Journal of the Italian Society of Anatomic Pathology and Diagnostic Cytopathology, Italian Division of the International Academy of Pathology

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1 ISSN Cited in Index Medicus/MEDLINE, BIOSIS Previews, SCOPUS Journal of the Italian Society of Anatomic Pathology and Diagnostic Cytopathology, Italian Division of the International Academy of Pathology ORIGINAL ARTICLE 93 Frequency of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype: a population-based study from Trentino, North East Italy S. Giuliani, E. Leonardi, D. Aldovini, D. Bernardi, M. Pellegrini, F. Soli, A. Ferro, P. Dalla Palma, N. Decarli, M. Barbareschi Vol. 104 June 2012 Periodico bimestrale POSTE ITALIANE SPA - Spedizione in Abbonamento Postale - D.L. 353/2003 conv. in L. 27/02/2004 n 46 art. 1, comma 1, DCB PISA Aut. Trib. di Genova n. 75 del 22/06/1949 CASE REPORTS 98 Oncocytic papillary renal cell carcinoma: potential pitfall in small enucleation E. Munari, A. Eccher, D. Segala, A. Iannucci, S. Gobbo, M. Chilosi, M. Brunelli, G. Martignoni 101 Clear cell papillary renal cell carcinoma with characteristic morphology and immunohistochemical staining pattern S.M. Gilani, R. Tashjian, H. Qu 105 Idiopathic granulomatous mastitis mimicking breast cancer: report of two cases F. Limaiem, S. Korbi, T. Tlili, I. Haddad, A. Lahmar, S. Bouraoui, F. Gara, S. Mzabi ATTI DI CONGRESSO 109 I Congresso Nazionale di Citopatologia SIAPEC-IAP Trieste, giugno 2012 Società Italiana di Anatomia Patologica e Citopatologia Diagnostica, Divisione Italiana della International Academy of Pathology

2 Ogni anno il carcinoma polmonare colpisce 1.3 milioni di persone e causa 1.18 milioni di decessi. Il tumore polmonare non a piccole cellule (NSCLC) è la forma più diffusa di questo carcinoma. La ricerca è giunta oggi a significativi progressi: specifiche alterazioni molecolari, come le mutazioni del gene EGFR, permettono di individuare i pazienti che risponderanno al trattamento personalizzato con i nuovi farmaci a bersaglio molecolare. La determinazione dello stato mutazionale di EGFR rappresenta un passaggio indispensabile per la completa diagnosi. La rapidità di esecuzione del test è il fattore determinante per l accesso dei pazienti alla migliore terapia disponibile. EGFR La chiave d accesso alla terapia personalizzata del NSCLC In Italia è attivo, grazie al supporto di AstraZeneca, il network EGFR FASTnet che consente a tutti gli ospedali di richiedere la determinazione dello stato mutazionale dell EGFR a selezionati laboratori di Biologia Molecolare EGFR FASTnet

3 Materiale destinato esclusivamente ai Professionisti Sanitari BenchMark Special Stains Colorazioni speciali in totale automazione Reagenti sempre freschi e pronti all uso Nessuna cross-contaminazione Funzione di sparaffinatura automatica Ampia gamma di colorazioni Roche Diagnostics SpA Roche Tissue Diagnostics Viale G.B. Stucchi, Monza (MB)

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5 Cited in Index Medicus/MEDLINE, BIOSIS Previews, SCOPUS Journal of the italian Society of anatomic Pathology and Diagnostic cytopathology, italian Division of the international academy of Pathology Editor-in-Chief Marco Chilosi, Verona Associate Editor Roberto Fiocca, Genova Managing Editor Roberto Bandelloni, Genova Scientific Board R. Alaggio, Padova G. Angeli, Vercelli M. Barbareschi, Trento C.A. Beltrami, Udine G. Bevilacqua, Pisa M. Bisceglia, S. Giovanni R. A. Bondi, Bologna F. Bonetti, Verona C. Bordi, Parma A.M. Buccoliero, Firenze G.P. Bulfamante, Milano G. Bussolati, Torino A. Cavazza, Reggio Emilia G. Cenacchi, Bologna P. Ceppa, Genova C. Clemente, Milano M. Colecchia, Milano G. Collina, Bologna P. Cossu-Rocca, Sassari P. Dalla Palma, Trento G. De Rosa, Napoli A.P. Dei Tos, Treviso L. Di Bonito, Trieste C. Doglioni, Milano V. Eusebi, Bologna G. Faa, Cagliari F. Facchetti, Brescia G. Fadda, Roma G. Fornaciari, Pisa M.P. Foschini, Bologna F. Fraggetta, Catania E. Fulcheri, Genova P. Gallo, Roma F. Giangaspero, Roma W.F. Grigioni, Bologna G. Inghirami, Torino L. Leoncini, Siena M. Lestani, Arzignano G. Magro, Catania A. Maiorana, Modena E. Maiorano, Bari T. Marafi oti, Londra A. Marchetti, Chieti D. Massi, Firenze M. Melato, Trieste F. Menestrina, Verona G. Monga, Novara R. Montironi, Ancona B. Murer, Mestre V. Ninfo, Padova M. Papotti, Torino M. Paulli, Pavia G. Pelosi, Milano G. Pettinato, Napoli S. Pileri, Bologna R. Pisa, Roma M.R. Raspollini, Firenze L. Resta, Bari G. Rindi, Parma M. Risio, Torino A. Rizzo, Palermo J. Rosai, Milano G. Rossi, Modena L. Ruco, Roma M. Rugge, Padova M. Santucci, Firenze A. Scarpa, Verona A. Sidoni, Perugia G. Stanta, Trieste G. Tallini, Bologna G. Thiene, Padova P. Tosi, Siena M. Truini, Genova V. Villanacci, Brescia G. Zamboni, Verona G.F. Zannoni, Roma Editorial Secretariat G. Martignoni, Verona M. Brunelli, Verona Governing Board SIAPEC-IAP President: C. Clemente, Milano Vice President: G. De Rosa, Napoli General Secretary: A. Sapino, Torino Past President: G.L. Taddei, Firenze Members: A. Bondi, Bologna P. Dalla Palma, Trento A. Fassina, Padova R. Fiocca, Genova D. Ientile, Palermo L. Resta, Bari L. Ruco, Roma M. Santucci, Firenze G. Zamboni, Verona Associate Members Representative: T. Zanin, Genova Copyright Società Italiana di Anatomia Patologica e Citopatologia Diagnostica, Divisione Italiana della International Academy of Pathology Publisher Pacini Editore S.p.A. Via Gherardesca, Pisa, Italy Tel Fax Vol. 104 June 2012 Società italiana di anatomia Patologica e citopatologia Diagnostica, Divisione italiana della international academy of Pathology

