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

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glands. These are perineural invasion, mucinous fibroplasia (collagenous micronodules), and glomerulations {160}. Although perineural indentation by benign prostatic glands has been reported, the glands in these cases appear totally benign and are present at only one edge of the nerve rather than circumferentially involving the perineural space, as can be seen in carcinoma {379,1676}. The second specific feature for prostate cancer is known as either mucinous fibroplasia or collagenous micronodules. It is typified by very delicate loose fibrous tissue with an ingrowth of fibroblasts, sometimes reflecting organization of intraluminal mucin. The final malignant specific feature is glomerulations, consisting of glands with a cribriform proliferation that is not transluminal. Rather, these cribriform formations are attached to only one edge of the gland resulting in a structure superficially resembling a glomerulus. Fig. 3.18 Intraluminal crystalloids in low grade adenocarcinoma. A B Fig. 3.19 A Adenocarcinoma with blue-tinged mucinous secretions. B Adenocarcinoma with straight rigid luminal borders, and dense pink secretions. Stromal features Ordinary acinar adenocarcinoma lacks a desmoplastic or myxoid stromal response, such that evaluation of the stroma is typically not useful in the diagnosis of prostate cancer. Typically adencarcinoma of the prostate does not elicit a stromal inflammatory response. Immunoprofile Prostate specific antigen (PSA) Following PSA’s discovery in 1979, it has become a useful immunohistochemical marker of prostatic differentiation in formalin-fixed, paraffin-embedded tissue, with both polyclonal and monoclonal antibodies available {702}. PSA is localized to the cytoplasm of non-neoplastic prostatic glandular cells in all prostatic zones, but is neither expressed by basal cells, seminal vesicle/ejaculatory duct glandular cells, nor urothelial cells. Because of its relatively high specificity for prostatic glandular cells, PSA is a useful tissue marker expressed by most prostatic adenocarcinomas {66, 702,1863,2905}. There is frequently intratumoural and intertumoural heterogeneity, with most studies indicating decreasing PSA expression with increasing tumour grade {702,906}. PSA is diagnostically helpful in distinguishing prostatic adenocarcinomas from other neoplasms secondarily involving the prostate and establishing prostatic origin in metastatic carcinomas of unknown primary {702,1863}. PSA is also helpful in excluding benign mimics of prostatic carcinoma, such as seminal vesicle/ejaculatory duct epithelium, nephrogenic adenoma, mesonephric duct remnants, Cowper’s glands, granulomatous prostatitis and malakoplakia {66,309,2905}. Whereas monoclonal antibodies to PSA do not label seminal vesicle tissue, polyclonal antibodies have been shown to occasionally label seminal vesicle epithelium {2714}. PSA in conjunction with a basal cell marker is useful in distinguishing intraglandular proliferations of basal cells from acinar cells, helping to separate prostatic intraepithelial neoplasia from basal cell hyperplasia and transitional cell metaplasia in equivocal cases {66, 2374,2905}. A minority of higher grade prostatic adenocarcinomas are PSA negative, although some of these tumours have been shown to express PSA mRNA. Some prostatic adenocarcinomas lose PSA immunoreactivity following androgen deprivation or radiation therapy. Prostate specific membrane antigen (PSMA) (membrane bound antigen expressed in benign and malignant prostatic acinar cells) and androgen receptor may be immunoreactive in some high grade, PSA immunonegative prostatic adenocarcinomas. Extraprostatic tissues which are variably immunoreactive for PSA, include urethral and periurethral glands (male and female), urothelial glandular metaplasia (cystitis cystitica and glandularis), anal glands (male), urachal remnants and neutrophils. Extraprostatic neoplasms and tumourlike conditions occasionally immunoreactive for PSA include urethral/periurethral adenocarcinoma (female), bladder adenocarcinoma, extramammary Paget disease of the penis, salivary gland neoplasms in males (pleomorphic adenoma, mucoepidermoid carcinoma, adenoid cystic carcinoma, salivary duct carcinoma), mammary carcinoma, mature teratoma, and some nephrogenic adenomas {66,702,2905}. Prostate specific acid phosphatase (PAP) Immunohistochemistry for PAP is active in formalin-fixed, paraffin-embedded tissues {26,66,702,1771,1862,2905}. The polyclonal antibody is more sensitive, but less specific than the monoclonal antibody {309}. PAP and PSA have similar diagnostic utility; since a small number of prostatic adenocarcinomas are immunoreactive for only one of the two markers, PAP is primarily reserved for cases of suspected prostatic carcinoma in which the PSA stain is negative {849}. Extraprostatic tissues reported to be immunoreactive for PAP include pancreatic islet cells, hepatocytes, gastric parietal cells, some renal tubular epithelial cells and neutrophils. Reported PAP immunoreactive neoplasms include some neuroendocrine tumours (pancreatic islet cell tumours, gastrointestinal carcinoids), mammary carcinoma, urothelial adenocarcinoma, anal cloacogenic carcinoma, salivary gland neoplasms (males) and mature teratoma {66,702,2905}. High molecular weight cytokeratins detected by 34βE12 (Cytokeratin-903) Prostatic secretory and basal cells are immunoreactive for antibodies to broad 172 Tumours of the prostate
