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

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expression of PSMA in serum of both normal individuals and prostate cancer patients using western blots have provided conflicting results in some laboratories {635,1838,1841,2214}. Reverse transcriptase-polymerase chain reaction RT-PCR is an extremely sensitive assay, capable of detecting one prostate cell diluted in 10 8 non-prostate cells. This high degree of sensitivity mandates that extreme precaution be taken to avoid both cross-sample and environmental contamination. Because of the high sensitivity of RT-PCR, there is the possibility that extremely low-level basal transcriptions of prostate-specific genes from non-prostate cells will result in a positive RT-PCR signal. More recently, basal PSA mRNA levels were detected in a quantitative RT-PCR in individuals without prostate cancer, thus suggesting the need to quantitate the RT- PCR assay in order to control for basal transcription {2730}. These problems with RT-PCR have limited its clinical utility {1780,1927}. Methods of tissue diagnosis Needle biopsies The current standard method for detection of prostate cancer is by transrectal ultrasound-guided core biopsies. Directed biopsies to either lesions detected on digital rectal examination or on ultrasound should be combined with systematic biopsies taken according to a standardized protocol {1008,1703}. The sextant protocol samples the apex, mid and base region bilaterally {1099}. Sextant biopsies aim at the centre of each half of the prostate equidistant from the midline and the lateral edge while the most common location of prostate cancer is in the dorsolateral region of the prostate. Several modifications of the sextant protocol have been proposed. Recent studies have shown that protocols with 10 to 13 systematic biopsies have a cancer detection rate up to 35% superior to the traditional sextant protocol {105,724, 2151}. This increased yield relates to the addition of biopsies sampling the more lateral part of the peripheral zone, where a significant number of cancers are located. Approximately 15-22% of prostate cancers arise in the transition zone, while sextant biopsies mainly sample the peripheral zone. Most studies have found few additional cancers by adding transition zone biopsies to the sextant protocol (1.8-4.3% of all cancers detected) and transition zone biopsies are usually not taken in the initial biopsy session {778,2598}. Handling of needle biopsies. Prostate biopsies from different regions of the gland should be identified separately. If two cores are taken from the same region, they can be placed into the same block. However, blocking more than two biopsy specimens together increases the loss of tissue at sectioning {1272}. When atypia suspicious for cancer is found, a repeat biopsy should concentrate on the initial atypical site in addition to sampling the rest of the prostate. This cannot be performed unless biopsies have been specifically designated as to their location. The normal histology of the prostate and its adjacent structures differs between base and apex and knowledge about biopsy location is helpful for the pathologist. The location and extent of cancer may be critical for the clinician when selecting treatment option {2151}. The most common fixative used for needle biopsies is formalin, although alternative fixatives, which enhance nuclear details are also in use. A potential problem with these alternative fixatives is that lesions such as high-grade prostatic intraepithelial neoplasia may be over-diagnosed. Immunohistochemistry for high molecular weight cytokeratins provides considerable help in decreasing the number of inconclusive cases from 6-2% {1923}. It has therefore been suggested that intervening unstained sections suitable for immunohistochemistry are retained in case immunohistochemistry would be necessary. Intervening slides are critical to establish a conclusive diagnosis in 2.8% of prostate biopsies, hence, sparing a repeat biopsy {939}. Transurethral resection of the prostate When transurethral resection of the prostate (TURP) is done without clinical suspicion of cancer, prostate cancer is incidentally detected in approximately 8- 10% of the specimens. Cancers detected at TURP are often transition zone tumours, but they may also be of peripheral zone origin, particularly when they are large {941,1685,1686}. It is recommended that the extent of tumour is reported as percentage of the total specimen area. If the tumour occupies less Fig. 3.09 Needle biopsies sampling the lateral part of the peripheral zone (PZ) improve detection of prostate cancer (red). than 5% of the specimen it is stage T1a, and otherwise stage T1b. However, in the uncommon situation of less than 5% of cancer with Gleason score 7 or higher, patients are treated as if they had stage T1b disease. Most men who undergo total prostatectomy for T1a cancer have no or minimal residual disease, but in a minority there is substantial tumour located in the periphery of the prostate {711}. Handling of TUR specimens. A TURP specimen may contain more than a hundred grams of tissue and it is often necessary to select a limited amount of tissue for histological examination. Submission should be random to ensure that the percentage of the specimen area involved with cancer is representative for the entire specimen. Several strategies for selection have been evaluated. Submission of 8 cassettes will identify almost all stage T1b cancers and approximately 90% of stage T1a tumours {1847,2223}. In young men, submission of the entire specimen may be considered to ensure detection of all T1a tumours. Guidelines have been developed for whether additional sampling is needed following the initial detection of cancer in a TURP specimen {1673}. Fine needle aspiration cytology Before the era of transrectal core biopsies, prostate cancer was traditionally diagnosed by fine needle aspiration (FNA). FNA is still used in some countries and has some advantages. The technique is cheap, quick, usually relatively painless and has low risk of complications. In early studies comparing FNA and limited core biopsy protocols, the sensitivity of FNA was usually found to be comparable with that of core biopsies {2765}. However, the use of FNA for diagnosing prostate cancer has disadvan- 168 Tumours of the prostate