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8 CONTENTS Original article Frequency of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype: a population-based study from Trentino, North East Italy S. Giuliani, E. Leonardi, D. Aldovini, D. Bernardi, M. Pellegrini, F. Soli, A. Ferro, P. Dalla Palma, N. Decarli, M. Barbareschi Objective. Triple negative breast carcinomas (TNT) are infiltrating breast carcinomas (BC) with negative oestrogen receptor (ER), progesterone receptor (PgR) and human epidermal growth factor receptor 2 (HER-2) expression, and are associated with frequent BRCA1/ BRCA2 mutations. The aim of the present study is to analyze the frequency and distribution of TNT in our population where a breast cancer screening program for women aged between 50 and 69 years is effective since 2001 with 85% accrual. Methods. We investigated the records of 2112 consecutive BC and 153 interval BC (i.e. BC detected in the screened negative women in the interval between screening rounds). Tumours with complete negative expression of ER, PgR and Her2 were considered TNT; tumours with negative ER and PgR status and faint Her2 expression (score 1) were considered as possible TNT (ptnt). Results. We identified 82 (3.8%) TNT and 20 (0.9%) ptnt in the series of 2112 consecutive BC and 7 TNT and 1 ptnt (5.2%) in the series of 153 interval BC. In the consecutive series, TNT/pTNT were observed in 6.5% patients below 50 years and in 4.3% of patients above 50 years. A high proliferation rate (Ki-67 labelling > 36%) was observed in 87.8% of TNT (median labelling 56.3%) and in 60% of ptnt (median labelling 48.4%). Conclusions. Since TNT/pTNT occurring in women < 50 years is a criterion for selecting patients whom genetic counselling and BRCA1 testing should be offered, our study is of help in foreseeing the workload of the Unit of Medical Genetics and the Laboratory of Molecular Pathology. Case reports Oncocytic papillary renal cell carcinoma: potential pitfall in small enucleation E. Munari, A. Eccher, D. Segala, A. Iannucci, S. Gobbo, M. Chilosi, M. Brunelli, G. Martignoni Objective. We describe an emerging entity, recently recognized as a pitfall in the diagnostic practice among eosinophilic renal cell tumours. Methods. A 60-year-old male underwent enucleation of a 1.2 cm nodule. Immunohistochemistry and FISH analysis were performed. Results. Histology revealed a neoplasm composed of large cells with eosinophilic cytoplasm, Fuhrman grade 3, arranged in papillae. At the immunohistochemical level, cells showed positivity for AMACR and CD10. Fluorescence in situ hybridization (FISH) demonstrated gains of chromosomes 7 and 17 and loss of Y. A diagnosis of oncocytic papillary renal cell carcinoma was made. Conclusions. The distinction between renal oncocytoma and oncocytic papillary renal cell carcinoma is of substantial importance because of their different behaviour and prognosis, since the latter has malignant potential. Although the available evidence supporting tumour enucleation as the surgical treatment for renal cortical tumours 4 cm, due to aforementioned clinicopathological features such tumours need to be evaluated using appropriate immunophenotypical and cytogenetic analyses. Clear cell papillary renal cell carcinoma with characteristic morphology and immunohistochemical staining pattern S.M. Gilani, R. Tashjian, H. Qu Clear cell papillary renal cell carcinoma is newly-defined entity initially believed to be associated with end stage renal disease. We report a rare case of this neoplasm in a 70-year-old female patient with no known history of end-stage renal disease who presented with haematuria lasting several days. After initial workup, a computed tomography (CT) scan was performed and revealed a cystic mass in the right kidney. Material obtained by fine needle aspiration (FNA) biopsy of the mass was felt to be suspicious for renal cell carcinoma. The patient subsequently underwent right nephrectomy, and the lesional tissue was examined microscopically. A 2.3 cm in greatest dimension cystic space circumscribed by a fibrous wall was surfaced by a single layer of bland cuboidal cells with abundant clear cytoplasm. The solid component of the tumour consisted of branching papillae with delicate fibrovascular cores and uniformly lined by cells similar to those of the inner wall of the cyst. Some of the fibrovascular cores were markedly expanded by a myxoid-appearing substance, but no foamy cells were appreciated. Immunohistochemically, the neoplastic cells were diffusely immunoreactive with cytokeratin 7 (CK7), epithelial membrane antigen (EMA), high molecular weight cytokeratin (HMWCK) and vimentin. Neoplastic cells were only focally immunoreactive with CD10, and were negative for both p63 and α-methylacyl-coa racemase (AMACR) (P504S). The cytomorphological features and immunohistochemical staining pattern of this tumour was consistent with that of clear cell papillary renal cell carcinoma (CCPRCC), as described by Gobbo et al. Idiopathic granulomatous mastitis mimicking breast cancer: report of two cases F. Limaiem, S. Korbi, T. Tlili, I. Haddad, A. Lahmar, S. Bouraoui, F. Gara, S. Mzabi Idiopathic granulomatous mastitis is a rare inflammatory breast disease of unknown aetiology that is frequently mistaken for breast carcinoma both clinically and mammographically. In this paper, the authors report two cases of idiopathic granulomatous mastitis that occurred in two parous women aged 38 and 45 years. Clinically, both patients presented with a tender palpable lump in the left breast. Mammography showed an poorly-defined mass in both patients with microcalcification in the first case and skin retraction in the second case. Breast lumpectomy was performed in both patients. Histological examination of the surgical specimen revealed non-caseating granulomas confined to breast lobules. Special staining for fungi and tuberculosis were all negative. Correct diagnosis of idiopathic granulomatous mastitis requires the exclusion of malignancy, other granulomatous disease and infectious aetiologies. Histopathologic examination remains the gold standard for diagnosis. This disease is rare, and therefore the optimum treatment protocol is still being established.

