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

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PSA positive. Associated acinar adenocarcinoma has been noted {34,2145}. In situ hybridization has been negative for <strong>Epstein</strong>-Barr virus {34}. Clinical significance is uncertain. Sarcomatoid variant (carcinosarcoma) There is considerable controversy in the literature regarding nomenclature and histogenesis of these tumours. In some series, carcinosarcoma and sarcomatoid carcinoma are considered as separate entities based on the presence of specific mesenchymal elements in the former. However, given their otherwise similar clinico-pathologic features and identically poor prognosis, these two lesions are best considered as one entity. Sarcomatoid carcinoma of the prostate is a rare neoplasm composed of both malignant epithelial and malignant spindle-cell and/or mesenchymal elements {207,588,644,1555,2175,2376}. Sarcomatoid carcinoma may be present in the initial pathologic material (synchronous presentation) or there may be a previous history of adenocarcinoma treated by radiation and/or hormonal therapy {1578}. The gross appearance often resembles sarcomas. Microscopically, sarcomatoid carcinoma is composed of a glandular component showing variable Gleason score {644,2093}. The sarcomatoid component often consists of a nonspecific malignant spindle-cell proliferation. Amongst the specific mesenchymal elements are osteosarcoma, chondrosarcoma, rhabdomyosarcoma, leiomyosarcoma, liposarcoma, angiosarcoma or multiple types of heterologous differentiation {644,1578}. Sarcomatoid carcinoma should be distinguished from the rare carcinoma with metaplastic, benignappearing bone or cartilage in the stroma. By immunohistochemistry, epithelial elements react with antibodies against PSA and/or pan-cytokeratins, whereas spindle-cell elements react with markers of soft tissue tumours and variably express cytokeratins. Serum PSA is within normal limits in most cases. Nodal and distant organ metastases at diagnosis are common {644,1578,2093}. There is less than a 40% five-year survival {644}. Treatment effects Radiation therapy Radiation therapy can be given as either external beam or interstitial seed implants or as a combination of the two. After radiation therapy the prostate gland is usually small and hard. Radiation therapy affects prostate cancer variably with some glands showing marked radiation effect and others showing no evidence of radiation damage. Architecturally, carcinoma showing treatment effect typically loses their glandular pattern, resulting in clustered cells or individual cells. Cytologically, the cytoplasm of the tumour cells is pale, increased in volume and often vacuolated. There is often a greater variation of nuclear size than in non-irradiated prostate cancer and the nuclei may be pyknotic or large with clumped chromatin. Nucleoli are often lost {607,842,1060,1061,1065,1086, 1584}. Paradoxically the nuclear atypia in prostate carcinoma showing radiation effect is less than that seen in radiation atypia of benign glands. By immunohistochemistry, tumour cells with treatment effect are usually positive for PAP and PSA. These antibodies along with pancytokeratins are very helpful to detect isolated residual tumour cells, which can be overlooked in H&E stained sections. The stroma is often sclerosed, particularly following radioactive seed implantation. In the latter the stromal hyalinization is often sharply delineated. Following radiation therapy, prostatic biopsy should be diagnosed as no evidence of cancer, cancer showing no or minimal radiation effect, or cancer showing significant radiation effect, or a combination of the above. Although there exists various systems to grade radiation effects, these are not recommended for routine clinical practice. Biopsy findings predict prognosis with positive biopsies showing no treatment effect having a worse outcome than negative biopsies, and cancer with treatment effect having an intermediate prognosis {511}. Hormone therapy The histology of prostate cancer may be significantly altered following its treatment with hormonal therapy {2358}. One pattern is that neoplastic glands develop pyknotic nuclei and abundant xanthomatous cytoplasm. These cells then desquamate into the lumen of the malignant glands where they resemble histiocytes and lymphocytes, sometimes resulting in empty clefts. In some areas, there may be only scattered cells within the stroma resembling foamy histiocytes with pyknotic nuclei and xanthomatous cytoplasm. A related pattern is the presence of individual tumour cells resembling inflammatory cells. At low power, these areas may be difficult to identify, and often the only clue to areas of hormonally treated carcinoma is a fibrotic background with scattered larger cells. A B Fig. 3.31 A Sarcomatoid carcinoma with adenosquamous carcinoma. B Sarcomatoid carcinoma with osteoid formation. 178 Tumours of the prostate
A B Fig. 3.32 A Sarcomatoid carcinoma. Note both epithelial (upper centre) and mesenchymal differentiation. B High-magnification view of spindle cell component of sarcomatoid carcinoma of prostate. A B Fig. 3.33 A Cancer with radiation effect. The degenerating tumour cells are ballooned. Note pleomorphic hyperchromatic nuclei. B Adenocarcinoma with cancer showing radiation effect adjacent to cancer without evidence of radiation effect. Immunohistochemistry for PSA or pancytokeratin can aid in the diagnosis of carcinoma in these cases by identifying the individual cells as epithelial cells of prostatic origin. Cancer cells following hormonal therapy demonstrate a lack of high molecular weight cytokeratin staining, identical to untreated prostate cancer. Following a response to combination endocrine therapy, the grade of the tumour appears artefactually higher, when compared to the grade of the pretreated tumour. As with radiation, the response to hormonal therapy may be variable, with areas of the cancer appearing unaffected {117,340,470, 1059,1852,2176,2447,2681}. Gleason grading system Numerous grading systems have been designed for histopathological grading of prostate cancer. The main controversies have been whether grading should be based on glandular differentiation alone or a combination of glandular differentiation and nuclear atypia, and also whether prostate cancer should be graded according to its least differentiated or dominant pattern. The Gleason grading system named after Donald F. Gleason is now the predominant grading system, and in 1993, it was recommended by a WHO consensus conference {1840}. The Gleason grading system is based on glandular architecture; nuclear atypia is not evaluated {894,895}. Nuclear atypia as adopted in some grading systems, correlates with prognosis of prostate cancer but there is no convincing evidence that it adds independent prognostic information to that obtained by grading glandular differentiation alone {1801}. The Gleason grading system defines five histological patterns or grades with decreasing differentiation. Normal prostate epithelial cells are arranged around a lumen. In patterns 1 to 3, there is retained epithelial polarity with luminal differentiation in virtually all glands. In pattern 4, there is partial loss of normal polarity and in pattern 5, there is an almost total loss of polarity with only occasional luminal differentiation. Prostate cancer has a pronounced morphological heterogeneity and usually more than one histological pattern is present. The primary and secondary pattern, i.e. the most prevalent and the second most prevalent pattern are added to obtain a Gleason score or sum. It is recommended that the primary and secondary pattern as well as the score be reported, e.g. Gleason score 3+4=7. If the tumour only has one pattern, Gleason score is obtained by doubling that pattern, e.g. Gleason score 3+3=6. Gleason scores 2 and 3 are only exceptionally Acinar adenocarcinoma 179
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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
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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
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 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: A Fig. 3.27 A, B Foamy gland adenoc
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
Page 219 and 220: Similar tumours as those of group 1
Page 221 and 222: crucial for the development of this
Page 223 and 224: 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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CCNB, 226 CCND1, 105, 108 CCND2, 22
Page 351 and 352:
J Juvenile type granulosa cell tumo
Page 353 and 354:
Promoter methylation, 21 Prostate s
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Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

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