A B Fig. 3.20 A, B Adenocarcinoma with mucinous fibroplasia (collagenous micronodules). A B Fig. 3.21 A Adenocarcinoma with perineural invasion. B Prostate cancer with glomerulations. spectrum and low molecular weight cytokeratins. However, only basal cells express high molecular weight cytokeratins {309}. One high molecular monoclonal cytokeratin antibody, clone 34βE12, recognizes 57 and 66 kilodalton cytokeratins in stratum corneum corresponding to Moll numbers 1, 5, 10 and 14, and is widely used as a basal cell specific marker active in paraffin-embedded tissue following proteolytic digestion {66,309,918,1048,1765,2374,2905}. 34βE12 is also immunoreactive against squamous, urothelial, bronchial/pneumocyte, thymic, some intestinal and ductal epithelium (breast, pancreas, bile duct, salivary gland, sweat duct, renal collecting duct), and mesothelium {918}. An immunoperoxidase cocktail containing monoclonal antibodies to cytokeratins 5 and 6 is also an effective basal cell stain {1286}. Since uniform absence of a basal cell layer in prostatic acinar proliferations is one important diagnostic feature of invasive carcinoma and basal cells may be inapparent by H&E stain, basal cell specific immunostains may help to distinguish invasive prostatic adenocarcinoma from benign small acinar cancer - mimics which retain their basal cell layer, e.g. glandular atrophy, post-atrophic hyperplasia, adenosis (atypical adenomatous hyperplasia), sclerosing adenosis and radiation induced atypia {66,1048,2905}. Because the basal cell layer may be interrupted or not demonstrable in small numbers of benign glands, the complete absence of a basal cell layer in a small focus of acini cannot be used alone as a definitive criterion for malignancy; rather, absence of a basal cell layer is supportive of invasive carcinoma only in acinar proliferations which exhibit suspicious cytologic and / or architectural features on H&E stain {1048}. Conversely, some early invasive prostatic carcinomas, e.g. microinvasive carcinomas arising in association with or independent of high grade prostatic intraepithelial neoplasia, may have residual basal cells {1952}. Intraductal spread of invasive carcinoma and entrapped benign glands are other proposed explanations for residual basal cells {66,2905}. Rare prostatic adenocarcinomas contain sparse neoplastic glandular cells, which are immunoreactive for 34βE12, yet these are not in a basal cell distribution {66,2374}. The use of antibodies for 34βE12 is especially helpful for the diagnosis for of deceptively benign appearing variants of prostate cancer. Immunohistochemistry for cytokeratins 7 and 20 have a limited diagnostic use in prostate pathology with the exception that negative staining for both markers, which can occur in prostate Acinar adenocarcinoma 173
Page 1 and 2:
World Health Organization Classific
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This volume was produced in collabo
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Contents 1 Tumours of the kidney 9
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CHAPTER 1 Tumours of the Kidney Can
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TNM classification of renal cell ca
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one quarter of kidney cancers in bo
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Familial renal cell carcinoma M.J.
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Table 1.02 Genotype - phenotype cor
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A B Fig. 1.11 A Multiple cutaneous
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A B Fig. 1.14 Birt-Hogg-Dubé syndr
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Clear cell renal cell carcinoma D.J
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Fig. 1.20 Clear cell renal cell car
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Papillary renal cell carcinoma B. D
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A B Fig. 1.29 Papillary renal cell
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Fig. 1.33 Chromophobe RCC with sarc
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Carcinoma of the collecting ducts o
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Renal medullary carcinoma C.J. Davi
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Renal carcinomas associated with Xp
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Renal cell carcinoma associated wit
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Papillary adenoma of the kidney J.N
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of this tumour. Microscopic extensi
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A B Fig. 1.59 Metanephric adenoma.
