and extent of sarcomatoid differentiation, ranging from no differentiation (n=326), to sarcomatoid differentiation in 50% (n=31) of tumour area. From H. Moch et al. {1753}. Copyright © 2000 American Cancer Society. Reprinted by permission of Wiley- Liss, Inc., a subsidiary of John Wiley & Sons, Inc. amplification of the EGFR gene on chromosome 7p13 is a major cause for EGFR expression in brain tumours, this pathway is uncommon in renal cell carcinoma {1756}. HER2/neu amplifications are rare or absent in renal cell carcinoma {2339,2799}. cDNA array analysis of clear cell renal carcinoma showed complex patterns of gene expression {1759,2887}. It has been shown that the integration of expression profile data with clinical data could serve to enhance the diagnosis and prognosis of clear cell RCC {2551}. Clear cell renal cell carcinoma 25
Page 1 and 2: World Health Organization Classific
Page 3 and 4: This volume was produced in collabo
Page 5 and 6: Contents 1 Tumours of the kidney 9
Page 7 and 8: CHAPTER 1 Tumours of the Kidney Can
Page 9 and 10: TNM classification of renal cell ca
Page 11 and 12: one quarter of kidney cancers in bo
Page 13 and 14: Familial renal cell carcinoma M.J.
Page 15 and 16: Table 1.02 Genotype - phenotype cor
Page 17 and 18: A B Fig. 1.11 A Multiple cutaneous
Page 19 and 20: A B Fig. 1.14 Birt-Hogg-Dubé syndr
Page 21: Clear cell renal cell carcinoma D.J
Page 25 and 26: Papillary renal cell carcinoma B. D
Page 27 and 28: A B Fig. 1.29 Papillary renal cell
Page 29 and 30: Fig. 1.33 Chromophobe RCC with sarc
Page 31 and 32: Carcinoma of the collecting ducts o
Page 33 and 34: Renal medullary carcinoma C.J. Davi
Page 35 and 36: Renal carcinomas associated with Xp
Page 37 and 38: Renal cell carcinoma associated wit
Page 39 and 40: Papillary adenoma of the kidney J.N
Page 41 and 42: of this tumour. Microscopic extensi
Page 43 and 44: A B Fig. 1.59 Metanephric adenoma.
Page 45 and 46: esults in intratumoral aneurysms. O
Page 47 and 48: peritumoural fibrous pseudocapsule.
Page 49 and 50: increases in prevalence to approxim
Page 51 and 52: Nephrogenic rests and nephroblastom
Page 53 and 54: Cystic partially differentiated nep
Page 55 and 56: A B Fig. 1.80 Clear cell sarcoma of
Page 57 and 58: A B Fig. 1.85 Rhabdoid tumour of th
Page 59 and 60: transcription factor is fused to th
Page 61 and 62: Leiomyosarcoma S.M. Bonsib Definiti
Page 63 and 64: Angiomyolipoma G. Martignoni M.B. A
Page 65 and 66: melanocytic and smooth muscle marke
Page 67 and 68: Multinucleated and enlarged ganglio
Page 69 and 70: Haemangioma P. Tamboli Definition H
Page 71 and 72: Fig. 1.107 Juxtaglomerular cell tum
Page 73 and 74:
Intrarenal schwannoma I. Alvarado-C
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Mixed epithelial and stromal tumour
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Synovial sarcoma of the kidney J.Y.
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Renal carcinoid tumour L.R. Bégin
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Primitive neuroectodermal tumour (E
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Paraganglioma / Phaeochromocytoma P
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Leukaemia A. Orazi Interstitial inf
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WHO histological classification of
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TNM classification of carcinomas of
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The risk of bladder cancer goes dow
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Tumour spread and staging Urinary b
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feature in such patients undergoing
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A Fig. 2.12 Infiltrative urothelial
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A Fig. 2.15 A Infiltrating urotheli
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A B Fig. 2.19 A Infiltrative urothe
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Fig. 2.23 Infiltrative urothelial c
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ing systems have been proposed on t
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Non-invasive urothelial tumours G.
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chronically inflamed urothelium and
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Inverted papilloma G. Sauter Defini
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muscle invasive disease, but there
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Fig. 2.42 Non-invasive urothelial n
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A Fig. 2.45 Non-invasive urothelial
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for DBCCR1 silencing {984,2476}. Th
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Squamous cell carcinoma D.J. Grigno
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Fig. 2.51 Squamous cell carcinoma.
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Adenocarcinoma A.G. Ayala P. Tambol
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A B Fig. 2.61 A Adenocarcinoma in s
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A B Fig. 2.65 Intramural urachal ca
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Müllerian origin is postulated for
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A Fig. 2.69 Small cell carcinoma. A
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Carcinoid L. Cheng Definition Carci
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Leiomyosarcoma J. Cheville Definiti
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Osteosarcoma L. Guillou Definition
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Leiomyoma J. Cheville Definition A
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Haemangioma L. Cheng Definition Hae
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Metastatic tumours and secondary ex
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Tumours of the renal pelvis and ure
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nodular, ulcerative or infiltrative
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Tumours of the urethra F. Hofstädt
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usually show enteric, colloid or si
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CHAPTER 3X Tumours of of the the Pr
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TNM classification of carcinomas of
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contrast, mortality among migrants
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Fig. 3.06 Transrectal ultrasound of
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PSA-related diagnostic strategies.