9 pathologica 2012;104:93-97 Original article Frequency of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triple-negative phenotype: a population-based study from Trentino, North East Italy S. Giuliani 1 2, E. Leonardi 1, D. Aldovini 1, D. Bernardi 3, M. Pellegrini 3, F. Soli 4, A. Ferro 5, P. Dalla Palma 1, N. Decarli 1, M. Barbareschi Unit of Surgical Pathology, S. Chiara Hospital, Trento, Italy; 2 Trentino Biobank, Unit of Surgical Pathology, S. Chiara Hospital, Trento, Italy; 3 Unit of Senology, Azienda provinciale Servizi Sanitari, Trento, Italy; 4 Unit of Medical Genetics, S. Chiara Hospital, Trento, Italy; 5 Unit of Medical Oncology, S. Chiara Hospital, Trento, Italy Key words Breast cancer Triple Negative BRCA1 BRCA2 Summary Objective. Triple negative breast carcinomas (TNT) are infiltrating breast carcinomas (BC) with negative oestrogen receptor (ER), progesterone receptor (PgR) and human epidermal growth factor receptor 2 (HER-2) expression, and are associated with frequent BRCA1/BRCA2 mutations. The aim of the present study is to analyze the frequency and distribution of TNT in our population where a breast cancer screening program for women aged between 50 and 69 years is effective since 2001 with 85% accrual. Methods. We investigated the records of 2112 consecutive BC and 153 interval BC (i.e. BC detected in the screened negative women in the interval between screening rounds). Tumours with complete negative expression of ER, PgR and Her2 were considered TNT; tumours with negative ER and PgR status and faint Her2 expression (score 1) were considered as possible TNT (ptnt). Results. We identified 82 (3.8%) TNT and 20 (0.9%) ptnt in the series of 2112 consecutive BC and 7 TNT and 1 ptnt (5.2%) in the series of 153 interval BC. In the consecutive series, TNT/ ptnt were observed in 6.5% patients below 50 years and in 4.3% of patients above 50 years. A high proliferation rate (Ki-67 labelling > 36%) was observed in 87.8% of TNT (median labelling 56.3%) and in 60% of ptnt (median labelling 48.4%). Conclusions. Since TNT/pTNT occurring in women < 50 years is a criterion for selecting patients whom genetic counselling and BRCA1 testing should be offered, our study is of help in foreseeing the workload of the Unit of Medical Genetics and the Laboratory of Molecular Pathology. Introduction Breast carcinomas (BC) with negative oestrogen receptor (ER), progesterone receptor (PgR) and human epidermal growth factor receptor 2 (HER-2/neu) expression are termed triple negative tumours (TNT), and partially correspond to basal-like carcinomas as detected by gene expression studies 1 2. TNT more frequently affect younger patients (< 50 years), and are associated with a high proliferation rate. TNT usually show high expression of p53, EGFR and high molecular weight cytokeratins 3. TNT are aggressive tumours with a unique pattern of early relapse within the first two years following diagnosis, with a peak within three years, followed by a rapid decline over the next five, and a very low risk of subsequent recurrence. Women with TNT do not benefit from hormonal or trastuzumab therapy, and are left with chemotherapy as their only option TNT arise more frequently in patients carrying germline BRCA1 and, to a lesser extent, BRCA2 gene mutations, and several studies have demonstrated that BRCA1-mutation carriers more likely are affected by TNT than non-carriers Due to this strict relationship, TNT can be considered as an index of sus- This work was supported by the Provincia Autonoma di Trento and the Fondazione Cassa di Risparmio di Trento e Rovereto. Correspondence Mattia Barbareschi, Unit of Surgical Pathology, Laboratory of Molecular Pathology, S. Chiara Hospital, largo Medaglie Oro 9, Trento, Italy - Tel Fax

10 94 S. Giuliani et al. Fig. 1. Immunohistochemistry in TNT showing complete negativity for ER (a), PR (b), and HER2 (c). 20x. Fig. 2. Immunohistochemistry in ptnt showing complete negativity for ER (a) and PR (b), and faint positivity for HER2 (score 1) (c). 20x. picious BRCA1 mutational status TNT occurring in patients younger than 50 years or with familiarity for breast cancer is one of the criteria to select patients whom genetic counselling and BRCA1 testing should be offered Given the relevant workload of genetic counselling and testing, it is important to know the incidence of TNT for appropriate organizational and Tab. I. Hormone receptor and Her2 status in 2112 infiltrating breast carcinomas. ER Negative Positive PR Negative Positive HER2 Her0 Her1 Her2 Her3 No. of patients % Abbreviations: ER, oestrogen receptor; PR, progesterone receptor; HER- 2, human epidermal growth factor 2; economical planning. The aim of the present study is to describe the frequency of TNT in a large series of consecutive unselected breast carcinomas in the general population in Trentino, Italy. Patients and methods The study population includes 2112 women affected by infiltrating BC observed at the Santa Chiara Hospital, Trento, Italy between 2005 and In our region, Trentino, North Italy, a breast cancer screening program for women aged between 50 and 69 years has been effective since 2001 with 85% accrual. Coded data on these markers were available in the database of the Unit of Surgical Pathology, and served as a basis for this study. We also investigated 153 interval BC detected between 2001 and 2009, which were defined as BC detected in screened negative women during the interval between screening rounds. All invasive BC specimens had been routinely evaluated for ER, PR, Ki-67 and HER-2/neu status using immunohistochemistry (IHC) at the time of diagnosis. Her2 immunoreactivity was evaluated using the HercepTest kit (DakoCytomation, Glostrup, Denmark) and scored according to the manufacturer s FDA-approved

11 Frequency of triple negative breast cancer 95 Tab. II. Age at diagnosis in all breast cancers (n=2112), in TNT (82) and ptnt (20). Age at diagnosis No. of patients TNT (%*) % of TNT within the age group Possible TNT (%**) % of Possible TNT within the age group < (1.2%) (9.8%) (5%) (22%) (5%) (19.5%) (25%) (20.7%) (40%) (19.5%) (10%) (7.3%) (15%) 1 * = percentage among all TNT ** = percentage among all possible TNT system. ER, PgR and Ki-67 were evaluated using 6F11 (Leica-Novocastra, Newcastle, UK.), Pgr636 (Dako) and MM1 (Leica-Novocastra) antibodies, respectively. ER and PgR were considered negative when no nuclear staining was seen in spite of positive appropriate internal and external controls 11. The Ki-67 labelling index was evaluated manually and with computer assisted image analysis in the most densely labelled areas, as previously described 12. Tumours with negative expression of all three markers were considered TNT (Fig. 1). Tumours with negative ER and PgR status but with faint Her2 expression (score 1) were considered as possible TNT (ptnt) (Fig. 2). Results Immunohistochemical data concerning ER, PgR and Her2 status of the entire series of 2112 cases of BC are shown in Tab. I. Among these cases, there were 82 (3.8%) TNT and 20 (0.9%) ptnt. Twenty-seven of 82 TNT (33%) were detected in women < 50 years at the time of diagnosis, corresponding to 6% of the 447 patients < 50 years old (detailed data on age distribution are shown in Tab. II and Fig. 3). Two of 20 (10%) ptnt were detected in women < 50 years old at the time of diagnosis, corresponding to 0.4% of the 447 patients < 50 years old (detailed data on age distribution are shown in Tab. II and Fig. 3). One patient affected by TNT was also affected by ovarian cancer. The age distribution of TNT and ptnt was slightly different, with TNT occurring at a younger age than ptnt: globally, their frequency was 6.5% for patients below 50 years and 4.3% for older patients (Fig. 4). The histopathological characteristics of the TNT and ptnt are shown in Tab. III. The most frequent histotype in both TNT and ptnt was infiltrating ductal carcinoma (86.6 % and 95%, respectively). A high proliferation rate (Ki-67 labelling >30% according to Goldhirsch et al 2009) 13 was observed in 87.8% of TNT with a median value of 56.3%, and in 60% of ptnt with a median value of 48.4%. Fig. 4. Distribution of TNT/pTNT among BC in patients under 50 and over 50 years in our series of 2112 infiltrating breast carcinomas. Fig. 3. Age at diagnosis in TNT and ptnt in our series of 2112 infiltrating breast carcinomas.