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esults in intratumoral aneurysms. O
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peritumoural fibrous pseudocapsule.
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increases in prevalence to approxim
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Nephrogenic rests and nephroblastom
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Cystic partially differentiated nep
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A B Fig. 1.80 Clear cell sarcoma of
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A B Fig. 1.85 Rhabdoid tumour of th
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transcription factor is fused to th
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Leiomyosarcoma S.M. Bonsib Definiti
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Angiomyolipoma G. Martignoni M.B. A
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melanocytic and smooth muscle marke
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Multinucleated and enlarged ganglio
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Haemangioma P. Tamboli Definition H
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Fig. 1.107 Juxtaglomerular cell tum
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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
Page 117 and 118: A Fig. 2.45 Non-invasive urothelial
Page 119 and 120: for DBCCR1 silencing {984,2476}. Th
Page 121 and 122: Squamous cell carcinoma D.J. Grigno
Page 123 and 124: Fig. 2.51 Squamous cell carcinoma.
Page 125 and 126: Adenocarcinoma A.G. Ayala P. Tambol
Page 127 and 128: A B Fig. 2.61 A Adenocarcinoma in s
Page 129 and 130: A B Fig. 2.65 Intramural urachal ca
Page 131 and 132: Müllerian origin is postulated for
Page 133 and 134: A Fig. 2.69 Small cell carcinoma. A
Page 135 and 136: Carcinoid L. Cheng Definition Carci
Page 137 and 138: Leiomyosarcoma J. Cheville Definiti
Page 139 and 140: Osteosarcoma L. Guillou Definition
Page 141 and 142: Leiomyoma J. Cheville Definition A
Page 143 and 144: Haemangioma L. Cheng Definition Hae
Page 145 and 146: Metastatic tumours and secondary ex
Page 147 and 148: Tumours of the renal pelvis and ure
Page 149 and 150: nodular, ulcerative or infiltrative
Page 151 and 152: Tumours of the urethra F. Hofstädt
Page 153 and 154: usually show enteric, colloid or si
Page 155 and 156: CHAPTER 3X Tumours of of the the Pr
Page 157 and 158: TNM classification of carcinomas of
Page 159 and 160: contrast, mortality among migrants
Page 161 and 162: Fig. 3.06 Transrectal ultrasound of
Page 163 and 164: PSA-related diagnostic strategies.
Page 165 and 166: A B C Fig. 3.10 A,B Section of pros
Page 167: pale-clear, similar to benign gland
Page 171 and 172: prostate adenocarcinomas exhibit AR
Page 173 and 174: A Fig. 3.27 A, B Foamy gland adenoc
Page 175 and 176: A B Fig. 3.32 A Sarcomatoid carcino
Page 177 and 178: A B Fig. 3.37 A Gleason score 1+1=2
Page 179 and 180: A B Fig. 3.43 A Prostate cancer Gle
Page 181 and 182: Fig. 3.48 Heat map-nature. From S.M
Page 183 and 184: Fig. 3.51 Prostate cancer. Major su
Page 185 and 186: many stage T1b cancers. Stage T2 Mo
Page 187 and 188: Fig. 3.58 Patterns of seminal vesic
Page 189 and 190: Prostatic intraepithelial neoplasia
Page 191 and 192: A B Fig. 3.63 A Micropapillary high
Page 193 and 194: A B Fig. 3.68 A Ductal carcinoma in
Page 195 and 196: Ductal adenocarcinoma X.J. Yang L.
Page 197 and 198: Papillary pattern can be seen in bo
Page 199 and 200: A B Fig. 3.74 A Inflammation withou
Page 201 and 202: Squamous neoplasms T.H. Van der Kwa
Page 203 and 204: Neuroendocrine tumours P.A. di Sant
Page 205 and 206: Mesenchymal tumours J. Cheville F.
Page 207 and 208: Fig. 3.89 Sarcoma of the prostate.
Page 209 and 210: Miscellaneous tumours P.H. Tan L. C
Page 211 and 212: A Fig. 3.96 A Adenocarcinoma of the
Page 213 and 214: WHO histological classification of
Page 215 and 216: Introduction F.K. Mostofi I.A. Sest
Page 217 and 218: 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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WHO histological classification of
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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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2070. Phillips G, Kumari-Subaiya S,
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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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