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

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Table 3.01 Prostate cancer susceptibility loci identified by linkage analysis Susceptibility loci Locus Mode Putative gene Reference HPC1 1q24-25 AD RNASEL {377,2451} PCAP 1q42.2-43 AD ? {230} CAPB 1p36 AD ? {871} HPCX Xq27-28 X-linked/AR ? {2855} HPC20 20q13 AD ? {229} HPC2 17p AD HPC2/ELAC2 {2584} 8p22-23 AD MSR1 {2857} ________ Key: Mode=suggested mode of inheritance; AD=autosomal dominant; AR=autosomal recessive. Fig. 3.50 Paradigm for gene discovery. sion of PTEN (i.e. haploinsufficiency) {1418}. A number of other genes have also been associated with prostate cancer including p27 {496, 975,2867} and E-cadherin {1989,2674}. p53 mutations are late events in prostate cancer and tend to occur in advanced and metastatic prostate tumours {1052}. Another very common somatic genomic alteration in prostate and other cancers is telomere shortening {1697,2461}. This molecular alteration is gaining heightened awareness as it has become clear that critically short telomere may lead to genetic instability and increased epithelial cancers in p53+/- mice {121,250}. Recent advances in genomic and proteomic technologies suggest that molecular signatures of disease can be used for diagnosis {33,907}, to predict survival {2238,2551}, and to define novel molecular subtypes of disease {2056}. Several studies have used cDNA microarrays to characterize the gene expression profiles of prostate cancer in comparison with benign prostate disease and normal prostate tissue {604, 1574,1576,1591, 2426,2807}. Several interesting candidates include AMACR, hepsin, KLF6 and EZH2. Alpha-methylacyl-CoA racemase (AMACR), an enzyme that plays an important role in bile acid biosynthesis and β- oxidation of branched-chain fatty acids {748,1366} was determined to be upregulated in prostate cancer {604,1220, 1574,1575,2259,2807}. AMACR protein expression was also determined to be upregulated in prostate cancer {604,1220, 1575,2259}. Hepsin is overexpressed in localized and metastatic prostate cancer when compared to benign prostate or benign prostatic hyperplasia {604,1574, 1591,2481}. By immunohistochemistry, hepsin was found to be highly expressed in prostatic intraepithelial neoplasia (PIN), suggesting that dysregulation of hepsin is an early event in the development of prostate cancer {604}. Kruppel-like factor 6 (KLF6) is a zinc finger is mutated in a subset of human prostate cancer {1870}. EZH2, a member of the polycomb gene family, is a transcriptional repressor known to be active early in embryogenesis {796, 1601}, showing decreased expression as cells differentiate. It has been demonstrated that EZH2 is highly over expressed in metastatic hormone refractory prostate cancer as determined by cDNA and TMA analysis {2711}. EZH2 was also seen to be overexpressed in localized prostate cancers that have a higher risk of developing biochemical recurrence following radical prostatectomy. The androgen receptor (AR) plays critical role in prostate development {2877}. It has been know for many years that withdrawal of androgens leads to a rapid decline in prostate cancer growth with significant clinical response. This response is short-lived and tumour cells reemerge, which are independent of androgen stimulation (androgen independent). Numerous mutations have been identified in the androgen receptor gene (reviewed by Gelmann {847}). It has been hypothesized that through mutation, prostate cancers can grow with significantly lower circulating levels of androgens. In addition to common mutations, the amino-terminal domain encoded by exon one demonstrates a high percentage of polymorphic CAG repeats {2638}. Shorter CAG repeat lengths have been associated with a greater risk of developing prostate cancer and prostate cancer progression {884, 2337}. Shorter CAG repeat lengths have been identified in African American men {208}. Prognosis and predictive factors The College of American Pathologists (CAP) have classified prognostic factors into three categories: Category I – Factors proven to be of prognostic importance and useful in clinical patient management. 186 Tumours of the prostate
Fig. 3.51 Prostate cancer. Major susceptibility locus for prostate cancer on chromosome 1 suggested by a genome-wide search. 91 families from Sweden and NA (10cM). Reprinted with permission from J.R. Smith et al. {2451}. Copyright 1996 American Association for the Advancement of Science. Category II – Factors that have been extensively studied biologically and clinically, but whose importance remains to be validated in statistically robust studies. Category III – All other factors not sufficiently studied to demonstrate their prognostic value. Factors included in category I, were preoperative PSA, histologic grade (Gleason score), TNM stage grouping, and surgical margin status. Category II included tumour volume, histologic type and DNA ploidy. Factors in Category III included such things as perineural invasion, neuroendorcrine differentiation, Table 3.02 Selected genes associated with prostate cancer progression. Abbreviation Gene Name(s) Locus Functional Role Molecular Alteration GST-pi Glutathione S-transferase pi 11q13 Caretaker gene Hypermethlyation NKX3.1 NK3 transcription factor homolog A 8p21 Homeobox gene No mutations PTEN Phosphatase and tensin homolog 10q23.3 Mutations and haplotype (mutated in multiple advanced insufficiency cancers 1) Tumour supressor gene insufficiency AMACR Alpha-methylacyl-CoA racemase 5p13.2-q11.1 B-oxidation of branched- Overexpressed in chain fatty acids PIN/Pca Hepsin Hepsin 19q11-q13.2 Transmembrane protease, Overexpressed in serine 1 PIN/Pca KLF-6 Kruppel-like factor 6/COPEB Zinc finger transcription Mutations and haplotype 10p15 factor insufficiency EZH2 Enhancer of zeste homolog 2 7q35 Transcriptional memory Overexpressed in aggressive Pca p27 Cyclin-dependent kinase inhibitor 1B 12p13 Cyclin dependent kinases Down regulated with Pca (p27, Kip1) 2 and 4 inhibitor progression E-cadherin E-cadherin 16q22.1 Cell adhesion molecule Down regulated with Pca progression ________ Key: Pca=prostate cancer; PIN=prostatic intraepithelial neoplasia Acinar adenocarcinoma 187
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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
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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
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 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: Fig. 3.48 Heat map-nature. From S.M
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
Page 225 and 226: A B Fig. 4.14 Intratubular germ cel
Page 227 and 228: A B Fig. 4.19 Seminoma. A Typical s
Page 229 and 230: Fig. 4.24 Seminoma. Vascular invasi
Page 231 and 232: 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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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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