A B C Fig. 3.10 A,B Section of prostate showing peripheral zone adenocarcinoma. C Section of prostate showing transition zone adenocarcinoma, difficult to distinguish from nodules of BPH. tages. Potential sources of false positive diagnosis with FNA are inflammatory atypia, prostatic intraepithelial neoplasia and contamination of seminal vesicle epithelium. Gleason grading, which is essential for the clinician, is based on the histological architecture of glands and cannot be applied on cytology. Core biopsies, unlike FNA, provide information about tumour extent and occasionally about extra-prostatic extension and seminal vesicle invasion. Before treatment of localized prostate cancer, the diagnosis should, therefore, be confirmed by core biopsies. Macroscopy On section, grossly evident cancers are firm, solid, and range in colour from white-grey to yellow-orange, the latter having increased cytoplasmic lipid; the tumours contrast with the adjacent benign parenchyma, which is typically tan and spongy {289,1001,1685,2905}. Fig. 3.11 A Transition zone cancer with yellow nodule in the anterior right area. B Transition zone cancer, microscopical extent of tumour. Tumours usually extend microscopically beyond their macroscopic border. Gross haemorrhage and necrosis are rare. Subtle tumours may be grossly recognized by structural asymmetry; for example, peripheral zone tumours may deform the periurethral fibromuscular concentric band demarcating the periurethral and peripheral prostate centrally, and peripherally may expand or obscure the outer boundaries of the prostate. Anterior and apical tumours are difficult to grossly identify because of admixed stromal and nodular hyperplasia {289,290,701, 1001,2905}. In general, grossly recognizable tumours tend to be larger, of higher grade and stage, and are frequently palpable, compared with grossly inapparent tumours (usually < 5 mm), which are often nonpalpable, small, low grade and low stage {2168}. Some large tumours are diffusely infiltrative, and may not be evident grossly {701,1001}. Causes of gross false positive diagnoses include confluent glandular atrophy, healed infarcts, stromal hyperplasia, granulomatous prostatitis and infection {1001}. In countries with widespread PSA testing, grossly evident prostate cancer has become relatively uncommon. Tumour spread and staging Local extraprostatic extension typically occurs along the anterior aspect of the gland for transition zone carcinomas, and in posterolateral sites for the more common peripheral zone carcinomas {1684}. The peripheral zone carcinomas often grow into periprostatic soft tissue by invading along nerves {2735} or by direct penetration out of the prostate. The term "capsule" has been used to denote the outer boundary of the prostate. However, as there is no well-defined capsule surrounding the entire prostate this term is no longer recommended. Extraprostatic invasion superiorly into the bladder neck can occur with larger tumours, and in advanced cases, this can lead to bladder neck and ureteral obstruction. Extension into the seminal vesicles can occur by several pathways, including direct extension from carcinoma in adjacent soft tissue, spread along the ejaculatory duct complex, and via lymphvascular space channels {1944}. Posteriorly, Denovillier’s fascia constitutes an effective physical barrier {2734}, and direct prostatic carcinoma spread into the rectum is a rare event. Metastatic spread of prostatic carcinoma begins when carcinoma invades into lymphvascular spaces. The most common sites of metastatic spread of prostatic carcinoma are the regional lymph nodes and bones of the pelvis and axial skeleton. The obturator and hypogastric nodes are usually the first ones to be involved, followed by external iliac, common iliac, presacral, and presciatic nodes. In a few patients, periprostatic/ periseminal vesicle lymph nodes may be the first ones to harbour metastatic carcinoma, but these nodes are found in less than 5% of radical prostatectomy specimens {1364}. Metastasis to bone marrow, with an osteoblastic response, is a hallmark of disseminated prostate cancer {835}. The bones most frequently infiltrated by metastatic disease are, in descending order, pelvic bones, dorsal and lumbar spine, ribs, cervical spine, femur, skull, sacrum, and humerus. Visceral metastatic deposits in the lung and liver are not often clinically apparent, but are common in end-stage disease. The TNM classification scheme {944, 2662} is the currently preferred system for clinical and pathologic staging of prostatic carcinoma. Histopathology Adenocarcinomas of the prostate range from well-differentiated gland forming cancers, where it is often difficult to dis- Acinar adenocarcinoma 169
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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
Page 113 and 114: muscle invasive disease, but there
Page 115 and 116: 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: PSA-related diagnostic strategies.
Page 167 and 168: pale-clear, similar to benign gland
Page 169 and 170: A B Fig. 3.20 A, B Adenocarcinoma w
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
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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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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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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
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J Juvenile type granulosa cell tumo
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Promoter methylation, 21 Prostate s
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