12 96 S. Giuliani et al. Tab. iii. Characteristics of TNT and ptnt in the consecutive series of 2112 patients. Variable Histotype Ductal Lobular Medullary Apocrine Squamous Metaplastic Tumour size 1a (< 5mm) 1b (6-10 mm) 1c (11 20 mm) 2 (> 20 mm < 50 mm) > 50 mm Unknown Grade Unknown MIB1/Ki67 Median value Low proliferation ( 20%) Medium proliferation (21-35%) High proliferation ( 36%) Unknown TNT (N=82) n % 71(86.6) 1 (1.2) 6 (7.3) 0 1 (1.2) 3 (3.7) 2 (2.4) 14 (17) 34 (41.5) 28 (34.2) 4 (4.9) (12.2) 66 (80.5) 6 (7.3) 56.3% 3 (3.7) 3 (3.7) 72 (87.8) 4 (4.8) Possible TNT (N=20), n % 19 (95) (5) 1 (5) 3 (15) 3(15) 8(40) 2 (10) 3 (15) - 3 (15) 15 (75) 2 (10) 48.4% 0 7 (35) 12 (60) 1 (5) Among 153 interval BC, we identified 7 TNT and 1 pt- NT, representing 5.2% of all interval BC. Five of these were detected in women between years of age and two in women between years old. Discussion The present study shows that in our region, in a population of Caucasian ethnicity and with an effective BC screening program for women between 50 and 69 years, TNT/pTNT represent a small subset (around 4.8%) of all BC. We show that TNT/pTNT occured in 6.5% of our patients below 50 years, in 4.3% of patients above 50 years, and in 5.2% of interval BC. At variance with our study, the average reported frequency of TNT in Caucasian populations is 10-17% (Tab. IV) This discrepancy could be related to several facts, including our strict criteria to define ER, PR and Her2 negativity, the impact of our screening program, and the genetic background of our population. The presence of a screening program, which is known to increase the detection of low grade, ER and PgR positive tumours, may indeed reduce the relative frequency of TNT. However, this does not seem to be the case as in our series the frequency of TNT/pTNT in young women not included in the screening program (i.e. younger than 50 years) is well below in the range of literature data for age-matched groups of patients The genetic background of our population may also be relevant since our population has been relatively stable in the past, and further studies could address this topic. Tab. IV. Frequencies of TNT in population-based studies. Authors Nation % TNT Sample size TNT definition criteria Rakha EA et al. (2007) UK ER-PR-HER2- Dent R et al. (2007) Canada ER-PR-HER2- Tischkowitz et al. (2007) Canada ER-PR-HER2- Bauer KR et al. (2007) Lund MJ et al. (2009 ) Morris GJ et al. ( 2007) Adamo et al. (2011 ) CA, USA GA, USA PA, USA Overall in non-hispanic white 24.6 in African-American 17.2 in Hispanic 11.7 Asian/Pacific Islander Overall in African-American 21.8 in Caucasian 20.8 in African-American 10.4 in Caucasian African American 360 Caucasian Italy Present study Italy ER < 5%, PR <5 %, HER2 score 0 or 1 ER-PR-HER ER-PR-HER2- ER-PgR 0-9% HER2 score 2 with no gene amplification ER- PR- HER score 0 ER- PR- HER2 score 1

