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

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and prostatectomy Gleason score {375,668,2498}. Exact correlation has been observed in 28.2-67.9% of the cases. The biopsies undergraded in 24.5- 60.0% and overgraded in 5.2-32.2%. Causes for biopsy grading discrepencies are undersampling of higher or lower grades, tumours borderline between two grade patterns, and misinterpretation of patterns {2498}. The concordance between biopsy and prostatectomy Gleason score is within one Gleason score in more than 90% of cases {668}. Reproducibility Pathologists tend to undergrade {665,2498}. The vast majority of tumours graded as Gleason score 2 to 4 on core biopsy are graded as Gleason score 5 to 6 or higher when reviewed by experts in urological pathology {2498}. In a recent study of interobserver reproducibility amongst general pathologists, the overall agreement for Gleason score groups 2-4, 5-6, 7, and 8-10 was just into the moderate range {67}. Undergrading is decreased with teaching efforts and a substantial interobserver reproducibility can be obtained {665,1400}. Prognosis Multiple studies have confirmed that Gleason score is a very powerful prognostic factor on all prostatic samples. This includes the prediction of the natural history of prostate cancer {54,667} and the assessment of the risk of recurrence after total prostatectomy {713,1144} or radiotherapy {937}. Several schedules for grouping of Gleason scores in prognostic categories have been proposed. Gleason scores 2 to 4 behave similarly and may be grouped. Likewise, Gleason scores 8 to 10 are usually grouped together, although they could be stratified with regard to disease progression in a large prostatectomy study {1446}. There is evidence that Gleason score 7 is a distinct entity with prognosis intermediate between that of Gleason scores 5-6 and 8 to 10, respectively {667,2590}. Although the presence and amount of high grade cancer (patterns 4 to 5) correlates with tumour prognosis, reporting the percentage pattern 4/5 is not routine clinical practice {666,2479}. Gleason score 7 cancers with a primary pattern 4 have worse prognosis than those with a primary pattern 3 {406,1447,2282}. Genetics In developed countries, prostate cancer is the most commonly diagnosed nonskin malignancy in males. It is estimated that 1 in 9 males will be diagnosed with prostate cancer during their lifetime. Multiple factors contribute to the high incidence and prevalence of prostate cancer. Risk factors include age, family history, and race. Environmental exposures are clearly involved as well. Although the exact exposures that increase prostate cancer risk are unclear, diet (especially those high in animal fat such as red meat, as well as, those with low levels of antioxidants such as selenium and vitamin E) job/industrial chemicals, sexually transmitted infections, and chronic prostatitis have been implicated to varying degrees. The marked increase in incidence in prostate cancer that occurred in the mid 1980s, which subsequently leveled off in the mid to late 1990s, indicates that wide spread awareness and serum prostate specific antigen screening can produce a transient marked increase in prostate cancer incidence. Hereditary prostate cancer Currently the evidence for a strong genetic component is compelling. Observations made in the 1950s by Morganti and colleagues suggested a strong familial predisposition for prostate cancer {1784}. Strengthening the genetic evidence is a high frequency for prostate cancer in monozygotic as compared to dizygotic twins in a study of twins from Sweden, Denmark, and Finland {1496}. Work over the past decade using genome wide scans in prostate cancer families has identified high risk alleles, displaying either an autosomal dominant or X-linked mode of inheritance for a hereditary prostate cancer gene, from at least 7 candidate genetic loci. Of these loci, three candidate genes have been identified HPC2/ELAC2 on 17p {2584}, RNASEL on 1q25 {377}, and MSR1 on 8p22-23 {2857}. These 3 genes do not account for the majority of hereditary prostate cancer cases. In addition, more than 10 other loci have been implicated by at least some groups. The discovery of highly penetrant prostate cancer genes has been particularly difficult for at least 2 main reasons. First, due to the advanced age of onset (median 60 years), identification of more than two generations to perform molecular studies on is difficult. Second, given the high frequency of prostate cancer, it is likely that cases considered to be hereditary during segregation studies actually repre- A Fig. 3.46 A Gleason score 3+4=7. B Gleason score 3+4=7. B 184 Tumours of the prostate
Fig. 3.48 Heat map-nature. From S.M. Dhanasekaran et al. {604}. Fig. 3.47 Meta-analysis heat map. From D.R. Rhodes et al. {2183a}. Fig. 3.49 Gleason score 7 tumours comprise a large percentage of prostate cancer in the radical prostatectomy specimens, and constitute an intermediate category in terms of prognosis between Gleason scores of 6 and those of 8. Within the score 7 tumours, the proportion of Gleason pattern 4 carcinoma is important, i.e. (4+3) are more aggressive than (3+4) tumours. sent phenocopies; currently it is not possible to distinguish sporadic (phenocopies) from hereditary cases in families with high rates of prostate cancer. In addition, hereditary prostate cancer does not occur in any of the known cancer syndromes and does not have any clinical (other than a somewhat early age of onset at times) or pathologic characteristics to allow researchers to distinguish it from sporadic cases {302}. Perhaps even more important in terms of inherited susceptibility for prostate cancer are common polymorphisms in a number of low penetrance alleles of other genes - the so-called genetic modifier alleles. The list of these variants is long, but the major pathways currently under examination include those involved in androgen action, DNA repair, carcinogen metabolism, and inflammation pathways {2246,2858}. It is widely assumed that the specific combinations of these variants, in the proper environmental setting, can profoundly affect the risk of developing prostate cancer. Molecular alterations in sporadic prostate cancer While mutations in any of the classic oncogenes and tumour suppressor genes are not found in high frequency in primary prostate cancers, a large number of studies have identified non-random somatic genome alterations. Using comparative genomic hybridization (CGH) to screen the DNA of prostate cancer, the most common chromosomal alterations in prostate cancer are losses at 1p, 6q, 8p, 10q, 13q, 16q, and 18q and gains at 1q, 2p, 7, 8q, 18q, and Xq {436,1246,1924,2737}. Numerous genes have now been implicated in prostate cancer progression. Several genes have been implicated in the earliest development of prostate cancer. The pi-class of Glutathione S-transferase (GST), which plays a caretaker role by normally preventing stress related damage, demonstrates hypermethylation in high percentage of prostate cancers, thus preventing expression of this protective gene {1465, 1505,1732}. NKX3.1, a homeobox gene located at 8p21 has also been implicated in prostate cancer {304,1047,1319, 2741}. Although no mutations have been identified in this gene {2741}, recent work suggests that decreased expression is associated with prostate caner progression {304}. PTEN encodes a phosphatase, active against both proteins and lipids, is also commonly altered in prostate cancer progression {1491, 2489}. PTEN is believed to regulate the phosphatidylinositol 3’-kinase/protein kinase B (PI3/Akt) signaling pathway and therefore mutations or alterations lead to tumour progression {2850}. Mutations are less common than initially thought in prostate cancer, however, tumour suppressor activity may occur from the loss of one allele, leading to decreased expres- Acinar adenocarcinoma 185
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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
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 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: A B Fig. 3.43 A Prostate cancer Gle
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
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
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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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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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