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A B C Fig. 3.10 A,B Section of pros
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pale-clear, similar to benign gland
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A B Fig. 3.20 A, B Adenocarcinoma w
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prostate adenocarcinomas exhibit AR
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A Fig. 3.27 A, B Foamy gland adenoc
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A B Fig. 3.32 A Sarcomatoid carcino
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A B Fig. 3.37 A Gleason score 1+1=2
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A B Fig. 3.43 A Prostate cancer Gle
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Fig. 3.48 Heat map-nature. From S.M
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Fig. 3.51 Prostate cancer. Major su
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many stage T1b cancers. Stage T2 Mo
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Fig. 3.58 Patterns of seminal vesic
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Prostatic intraepithelial neoplasia
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A B Fig. 3.63 A Micropapillary high
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A B Fig. 3.68 A Ductal carcinoma in
Page 195 and 196:
Ductal adenocarcinoma X.J. Yang L.
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Papillary pattern can be seen in bo
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A B Fig. 3.74 A Inflammation withou
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Squamous neoplasms T.H. Van der Kwa
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Neuroendocrine tumours P.A. di Sant
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Mesenchymal tumours J. Cheville F.
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Fig. 3.89 Sarcoma of the prostate.
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Miscellaneous tumours P.H. Tan L. C
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A Fig. 3.96 A Adenocarcinoma of the
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Page 215 and 216:
Introduction F.K. Mostofi I.A. Sest
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wartime birth cohorts illustrate th
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Similar tumours as those of group 1
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crucial for the development of this
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A B Fig. 4.09 Spermatocytic seminom
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A B Fig. 4.14 Intratubular germ cel
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A B Fig. 4.19 Seminoma. A Typical s
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Fig. 4.24 Seminoma. Vascular invasi
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Fig. 4.28 Spermatocytic seminoma wi
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A B Fig. 4.33 Embryonal carcinoma.
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A B Fig. 4.38 Yolk sac tumour. A En
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have cytoplasmic lacunae that conta
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A Fig. 4.46 Teratoma. A Longitudina
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A B Fig. 4.51 A Cut surface of derm
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Fig. 4.54 Mixed germ cell tumour. L
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Sex cord / gonadal stromal tumours
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A B C Fig. 4.67 Malignant Leydig ce
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A Fig. 4.73 A Sertoli cell tumour.
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ICD-O codes Granulosa cell tumour 8
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ICD-O code 8592/1 Clinical features
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A B Fig. 4.83 Germ cell-sex cord/go
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A Fig. 4.85 A, B Brenner tumour of
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typical grade III follicular morpho
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testicular parenchyma and tumour te
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A B the surgical scar and adjacent
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Immunoprofile Ordóñez and associa
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often have a grey-white cut surface
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Fig. 4.111 Angiomyofibroblastoma-li
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A B Fig. 4.119 Embryonal rhabdomyos
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Table 4.05 Secondary tumours of the
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Page 277 and 278:
A Fig. 5.04 A, B Squamous cell carc
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deformed by an exophytic mass. In s
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A B C Fig. 5.12 A Warty (condylomat
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A Fig. 5.20 Bowenoid papulosis. A,
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three had been circumcized by 9 yea
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Mesenchymal tumours J.F. Fetsch M.
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Fig. 5.31 Neurofibroma of the penis
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oectodermal tumour/Ewing sarcoma [p
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Secondary tumours of the penis C.J.
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Dr John N. EBLE* Dept. of Pathology
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Dr Ricardo PANIAGUA Department of C
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Source of charts and photographs 1.
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References 1. Anon. (1955). Case re
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115. Ariel I, Sughayer M, Fellig Y,
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246. Birt AR, Hogg GR, Dube WJ (197
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374. Cardone G, Malventi M, Roffi M
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502. Corti B, Carella R, Gabusi E,
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633. Donhuijsen K, Schmidt U, Richt
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768. Fischer J, Palmedo G, von Knob
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900. Goedert JJ, Cote TR, Virgo P,
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1028. Hartmann A, Dietmaier W, Hofs
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1162. Iezzoni JC, Fechner RE, Wong
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1293. Keetch DW, Catalona WJ (1995)
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1424. Ladanyi M, Lui MY, Antonescu
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1548. Lopez-Beltran A, Croghan GA,
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1681. McLaughlin JK, Silverman DT,
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1816. Moudouni SM, En-Nia I, Rioux-
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1945. Ohori M, Wheeler TM, Kattan M
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2070. Phillips G, Kumari-Subaiya S,
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2199. Riou G, Barrois M, Prost S, T
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2327. Schmidt L, Junker K, Weirich
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2450. Smith G, Elton RA, Beynon LL,
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2572. Tamboli P, Mohsin SK, Hailema
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2693. van Echten J, Timmer A, van d
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2816. Wick MR, Berg LC, Hertz MI (1
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2937. Zhuang Z, Park WS, Pack S, Sc
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CCNB, 226 CCND1, 105, 108 CCND2, 22
Page 351 and 352:
J Juvenile type granulosa cell tumo
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Promoter methylation, 21 Prostate s
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