13 Frequency of triple negative breast cancer 97 Interval BC are usually considered rapidly growing tumours with reduced ER expression 22 23, and it could be hypothesized that they should be more frequently of the basal cell type. However, the frequency of TNT in our series of interval BC is low, and does not differ significantly from the one observed in the entire group of our consecutive patients. Beside concerns about the reasons for the lower frequency of TNT observed in this series, our data are important to anticipate the workload of the Unit of Medical Genetics and the Laboratory of Molecular Pathology. In fact, TNT occurring in young women (< 50 years) or in women with familiar history of breast cancer represent a criterion for selecting patients to whom genetic counselling and BRCA1 testing should be offered Both genetic counselling and laboratory testing are time consuming, expensive and not always clear (e.g. because of variants, polymorphisms, etc.), and it is important to accurately plan their activity. This is even more important when psychological and emotional aspects of the genetic investigations are taken in account: once a patient has been told that she could be a BRCA1 mutation carrier, it is mandatory to provide the results of the genetic test within a reasonable time to avoid unnecessary anxiety for herself and her family. The role of TNT as an index of suspicious BRCA1 mutational status highlights the importance of proper communication between the Units of Pathology and Medical Genetics. Because of progressive reduction of the members of modern families, which among Western countries is especially evident in Italy, it will become progressively more difficult to identify probands to submit for genetic testing, based on criteria of familiarity. Therefore, the relevance of identifying TNT, not only for therapeutic purposes but also for genetic purposes, highlights the important role of pathologists in early detection and prevention of familial BC. References 1 Perou CM, Sørlie T, Eisen MB, et al. Molecular portraits of human breast tumours. Nature 2000;406: Irvin WJ Jr, Carey LA. What is triple-negative breast cancer? Eur J Cancer 2008;44: Reis-Filho JS, Tutt AN. Triple negative tumours: a critical review. Histopathology 2008;52: Dent R, Trudeau M, Pritchard KI, et al. Triple-negative breast cancer: clinical features and patterns of recurrence. Clin Cancer Res 2007;13: Minami CA, Chung DU, Chang HR. Management options in triple-negative breast cancer. Breast Cancer: Basic and Clinical Research 2011;5: Nanda R. Targeting triple-negative breast cancer: the lessons learned from BRCA1-associated breast cancers. Semin Oncol 2011;38: Gadzicki D, Schubert A, Fischer C, et al. Histophatological criteria and selection algorithms for BRCA1 genetic testing. Cancer Genetics and Cytogenetics 2009;189: Atchley DP, Albarracin CT, Lopez A, et al. Clinical and pathologic characteristics of patients with BRCA-positive and BRCAnegative breast cancer. J Clin Oncol 2008;26: Gonzalez-Angulo AM, Timms KM, Liu S, et al. Incidence and outcome of BRCA mutations in unselected patients with triple receptor-negative breast cancer. Clin Cancer Res 2011;17: Kwon JS, Gutierrez-Barrera AM, Young D, et al. Expanding the criteria for brca mutation testing in breast cancer survivors. J Clin Oncol 2010;28: Mauri FA, Veronese S, Frigo B, et al. Er1d5 and h222 (er-ica) antibodies to human estrogen receptor protein in breas carcinomas: a result of a multicentric comparative study. Appl Immunohistochem 1994;2: Fasanella S, Leonardi E, Cantaloni C, et al. Proliferative activity in human breast cancer: Ki-67 automated evaluation and the influence of different Ki-67 equivalent antibodies. Diagn Pathol 2011;6 Suppl 1:S7. 14 Goldhirsch A, Ingle JN, Gelber RD, et al. Thresholds for therapies: highlights of the St Gallen International Expert Consensus on the primary therapy of early breast cancer. Ann Oncol 2009;20: Rakha EA, El-Sayed ME, Green AR, et al. Prognostic markers in triple-negative breast cancer. Cancer 2007;109: Tischkowitz M, Brunet JS, Bégin LR, et al. Use of immunohistochemical markers can refine prognosis in triple negative breast cancer. BMC Cancer 2007;24: Bauer KR, Brown M, Cress RD, et al. Descriptive analysis of estrogen receptor (ER)-negative, progesterone receptor (PR)-negative, and HER2-negative invasive breast cancer, the so-called triplenegative phenotype: a population-based study from the California cancer Registry. Cancer 2007;109: Lund MJ, Trivers KF, Porter PL, et al. Race and triple negative threats to breast cancer survival: a population-based study in Atlanta, GA. Breast Cancer Res Treat 2009;113: Morris GJ, Naidu S, Topham AK, et al. Differences in breast carcinoma characteristics in newly diagnosed African-American and Caucasian patients: a single-institution compilation compared with the National Cancer Institute s Surveillance, Epidemiology, and End Results database. Cancer 2007;110: Adamo V, Ricciardi GRR, De Placido S, et al. Management and treatment of triple-negative breast cancer patients from the NEM- ESI study: an Italian experience. European Journal of Cancer Epub ahead of print. 21 Saunders KH, Nazareth S, Pressman PI. Case report: BRCA in the Ashkenazi population: are current testing guidelines too exclusive? Hered Cancer Clin Pract 2011;9:3. 22 Halbert CH, Kessler L, Troxel AB, et al. Effect of genetic counseling and testing for BRCA1 and BRCA2 mutations in African American women: a randomized trial. Public Health Genomics 2010;13: Van der Vegt B,Wesseling J, Pijnappel RM, et al. Aggressiveness of true interval invasive ductal carcinomas of the breast in postmenopausal women. Mod Pathol 2010;23: Raja Ma, Hubbard A, Salman AR. Interval breast cancer: is it a different type of breast cancer? Breast 2001;10: Foulkes WD, Stefansson IM, Chappuis PO, et al. Germline BRCA1 mutations and a basal epithelial phenotype in breast cancer. J Natl Cancer Inst 2003;95:

14 pathologica 2012;104: Case report Oncocytic papillary renal cell carcinoma: potential pitfall in small enucleation E. Munari, A. Eccher, D. Segala, A. Iannucci *, S. Gobbo, M. Chilosi, M. Brunelli, G. Martignoni Department of Pathology and Diagnostic, University of Verona, Italy; * Anatomic Pathology, Ospedale Maggiore, Azienda Ospedaliera Universitaria Integrata, Verona, Italy Key words Oncocytic papillary RCC Renal oncocytoma FISH Summary Objective. We describe an emerging entity, recently recognized as a pitfall in the diagnostic practice among eosinophilic renal cell tumours. Methods. A 60-year-old male underwent enucleation of a 1.2 cm nodule. Immunohistochemistry and FISH analysis were performed. Results. Histology revealed a neoplasm composed of large cells with eosinophilic cytoplasm, Fuhrman grade 3, arranged in papillae. At the immunohistochemical level, cells showed positivity for AMACR and CD10. Fluorescence in situ hybridization (FISH) demonstrated gains of chromosomes 7 and 17 and loss of Y. A diagnosis of oncocytic papillary renal cell carcinoma was made. Conclusions. The distinction between renal oncocytoma and oncocytic papillary renal cell carcinoma is of substantial importance because of their different behaviour and prognosis, since the latter has malignant potential. Although the available evidence supporting tumour enucleation as the surgical treatment for renal cortical tumours 4 cm, due to aforementioned clinicopathological features such tumours need to be evaluated using appropriate immunophenotypical and cytogenetic analyses. Introduction Papillary renal cell carcinoma (RCC) is a well-established subtype of RCC with characteristic macroscopic and histological features, comprising approximately 10-15% of RCCs 1. This tumour can be subdivided into two morphologic types with different prognostic implications: type 1, with small cells arranged in a single layer on delicate papillary cores, and type 2 with large eosinophilic cytoplasm and pseudostratified nuclei with higher Fuhrman grade arranged on broader papillae 2. Cytogenetically, papillary RCC is mostly characterized by trisomies of chromosomes 7 and 17 and deletion of chromosome Y as well as additional gains of chromosomes 12, 16, and The existence of additional variants of papillary RCC may be inferred by the recognition of a few cases with different morphological features, such as those composed entirely of oncocytes 4 ; typical signs of oncocytic papillary RCC in routine clinical practice has also been highlighted 5. In contrast, renal oncocytomas represent 3-7% of all renal tumours and are characterized by compact nests, acini, tubules or microcysts composed of round to polygonal cells, with a densely granular eosinophilic cytoplasm and regular nuclei with centrally placed nucleoli 6. The distinction between the aforementioned tumours is of significant importance since renal oncocytomas are benign neoplasms with an indolent course, whereas papillary RCCs are malignant tumours characterized by potential malignant behaviour 1. The morphologic features are usually sufficient to distinguish renal oncocytomas from papillary RCCs among most routine cases. In certain scenarios, such as small enucleation or renal biopsies from small renal masses, there are challenging neoplasms combining both an extensive papillary pattern together with true oncocytic cells 7. Herein we describe a case of a 60-year-old male who underwent enucleation after the incidental finding of a renal nodule 1.2 cm in maximum diameter localized to the left kidney and finally diagnosed as oncocytic papillary RCC. Correspondence Enrico Munari, Department of Pathology and Diagnostic, University of Verona, piazzale L.A. Scuro, Verona, Italy - Tel Fax enrico_

15 Pitfall in oncocytic papillary RCC 99 Case report A 60-year-old man was incidentally found to have a nodule 1.2 cm in diameter on the left kidney and underwent enucleation. On intraoperative consultation, the lesion appeared macroscopically solid and browncoloured, with a 4 mm adjacent wide rim of normal renal parenchyma. Histological examination of the tumour tissue with frozen-sections revealed that the neoplasm was mainly composed of large cells with dense eosinophilic cytoplasm, Fuhrman grade 3 nuclei, and arranged mainly in papillary structures with delicate fibrovascular stalks. Areas of oncocytic cells arranged in a solid pattern were also present. Foamy macrophages were also observed within the fibrovascular cores of the papillae. Necrosis was not present. A diagnosis of oncocytic renal cell neoplasm, not otherwise specified, was made (Fig. 1a). On definitive examination, the tumour was completely confined by a thick pseudo-capsule without infiltrating the renal parenchyma. Morphology revealed a neoplasm composed of both papillary and solid-papillary arranged neoplastic cells, with oncocytic features (Fig. 1b). The differential diagnosis was for papillary RCC or renal oncocytoma. At the immunohistochemical level, neoplastic cells showed strong and diffuse positivity for α-methylacyl- CoA racemase (AMACR) (Fig. 2a), together with positivity for CD10. Tumour cells showed dim immunostaining for CK7, and no labelling for parvalbumin. In situ hybridization (FISH) demonstrated three or more signals for both chromosomes 7 and 17 in 21% of the nuclei, while no signal for chromosome Y was detected in 41% of nuclei (Fig. 2b). Discussion Papillary RCC was first recognized as an independent entity based on its particular morphology characterized Fig. 1. Small solid neoplasm (a) composed of large cells with dense eosinophilic cytoplasm and Fuhrman grade 3 nuclei, arranged mainly in papillary structures with delicate fibrovascular stalks (b). Fig. 2. Strong and diffuse AMACR immunoexpression in neoplastic cells (a); FISH showing three or more signals for both chromosomes 7 and 17 in neoplastic nuclei (b).

16 100 E. Munari et al. Tab. I. Case series of oncocytic papillary RCCs treated with nephrectomy or partial nephrectomy/enucleation reported in the literature. Author No. of cases Median age (years) Median tumour size (mm) Nephrectomy Partial Nephrectomy/ Enucleation (%) Lefévre et al (0) Hes et al (0) kunju et al (71) Masuzawa et al (0) Park et al (71) Okada et al (0) Ürge et al (42) Total (30) by a papillary architecture 2. It was then divided into two types based on morphological characteristics and clinical behaviour: type 1 with small cells and low nuclear grade (grade 1-2), and type 2 composed of large cells with a higher nuclear grade (grade 3-4) 8. The clinical utility of dividing papillary RCCs into 2 types according to histological characteristics was demonstrated to have prognostic significance 8. Here we described a case of oncocytic papillary RCC, a neoplasm characterized by oncocytic cells arranged in a papillary pattern with a specific immunophenotypic and cytogenetic profile. Oncocytic papillary RCC have been discussed in terms of morphological characteristics and immunophenotype in different studies with particular attention to the features that distinguish it from renal oncocytoma. The distinction between renal oncocytoma and oncocytic papillary RCC is of primary importance because of their different clinical behaviour and prognosis, as the latter has malignant potential 4. The case described here showed morphology characterized by a population of large cells with eosinophilic cytoplasm and Fuhrman grade 3 nuclei arranged mainly in papillary structures with delicate fibrovascular stalks. Areas of oncocytic cells arranged in a solid pattern were also present, and a diagnosis of oncocytic renal cell neoplasm was made during intraoperative consultation. In differential diagnosis, all renal neoplasms with granular cytoplasm must be considered, i.e., renal oncocytoma, chromophobe RCC, clear cell RCC with extensive granular areas, oncocytoid RCC after neuroblastoma and oncocytoma-like angiomyolipoma. The tumour in the pres- ent case differs from chromophobe RCC and clear cell RCC for the presence of papillary areas. The most difficult differential diagnosis is renal oncocytoma because of the oncocytic features of cells. Moreover, oncocytoma can show papillary foci; similarly, papillary neoplasms may show extensive areas of solid components. Thus, differential diagnosis based solely on morphology can be extremely difficult. In these cases, the use of an immunohistochemical panel including racemase, CD10 and parvalbumin can be very useful 9. However, the specificity of some of these antibodies is limited. In particular, racemase has been described in 15% of renal oncocytoma and parvalbumin, a marker present in 70% of renal oncocytomas, has been reported to be positive in some cases 9. On definitive diagnosis, immunohistochemistry demonstrated that cells stained for AMACR and CD10, while immunostaining for parvalbumin was negative. The numerical abnormalities on chromosomes 7 and 17 and loss of chromosome Y are specific for papillary RCC, but not for oncocytoma; we found the presence of three or more signals for chromosomes 7, 17 and the loss of chromosome Y. Considering the above-mentioned features, a diagnosis of oncocytic papillary RCC was made. Although the available evidence supports tumour enucleation or partial nephrectomy as the standard surgical treatment for renal cortical tumours 4 cm 10, including oncocytic papillary RCC (Tab. I), it should be kept in mind that these latter tumours rarely develop metastases 4. Due to aforementioned clinicopathological features, these tumours must be diagnosed with appropriate immunophenotypical and cytogenentic analyses. References 1 Eble JN, Sauter G, Epstein JI, et al. WHO: Tumours of the Urinary System and Male Genital Organs. Lyon: IARC Press Delahunt B, Eble JN. Papillary renal cell carcinoma: a clinicopathologic and immunohistochemical study of 105 tumors. Mod Pathol 1997;10: Brunelli M, Eble JN, Zhang S, et al. Gains of chromosomes 7, 17, 12, 16, and 20 and loss of Y occur early in the evolution of papillary renal cell neoplasia: a fluorescent in situ hybridization study. Mod Pathol 2003;16: Hes O, Brunelli M, Michal M, et al. Oncocytic papillary renal cell carcinoma: a clinicopathologic, immunohistochemical, ultrastructural, and interphase cytogenetic study of 12 cases. Ann Diagn Pathol 2006;10: Urge T, Hes O, Ferda J, et al. Typical signs of oncocytic papillary renal cell carcinoma in everyday clinical praxis. World J Urol 2010;28: Trpkov K, Yilmaz A, Uzer D, et al. Renal oncocytoma revisited: a clinicopathological study of 109 cases with emphasis on problematic diagnostic features. Histopathology 2010;57: Russo P, Goetzl M, Simmons R, et al. Partial nephrectomy: the rationale for expanding the indications. Ann Surg Oncol 2002;9: Delahunt B, Eble JN, McCredie MR, et al. Morphologic typing of papillary renal cell carcinoma: comparison of growth kinetics and patient survival in 66 cases. Hum Pathol 2001;32: Martignoni G, Brunelli M, Gobbo S, et al. Role of molecular markers in diagnosis and prognosis of renal cell carcinoma. Anal Quant Cytol Histol 2007;29: Thompson RH, Kurta JM, Kaag M, et al. Tumor size is associated with malignant potential in renal cell carcinoma cases. J Urol 2009;181:

17 pathologica 2012;104: Case report Clear cell papillary renal cell carcinoma with characteristic morphology and immunohistochemical staining pattern S.M. Gilani, R. Tashjian, H. Qu Department of Pathology, St. John Hospital & Medical Center, Detroit MI, USA Key words Renal cell carcinoma Clear cell papillary type Classification Immunohistochemical staining Cytokeratin 7 Summary Clear cell papillary renal cell carcinoma is newly-defined entity initially believed to be associated with end stage renal disease. We report a rare case of this neoplasm in a 70-year-old female patient with no known history of end-stage renal disease who presented with haematuria lasting several days. After initial workup, a computed tomography (CT) scan was performed and revealed a cystic mass in the right kidney. Material obtained by fine needle aspiration (FNA) biopsy of the mass was felt to be suspicious for renal cell carcinoma. The patient subsequently underwent right nephrectomy, and the lesional tissue was examined microscopically. A 2.3 cm in greatest dimension cystic space circumscribed by a fibrous wall was surfaced by a single layer of bland cuboidal cells with abundant clear cytoplasm. The solid component of the tumour consisted of branching papillae with delicate fibrovascular cores and uniformly lined by cells similar to those of the inner wall of the cyst. Some of the fibrovascular cores were markedly expanded by a myxoid-appearing substance, but no foamy cells were appreciated. Immunohistochemically, the neoplastic cells were diffusely immunoreactive with cytokeratin 7 (CK7), epithelial membrane antigen (EMA), high molecular weight cytokeratin (HMWCK) and vimentin. Neoplastic cells were only focally immunoreactive with CD10, and were negative for both p63 and α-methylacyl-coa racemase (AMACR) (P504S). The cytomorphological features and immunohistochemical staining pattern of this tumour was consistent with that of clear cell papillary renal cell carcinoma (CCPRCC), as described by Gobbo et al. Introduction Clear cell papillary renal cell carcinoma (CCPRCC) is a rare, newly-defined entity with very few reported cases in the English language literature. Typically, CCPRCC is associated with end stage renal disease (ESRD) and should be distinguished from the other variants of renal cell carcinoma. We report a unique case of CCPRCC appearing in a patient with no known history of ESRD. Case report A 70-year-old female with a past medical history significant for colon cancer, hypertension and coronary artery disease presented with the history of haematuria lasting several days. After initial workup, a computed tomography (CT) scan demonstrated a partially-calcified cystic mass in the right kidney. The patient underwent CTguided fine needle aspiration (FNA) biopsy of the lesion, which showed atypical cells suspicious for, but not diagnostic of, renal cell carcinoma. The subsequent laparoscopic total nephrectomy specimen weighed 771 grams. Serial sectioning of the specimen revealed multiple 1.0 to 8.5 cm in the greatest dimension cystic foci, the majority of which were lined by a pale-tan to grey, smooth inner surface. However, a 2.3 cm in greatest dimension cavity in the mid-portion of the kidney contained a red-tan, solid focus that projected from the fibrous cyst wall. Microscopic examination of this focus revealed a neoplasm with branching papillae and well-formed fibrovascular cores. The papillae were uniformly lined by a single layer of bland cuboidal cells with abundant, clear cytoplasm (Figs. 1-2). Some of the papillae were markedly expanded by a myxoid-appearing substance, but no foamy cells were identified. The inner lining of the cyst was composed of neoplastic cells with features similar to those lining the papillae. Immunohistochemically, the neoplastic cells were diffusely immunoreactive with cytokeratin 7 (Fig. 3), epithelial membrane antigen (EMA), high Correspondence Syed M. Gilani, St. John Hospital & Medical Center, Detroit, MI Fax

18 102 S.M. Gilani et al. Fig. 1. Low-power view of neoplastic cells within the cystic cavity. (H&E, Original magnification x40). Fig. 3. Branching papillae with fibrovascular cores. (H&E, Original magnification x200). Fig. 2. Histological features of clear cell papillary renal cell carcinoma. The papillae are uniformly lined by a single layer of bland cuboidal cells with abundant clear cytoplasm. (H&E, Original magnification x100). Fig. 4. Immunohistochemical features of clear cell papillary renal cell carcinoma. Neoplastic cells diffusely immunoreactive for cytokeratin 7. (Original magnification x100). molecular weight cytokeratin (HMWCK) and vimentin. The same cells were only focally immunoreactive with CD10 and were negative for both p63 and α-methylacyl- CoA racemase (AMACR) (P504S). Based upon the cytomorphological features and immunohistochemical staining pattern, a diagnosis of clear cell papillary renal cell carcinoma (CCPRCC) was rendered. Recent studies have demonstrated that conventional clear cell renal cell carcinoma, papillary renal cell carcinoma, renal cell carcinoma with Xp11.2 translocation and clear cell papillary renal cell carcinoma are distinct entities, each with characteristic morphology, immunohistochemical staining profile and cytogenetic characteristics. Discussion Several variants of renal cell carcinoma have been described in the literature. The criteria for classification of renal epithelial neoplasia are based on the histological, immunohistochemical and cytogenetic characteristics of the neoplasm in question. In the past, classification of renal cell carcinomas with both papillary architecture and clear cell features had presented a diagnostic challenge. However, a new entity designated as clear cell papillary renal cell carcinoma (CCPRCC) has recently been described by Gobbo et al. 1, allowing for better categorization of such lesions. This variant of renal cell carcinoma has distinctive histological and immunohistochemical features and should not be mistaken for either clear cell renal carcinoma or papillary renal cell carcinoma. Some investigators have postulated an association between CCPRCC and end-stage renal disease (ESRD) 2. Clear cell papillary renal cell carcinoma is a low stage and low Fuhrman grade neoplasm with distinct histological features. Microscopically, these predominantly cystic neoplasms are surrounded by a fibrous stroma with branching papillae containing well-formed fibro-

19 Clear Cell Papillary Renal Cell Carcinoma 103 vascular cores. These papillae are lined by small- to intermediate-sized neoplastic epithelial cells with abundant clear cytoplasm. Nuclei tend to be small, round, and polarized towards the luminal aspect of the cells. The chromatin pattern corresponds to a low Fuhrman nuclear grade (Fuhrman grades 1 or 2). Foamy macrophages are not identified, a key feature that distinguished CCPRCC from papillary renal cell carcinoma. Necrosis is typically not present, and there is minimal to no mitotic activity. The immunohistochemical staining patterns show positive immunoreactivity with cytokeratin 7 (CK7) and carbonic anhydrase 9 (CA IX). CD10, α-methylacyl-coa racemase (AMACR) (P504S), translocation factor E3 (TFE3), and translocation factor EB (TFEB) 3 are generally negative. Based on the limited data, it is suggested that this tumour has low potential for malignancy 3. Cytogenetic analysis is increasingly being utilized to aid in the differentiation between variants of renal cell carcinoma. Each of the most common histologic subtypes harbours specific recurrent genetic abnormalities, such as deletion of 3p in conventional clear cell renal cell carcinoma and trisomies 7 and 17 in papillary renal cell carcinoma 4. Several genetic mutations associated with 3p deletions have been described for clear cell renal cell carcinomas. Furthermore, Rohan et al. emphasized the role of hypoxia-inducible factor (HIF-1α) pathway in the pathogenesis of CCPRCC 5. Renal cell carcinomas with Xp11.2 translocation have also shown multiple genetic alterations involving the Transcription Factor E3 (TFE3) gene on Xp11.2 and various other fusion partners. The differential diagnosis of CCPRCC includes conventional clear cell renal cell carcinoma, papillary renal cell carcinoma, cystic clear cell carcinoma and renal cell carcinoma with Xp11.2 translocation. Neoplastic cells found in conventional clear cell renal cell carcinoma are typically immunoreactive for CD10 and AMACR (P504S), but not for CK7. A VHL gene mutation has been detected in conventional clear cell renal cell carcinoma, but not in CCPRCC 6. Papillary renal cell carcinoma can be distinguished from CCPRCC based on immunohistochemical staining patterns. The former is immunoreactive for CK7, CD10, and AMACR (P504S) and not for CA IX 7. The presence of clear cells in papillary renal cell carcinoma is associated with more aggressive lesions and a poorer prognosis 8. Renal cell carcinoma with Xp11.2 translocation is a rare entity and predominantly reported in children and young adults 9. They are positive for CD10 and TFE3. Based on recent studies, it has been postulated that conventional clear cell renal cell carcinoma, papillary renal cell carcinoma, CCPRCC and renal cell carcinoma with Xp11.2 translocation are four discrete entities 10, each with distinct cytomorphological, immunohistochemical (Tab. I) and cytogenetic characteristics. In our patient, a few months of postoperative follow-up showed that the symptoms were markedly diminished and there were no post-operative complications. CCPRCC is a unique entity with distinct cytomorphological, immunohistochemical and cytogenetic characteristics. It is critical to recognize and accurately diagnose CCPRCC because of its tendency to mimic other subtypes of renal cell carcinoma, especially in borderline neoplasms that possess both papillary architecture and clear cell histology. Definitive pathological diagnosis depends on the collective interpretation of histopathological findings, immunohistochemical staining pattern and cytogenetic analysis. Surgical resection is the mainstay of treatment. Tab. I. Differential diagnosis of clear cell papillary renal cell carcinoma. Histopathologic findings Immunostaining Prognosis RCC, Conventional Clear Cell Type Papillary RCC with Clear Cell Features Multiple architectural patterns with network of small, thin-walled vessels. Neoplastic cells with abundant clear cytoplasm filled with lipid and glycogen Malignant epithelial cells forming papillae and tubules. Papillae contain fibrovascular cores, aggregates of foamy macrophages, and cholesterol crystals. Positive for CD10, AMACR, Usually negative for CK7. Positive for CK7 and AMACR Tumour stage is the most important prognostic feature. Nuclear grade is the second most important prognostic feature. Five-year survival depends on tumour grade, stage and presence of sarcomatoid dedifferentiation (Type I tumours have longer survival than Type II tumours). RCC, Xp11.2 Translocation Malignant epithelial cells with clear to eosinophilic, granular cytoplasm forming papillae or arranged in a nested pattern. Positive for CD10, AMACR and TEF3 Usually present at an advanced stage. Poor prognosis in adults. AMACR = Alpha-Methylacyl-CoA Racemase, TEF3 = Transcription Factor E3.

20 104 S.M. Gilani et al. References 1 Gobbo S, Eble JN, Maclennan GT, et al. Renal cell carcinomas with papillary architecture and clear cell components: the utility of immunohistochemical and cytogenetical analyses in differential diagnosis. Am J Surg Pathol 2008; 32: Tickoo SK, deperalta-venturina MN, Harik LR, et al. Spectrum of epithelial neoplasms in end-stage renal disease: an experience from 66 tumor-bearing kidneys with emphasis on histologic patterns distinct from those in sporadic adult renal neoplasia. Am J Surg Pathol 2006;30: Adam J, Couturier J, Molinié V, et al. Clear-cell papillary renal cell carcinoma: 24 cases of a distinct low-grade renal tumor and a comparative genomic hybridization array study of seven cases. Histopathology 2011; 58: Hagenkord JM, Gatalica Z, Jonasch E, et al. Clinical genomics of renal epithelial tumors. Cancer Genet 2004;204: Rohan SM, Xiao Y, Liang Y, et al. Clear-cell papillary renal cell carcinoma: molecular and immunohistochemical analysis with emphasis on the von Hippel-Lindau gene and hypoxia-inducible factor pathway-related proteins. Mod Pathol 2011;24: Kuroda N, Shiotsu T, Kawada C, et al. Clear cell papillary renal cell carcinoma and clear cell renal cell carcinoma arising in acquired cystic disease of the kidney: an immunohistochemical and genetic study. Ann Diagn Pathol 2011;15: Molinié V, Balaton A, Rotman S, et al. Alpha-methyl CoA racemase expression in renal cell carcinomas. Hum Pathol 2006;37: Klatte T, Said JW, Seligson DB, et al. Pathological, immunohistochemical and cytogenetic features of papillary renal cell carcinoma with clear cell features. J Urol 2011;185: Armah HB, Parwani AV. Xp11.2 translocation renal cell carcinoma. Arch Pathol Lab Med 2010;134: Kato H, Kanematsu M, Yokoi S, et al. Renal cell carcinoma associated with Xp11.2 translocation/tfe3 gene fusion: radiological findings mimicking papillary subtype. J Magn Reson Imaging 2011;33:

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